Dr. Ross is assistant professor of psychiatry and director of the Division of Alcoholism and Drug Abuse at Bellevue Hospital, and associate director for education at New York University School of Medicine in New York City.

Disclosures: Dr. Ross reports no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Stephen Ross, MD, 104 E 40th St, Suite 802, New York, NY, 10016; Tel: 212-562-4097; Fax: 212-562-2041; E-mail: stephen.ross@nyumc.org.

 

 
 

Abstract

Ketamine is a schedule III drug with a well-established safety profile that has been used extensively as an anesthetic for close to 4 decades. It has long been described as a drug of abuse and has become known as one of the “club drugs,” used by adolescents and young adults in rave and circuit party settings. Ketamine is a congener of phencyclidine and acts as a noncompetitive N-methyl-d-aspartate (NMDA) antagonist. Through a complicated and not completely understood process, NMDA antagonism increases dopamine levels in reward-related areas such as the ventral tegmental area and the nucleus accumbens. In addition to its addictive liability, there is also evidence to suggest that ketamine might have anti-addictive properties when used as an adjunct to psychotherapy that takes advantage of its ability to produce spiritually oriented altered states of consciousness. This technique has been applied to patients with alcohol and opiate use disorders. Ketamine’s potential anti-addictive properties can be understood by looking at biologic and psycho-spiritual models.

 

Introduction

Ketamine is a commonly used, safe, effective and well-known anesthetic agent that has been available as a schedule III agent for close to 4 decades. It has been known as a drug of abuse since its discovery and introduction as a medicine and has most recently become associated as a “club drug” used primarily by adolescents, young adults, and gay men at “raves” and “circuit parties.”1 It is primarily thought of as a drug of abuse; however, it is also starting to find its way into the pharmacopoeia of agents used to treat addictive disorders by taking advantage of its ability to be used as an adjunct to psychotherapy, where its ability to produce psychedelic and spiritual states of consciousness has been successfully applied to induce sobriety in addicted individuals, mostly in Russia.2 It is worth trying to understand this contradictory phenomenon. This can be addressed by looking at biologic and psycho-spiritual etiologic models. This article includes a brief historic review of research and use of ketamine for a variety of medical and psychiatric conditions, addictive liability of ketamine including biologic mechanisms, and potential anti-addictive properties of ketamine with an exploration of biologic and psycho-spiritual mechanisms of action.

 

History of Research and Current Use Practices of Ketamine

Ketamine was synthesized by the American chemist Calvin Stevens in 1962 at the University of Michigan for use as a novel anesthetic agent after phencyclidine (PCP) was discovered to be too psychotigenic when used as an anesthetic.1 In 1965, Domino coined the term “dissociative anesthetic”3 to describe its properties of disconnecting mind from body unlike conventional anesthetics that completely suppressed consciousness. It was patented in 1966 by Parke-Davis and in 1970 the Food and Drug Administration approved its use for anesthesia in children, adults, and the elderly. Since then, it has been used extensively for this purpose as a result of the properties of rapid onset, rapid patient recovery, and its ability to suppress conscious experience without altering respiratory and circulatory functioning. It has a well-established biologic safety profile based on >7,000 published reports. There is some evidence it may prevent neurotoxicity from strokes, head trauma, and seizures, likely a result of its antagonist properties at the N-methyl-d-aspartate (NMDA) receptor.2 In addition, there is no evidence of long-term neurotoxicity or prolonged adverse psychological effects when used in controlled environments.4-7

In the 1970s and 1980s, ketamine was used and studied as an adjunct to psychotherapy in patients with depressive, anxiety, and psychosomatic spectrum disorders with anecdotal reports suggesting an effect on reducing symptom distress.8-10 Current research with ketamine has strongly suggested a role in treating refractory pain syndromes such as complex regional pain syndrome,11-13 and breakthrough pain in chronic pain syndromes such as that related to advanced cancer.14 Krystal15 has successfully used ketamine as a research tool for over a decade in normal volunteers and schizophrenics to explore the NMDA antagonist hypothesis of schizophrenia. As a serendipitous finding in Krystal’s research, subjects reported acute reductions in depressive symptomatology after ketamine administration.16 This laid the foundation for subsequent work by several investigators where ketamine was found to be the first known agent to effect acute antidepressant properties in patients with major depressive disorder (MDD) in randomized, placebo-controlled trials.17-19 Further research into this effect is actively being pursued at several centers in the country.

 

Addictive Liability

Illicit use and abuse of ketamine started soon after its introduction in 1970. Soldiers returning from Vietnam who received ketamine as an anesthetic reported vivid hallucinogenic experiences. It became linked with “intellectual hedonism” in the 1970s and 1980s, particularly in the United States, and the first reports of abuse by healthcare workers began to appear.20 Over the past decade, an increase in non-medical use of ketamine in Australia, Great Britain, Sweden, and the US (particularly in New York City) has been reported, with diversion from veterinary supplies a major source of obtaining the drug.1,21 There are two main groups of users, namely those who use in a solitary fashion seeking transcendental, psychedelic experiences and seeking spiritual growth, and those who use ketamine as a ‘“club drug” as part of the rave and circuit party scene. It is difficult to establish the true prevalence of ketamine use disorders as the users remain a mostly hidden group. One study21 in Britain reported that close to 30% of club-goers surveyed reported a lifetime use of ketamine. Another survey22 of mostly gay, Caucasian men who attended a “circuit party” in the New York City area in 1998 found that 86% of the 173 subjects reported drug or alcohol use at the party with ketamine being the second most common drug used (53%) after methylenedioxymethamphetamine (“ecstasy”; 71%). Several converging pieces of data point to ketamine having real addictive liability. These include positron emission tomography studies demonstrating that ketamine leads to increases in dopamine in the ventral tegmental area (VTA) in humans correlating with elevated mood23; ketamine induces increases in dopamine in the nucleus accumbens in humans24; ketamine induces self-administration in animal models25,26; repeated ketamine administration causes behavioral tolerance in animals27,28 and humans21; and heavy, habitual use of ketamine has been described in humans, including in anesthesiologists.29,30

Understanding ketamine’s addictive properties involves considering its mechanism of action. Ketamine is an arylcyclohexylamine and is part of the class of dissociative anesthetics, which also includes PCP (“angel dust”) and dextromethorphan. Its main receptor action is antagonism at the NMDA glutamate receptor complex at the same site as PCP, located inside the calcium channel leading to blockade of calcium influx through the channel.31 This action underlies its analgesic, dissociative, psychotigenic, psycho-spiritual, and neuroprotective properties. Ketamine mainly acts at the pre-frontal cortex (PFC) and limbic system, with the highest density of NMDA receptors being in the PFC and hippocampus.32 Alcohol, as one of its several mechanisms of action, also antagonizes the NMDA receptor, and ketamine produces alcohol-like subjective effects in humans.33 In addition, ketamine has opioidergic effects (mu and sigma opiate agonism)16 contributing to its analgesic properties and stimulant-like properties by enhancing monoaminergic transmission (dopamine, norepinephrine, serotonin) through inhibition of re-uptake pumps.34 The above effects have led some to describe ketamine’s subjective state as “alcohol-like intoxication, cocaine-like stimulation, opiate-like calming, and cannabis-like imagery.”35

Next, it is first important to look at the biologic underpinning of the addicted state. Two effects that likely contribute significantly to the addicted state are changes in midbrain dopamine as well as PFC dopamine and glutamate function. Damage to the dopamine system leads to decreased dopamine receptor density and release in the nucleus accumbens and PFC, diminishing the ability of dopamine to signal novel salient events, leading to under-excitability to biologically relevant stimuli.36,37 As addiction progresses, the neurocircuity of the reward pathway becomes corrupted, re-organized, and dysregulated whereby the behavioral system changes from a dopamine-oriented one in the nucleus accumbens (involved in the acute high and the initiation of learning and conditioned responses) to a glutamate-based system in the PFC (especially the anterior cingulate and orbitofrontal cortex) marked by altered glutamatergic transmission in projections from the PFC to the nucleus accumbens.38 Specifically, the system becomes hyperexcitable to drug-conditioned cues and under-excitable to biologically oriented ones. As part of these dopaminergic and glutamatergic changes, pharmacotherapy development of anti-addictive agents is currently focusing on agents that can strengthen the saliency of natural reinforcers, such as enhancing dopamine function, and agents that can alter the dysfunctional response to conditioned cues (either drug related or biologically relevant) by altering glutamatergic transmission.

Along the lines of hyperglutamatergic states being associated with addiction, it is key to consider that subanesthetic doses of NMDA antagonists (ie, ketamine) may actually enhance glutamatergic transmission by disinhibiting glutamate release, shunting glutamate to the other glutamatergic receptors other than NMDA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid [AMPA], kainite, and the metabotropic G protein coupled glutamate receptor) and causing a hyperglutamatergic state.15 One may ask how this is possible and what is its significance. There is some evidence to suggest that NMDA receptor blockers may antagonize γ-aminobutyric acid (GABA) neurons with a greater potency than their inhibition at the NMDA receptor. The NMDA antagonism may therefore diminish activation of GABA inhibitory neurons, with a diminution of cortical extracellular GABA levels,39 which in turn would decrease GABA’s normal inhibition of glutamate neurons, causing a net disinhibition of glutamate neurons and an increase in glutamatergic transmission in non-NMDA glutamate receptors.40 In turn, cortical glutamatergic activation stimulates monoaminergic terminals within the cortex, limbic system, midbrain, and brainstem.15 As part of this, extracellular dopamine levels are increased in reward-related areas (ie, VTA and nucleus accumbens) thereby likely explaining ketamine’s addictive liability. Given this, one can ask how we can understand a possible explanation—biologic or otherwise—for ketamine’s putative anti-addictive properties.

 

Anti-Addictive Properties

Brief History of the Use of Hallucinogens to Treat Addictive Disorders

Ketamine is not the first psychedelic agent to be tested to treat addictive disorders. In the 1950s and 1960s, serotonergic hallucinogens (predominantly d-lysergic acid diethylamide [LSD]; “acid”) were applied to patients with addictive disorders, mostly alcohol dependence and to a lesser degree opiate dependence. The most prominent researcher who studied this application was Humphrey Osmond, MD. He, in conjunction with Abram Hoffer, MD,41 treated >1,000 alcoholics using high-dose LSD. Their initial mechanistic hypothesis was based on aversive counterconditioning where they likened the intense LSD experience to the frightening altered state seen in the delirium tremens, which, in their experience, often served as a transformative, near-death (“bottoming out”) state that led to a sober conversion. However, soon after treating alcoholic patients with LSD in highly controlled environments paying careful attention to set and setting, they changed to a more positivist paradigm where they described that such agents had the capacity to produce a transcendental feeling of unity with the world, personal insights, self-understanding, increased sense of responsibility to self and others, and spiritual enlightenment.41 They reported high success rates including improved rates of abstinence, but the research was methodologically flawed with no randomization, no placebo controls, lack of blind raters, the use of unsophisticated severity measures, inadequate diagnostic specificity, inclusion of co-occurring psychiatric and substance use disorders (SUDs) other than alcohol, inadequate informed consent, and inadequate follow up.

Other studies looking at LSDs effect in alcoholism varied widely from astonishingly positive results to worsening of the alcoholism, depending on the design of the study and the set and setting. Unfortunately, almost all studies were methodologically flawed, leaving others unable to determine what if any effect might have existed.42 However, this has laid the groundwork for current studies using these and similar agents (ie, ketamine) to determine if there is a true treatment efficacy signal. The correct methodology would have to include randomization, placebo control, use of specific diagnoses using validated measures (ie, Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition), inclusion of severity measures, standardized psychotherapy dose, objective “blind” raters, and having adequate follow up.43

 

Current Use of Ketamine to Treat Addictive Disorders   

The first psychiatrist to rigorously study the potential of ketamine to treat addictive disorders was Evgeny Krupitsky, MD, PhD. In 1985, he developed a technique using ketamine—ketamine psychedelic psychotherapy (KPT)—to treat patients with alcohol use disorders.2 Similar to Osmond, he first conceptualized an aversive counter-conditioning model utilizing preparation and suggestion in combination with the altered state of consciousness induced by ketamine to induce and amplify a negative psychological state paired with the continued negative consequences of alcoholism. It is worth considering a model of a pharmacologically initiated, precipitated or enhanced “hitting of rock bottom.” In the addiction field, we often hear the adage of needing to hit “rock bottom” before the initiation of sobriety. This event may be similar to near-death experiences, which have been described as triggering transformative and positive life changes,44 and may serve to initiate a rapid change to a sober state. In Alcoholics Anonymous (AA), it is taught that this is what is needed before the individual can really get sober. Although this may be true for some, “rock bottom” for other addicts may be death. Rather than disengaging from the patient and waiting for this to happen, one may wonder if it could be possible to chemically induce or enhance this phenomenon, thereby speeding up the process to recovery initiation.

From an adverse psychiatric perspective, ketamine can induce frank psychotic states (with both positive and negative symptoms), dissociation, and cognitive impairment (including impaired attention, memory, and performance).21 However, this does not capture the phenomenology of the profound psychological, mystical, and spiritually oriented altered state of consciousness induced by ketamine. It is useful to define what is meant by “spirituality,” a broad construct that encompasses both faith and meaning.45,46 Faith can be defined as the belief in and relationship with a transcendent higher power, which does not have to be identified as “God” and does not have to occur through participation in traditional organized religion, while meaning can include feeling that one has a unique purpose in life and can achieve a sense of fulfillment and “even transcendence through connectedness with something greater than one’s self.”47 The spiritual types of experiences induced by ketamine, separate from its dissociative properties (ie, out of body experiences) and perhaps overlapping with and traditionally understood as psychotic phenomenon, can include feelings of ego dissolution and loss of identity; experience of psychological death and re-birth; emotionally intense visions and dream-like states; enhanced insight/self-reflection and meaning in life; and feelings of unity with humanity, nature, the universe and God.2 These effects led Krupitsky to change his model from an aversive one to an existential, spiritual model within a positivist framework with the goal of inducing peak/transcendental states to effect conversion to a sober state in addicted patients. He extended his research to include patients with opiate addiction, and from 1985 until 2002 treated >1,000 patients with addictive disorders using KPT.2 KPT includes three stages, namely, preparation, administration, and integration. The preparatory phase includes 5–10 hours of suggestive psychotherapy where the patient is told the ketamine experience may induce important insights related to personal problems, value systems, and the meaning of their lives and that these insights may lead to changes associated with sobriety. During administration, the patients receive 2–2.5 mg/kg intramuscular (IM) of ketamine with onset of action in 10 minutes and the duration of the experience lasting approximately 1 hour. Patients are told they will enter an altered state and to surrender to the experience. They lie supine with eyeshades and headphones, hearing pre-selected music. In the integration phase, a combination of individual and group psychotherapy is administered over time to help subjects interpret and integrate the ketamine experience with the goal of leveraging the experience to effect behavioral changes associated with abstinence. The therapist assists in the integration of the spiritual transformation.2

In a controlled trial48 of patients with alcohol dependence, a one-time dose of ketamine as part of KPT (added to standard psychosocial care for patients with alcohol dependence in Krupitsky’s treatment center) added considerable benefit to the standard treatment. Total abstinence from alcohol for >1 year was reported in approximately 66% (73 out of 111) of alcoholic subjects in the KPT group compared to 24% (24 out of 100) in the conventional treatment control group (P<.01). In addition, based on psychological measures administered in the study, the group receiving KPT had positive changes in their emotions and perception of themselves and others, positive changes in life values and purposes, important insights into the meaning of life, and increased spiritual development compared to the placebo group. Krupitsky further tested the use of KPT in patients with heroin dependence in a double-blind placebo-controlled, randomized trial49 where 70 detoxified heroin-dependent subjects were randomly assigned to two groups—one with a one-time hallucinogenic dose of ketamine (2 mg/kg IM), versus one group with a control, non-hallucinogenic dose (0.2 mg/kg IM). All patients received the same standardized dose of psychotherapy during the preparatory and integration phases. The experimental group had significantly higher rates of abstinence at multiple prospective points in time out until 2 years follow-up, compared to the active placebo group (Table 1).49 As with the above alcohol studies, compared to the control group, the experimental group also displayed improvements in other dimensions of psychological well being including decreased levels of anxiety/depression, enhanced understanding of the meaning and purpose of life, and increased spiritual development. In this study,49 there were no significant adverse physiologic or psychological events and no subjects became addicted to ketamine.

 

 

In these studies, it is unclear as to the exact nature of the pharmacologic or psychosocial component of substance abuse treatment before receiving KPT and especially following the administration stage. For example, in the above study with heroin dependent subjects,49 the integration phase appears to only consist of 5 hours of psychotherapy “carried out within several days after the KPT session” to help “integrate the insights from the ketamine session into everyday life.”49 It is not clear as to exactly what this entails and how such a brief “existentially oriented psychotherapy” intervention could promote long-term abstinence up to 2 years follow up. The follow-up treatment is not described in any detail and it is unknown if these patients received standard evidence-based addiction pharmacologic treatments, such as naltrexone (opiate agonist or partial agonist treatment is banned in Russia), or psychosocial ones, such as motivational interviewing, relapse prevention, contingency management, community reinforcement, or coercion. Furthermore, this was described as a double-blind study. However, there is no description of the integrity of the blinding procedures in terms of any reporting of the percentage of accurate identification, by either subjects or experimenters, of whether the experimental or placebo dose of ketamine was administered. A complete hallucinogenic or psychedelic ketamine experience would seem easily discernible from one that is sub-hallucinogenic given the pronounced phenomenology of the experience. Without data on the blinding integrity, it is unknown how much of the treatment effect could be influenced by either subject or experimenter expectancy biases.

 

Potential Biologic Anti-addictive Mechanisms of Ketamine

Ketamine, Alcohol Dependence, and the NMDA Receptor
In addition to ketamine, there are other examples of NMDA antagonists that have been associated with anti-addictive effects in humans. One such example is memantine, although the studies have had small sample sizes and the efficacy data has been mixed. For example, in a study50 of frequent cocaine smokers, memantine failed to attenuate the subjective or reinforcing properties of cocaine use and was even associated with significant increases in the subjective effects of smoked cocaine. Regarding alcohol use in humans, memantine has been associated with a reduction in the level of alcohol craving preceding alcohol consumption in moderate drinkers but without diminishing the increase in craving following alcohol use.51

In a study52 of abstinent subjects with alcohol dependence, memantine diminished alcohol cue-induced craving in a dose-dependent manner. Finally, in a study53 of heroin dependent subjects, memantine was associated with modest reductions in the subjective but not reinforcing effects of heroin administration. It should be noted that memantine does not cause the pronounced altered states of consciousness seen with ketamine and so its anti-addictive properties can likely only be explained by its biologic mechanism. Other examples of anti-glutamatergic agents that have anti-addictive potential in humans include acamprosate (weak direct NMDA antagonism and direct interaction with the metabotropic glutamate receptor type 5, thereby indirectly acting as an inhibitory modulator at the NMDA receptor) for alcoholism,54 ibogaine (NMDA antagonism as one of its many receptor actions, although its exact anti-addictive mechanism remains unknown as 18-methoxycoronaridine, a congener of ibogaine, has anti-addictive properties without appreciably antagonizing the NMDA receptor) for opiate withdrawal,55 lamotrigine (a glutamate release inhibitor) for alcoholism,56 and topiramate (AMPA/kainite receptor inhibitor) for alcoholism.57

Regarding alcohol use disorders in particular, ketamine’s action as an NMDA antagonist might be helpful at various stages of the illness. For one, we know that neurotoxicity associated with alcohol withdrawal such as seizures and the delirium tremens, are likely mediated by hyperglutamatergic states from both upregulation at the NMDA receptor and increase glutamate release.58,59 Theoretically, it would make sense that administering an NMDA antagonist would suppress withdrawal by replacing the NMDA antagonist effect previously provided by alcohol, and acting like a replacement therapy. There is a growing literature to support the use of anti-glutamatergic agents to treat acute alcohol withdrawal.60 Protracted withdrawal is another stage of illness that might benefit from modulation at the NMDA receptor. Acamprosate is an example of a pharmacotherapy for alcoholism that weakly suppresses acute alcohol withdrawal in humans61 but seems more effective when given in the time period initially following the cessation of acute withdrawal.62

Another strategy in alcoholism pharmacotherapy is prevention of disease progression, such as preventing the expression of ethanol abuse or dependence in those at high risk (ie, strongly positive family history); preventing the transition from alcohol abuse (ie, heavy social drinkers) to alcohol dependence, or preventing relapse in newly abstinent patients. There is evidence to suggest that alcohol’s NMDA antagonist properties mediate negative physiologic, subjective, and cognitive effects associated with high-dose ethanol intoxication that would normally relay an inhibitory feedback signal to stop drinking.60 Furthermore, there is some evidence to suggest that healthy, at-risk individuals for alcoholism with positive family histories63 and alcoholics in early recovery64 demonstrate diminished sensitivity to biologic markers of heavy alcohol ingestion, which may constitute a deficit in the inhibitory feedback signal that would normally halt the progression to heavy drinking. Thus, an NMDA antagonist might theoretically be used to substitute, restore, or maintain the deficient inhibitory feedback signal.60 Ketamine administration to patients with alcohol dependence has been associated with pronounced cognitive impairment and sedation similar subjectively to heavy (ie, ≥8 standard drinks) alcohol ingestion and without causing craving for alcohol.65,66 Taken together, this suggests that the intoxicated state from ketamine’s NMDA antagonism might serve as an inhibitory feedback signal on drinking behavior in humans. This may serve as an aversive stimuli for preventing alcohol use disorders in vulnerable, at-risk populations; interrupting the transition from abuse to dependence; and preventing relapse in those in early recovery.

Ketamine, the NMDA Receptor, and Other Drugs of Abuse
Regarding the above data suggesting the efficacy of ketamine in an opiate-dependent patient population, it is worth considering ketamine’s action as a mu opiate agonist, even though its affinity for the receptor is only 20% compared to its affinity for the NMDA receptor.67 Furthermore, ketamine, like d-methadone (NMDA antagonist properties) can inhibit the development of opiate tolerance and dependence in animals.68 How this translates clinically in humans is unclear. It is possible that this effect might prevent the expression of opiate dependence in vulnerable individuals and those with opiate abuse. However, it is unclear how this might constitute an anti-addictive effect in actively using opiate-dependent patients or how a one-time dose of ketamine (as in the above-mentioned ketamine study in heroin addicts49 could lead to higher abstinence rates relative to placebo up to 2 years follow up.

To try and understand more broadly how ketamine might have anti-addictive properties, one possibility is to consider the level of the reward system activated. For example, NMDA antagonists are reinforcing when injected into the PFC and nucleus accumbens in lab animals but not the VTA where they block the rewarding effects of direct electrical stimulation.69 Thus, the relative degree and variability by which ketamine might be acting in the critical neuroanatomic reward substrates in a given individual might make the difference in determining its relative addictive liability. Another factor might relate to dose. It may be that there is an optimal dose range that confers anti-addictive properties and, above this, the addictive properties start to predominate. Those who become addicted to ketamine tend to continue to escalate their dose and in general use higher doses than those who use it intermittently (ie, occasional use for spiritual enhancement). It may be that higher doses of ketamine lead to a greater relative increase in glutamate transmission compared to lower doses and as stated previously enhanced cortical glutamatergic activation causes dopamine elevation in the VTA and nucleus accumbens, a property associated with addictive liability. One simplistic heuristic divide might be that antagonist effects at the NMDA receptor might confer the relative anti-addictive properties of ketamine and its hyperglutamatergic effects may confer its addictive liability. Thus, the relative balance or ratio of NMDA blockade to enhanced glutamate transmission (which may be a function of dose, route of administration, relative potency at the NMDA receptor, and pharmacokinetic/pharmacodynamic inter-individual variation) may explain why some NMDA antagonists are more reinforcing than others and why some may have greater anti-addictive properties.


Indirect Mechanism: Antidepressant Effects of Ketamine

Rather than a direct anti-addictive effect of ketamine on substance abuse behavior, it may be that ketamine indirectly diminishes addiction by its acute antidepressant properties. As described above, ketamine is emerging as a promising and novel treatment for depressive spectrum disorders.17-19 In the above study49 utilizing KPT in heroin-dependent patients, both high- and low-dose ketamine groups reported significant reductions in depressive symptomatology. There is some evidence to suggest that in patients with depression and co-occurring SUDs, improvements in depression with anti-depressant treatment can be associated with decreased substance abuse. For example, in a 12-week, placebo-controlled trial of imipramine treatment in a cohort of actively drinking patients with alcohol dependence and comorbid depression, McGrath and colleagues70 reported that although imipramine did not have a direct effect on drinking behavior, it was associated with a decrease in depressive symptoms, and the patients with improved mood demonstrated a more pronounced reduction in alcohol intake. In addition, it has been reported that elevated depressive symptoms in patients with heroin dependence may serve as a trigger for relapse in abstinent individuals.71 Further research would be necessary to discern if ketamine’s effects on addictive behavior is independent of its effects on depression.

 

Putative Psycho-Spiritual Anti-Addictive Mechanisms

Perhaps ketamine’s anti-addictive properties have little or nothing to do with its biologic properties and everything to do with its pronounced psychological and spiritual (psycho-spiritual) effects. Alternatively, it may be that its biologic reinforcing properties may be countered by anti-addictive psycho-spiritual effects.

In Krupitsky’s work he lists several psycho-spiritual effects, induced by ketamine’s altered state, that might underlie its anti-addictive properties including…

…important insights into existential problems and the meaning of life, transformation of one’s life value system, a change of view of one’s self and the world around, insight into life and death, enhancing personal growth and self-awareness, increase in creative activities, stabilizing positive psychological changes, broadening of spiritual horizons, and harmonization of a person’s relationship with the world and other people.2

Although this is highly speculative, several aspects here are worth exploring in some detail. For one, the added capacity for insight, self reflection, and learning as it relates to changing addictive behavior are important because these are factors we seek to change in addiction psychotherapy especially in addressing resistance and denial. Another potential factor relates to the phenomenon of ego dissolution or death and then re-birth. There are similarities to this substance-induced state and reports of “near death” experiences, which can be frightening but are usually marked by feelings of calm and peace; transcendent spiritual states are common in these experiences, with past memories often organized into a life review, including important figures from one’s past, and archetypal images of God often experienced as an “ocean of luminescent white light.”2 As mentioned above, these near-death experiences often trigger transformative and positive life changes.44 This death-re-birth experience in the context of enhanced spirituality has some parallels to the core treatment philosophy inherent in AA and other 12-step treatments whereby addicts undergo a spiritual conversion with a concomitant and rapid transformation in identity from an “addict” to one in “recovery.” In fact, Bill Wilson, one of the founders of AA, underwent several sessions of LSD psychotherapy in the 1950s and likened the experience to his spiritually redemptive experiences that led him to sobriety and to form AA.72 He felt so strongly about this, he attempted to introduce LSD use into the bylaws of AA, an attempt rejected by the board at the time. Predating this, both James and Jung recognized the importance of spiritual factors in treating addiction. James famously commented, “the best cure for dipsomania is religiomania” and Jung stated “Spiritus contra spiritum” (ie, spirituality combats alcoholism).72

The idea that spirituality can be a useful anti-addictive tool, as seen in AA, is worth considering in the two instances in the US where a particular religious group is legally allowed to use a schedule I serotonergic hallucinogen or sacrament—the use of peyote in the Native American Church (NAC) and the use of ayahuasca (dimethyltryptamine as the psychoactive compound) in the Brazilian syncretic religion, the Uniao do Vegetal (UDV). These religious groups have similarities to AA (although in AA the spiritual state is not drug induced), where spirituality is combined with social factors such as group cohesion and coercion to effect sobriety.73 There are anecdotal reports of low rates of addiction in the NAC and UDV, where substances (ie, alcohol, nicotine, illicit drugs), other than their respective sacramental hallucinogens, are prohibited.74 Formal epidemiologic study of the prevalence of substance use disorders in these two groups would be an important starting point. If the NAC and UDV were found to have significantly lower rates of addiction compared to the general population or some appropriate comparison group (ie, the NAC versus other Native American groups), one could then speculate on possible etiologies such as biologic effects of the prescribed sacramental hallucinogens; psychosocial factors, such as group cohort effects (ie, proscribed alcohol/drug abuse, cohesion, shared sober identity formation/maintenance, enhanced spiritual or religious affiliation); or some combination of factors.
It would be naïve to think that a one-time experience with ketamine, however profound, could effect long-term sobriety, especially without linkage to after-care and psychosocial treatment. For some addicts, a spiritual conversion experience can last a lifetime. However, for the vast majority, they need multiple repeated attempts included with 12-step treatment. Thus, it may be that repeated dosing is necessary, similar to an electroconvulsive therapy type model. Biologically, it would seem that if ketamine can truly have anti-addictive properties by optimally modulating or re-altering glutamatergic imbalance in the addicted state, it would need to be dosed repeatedly. It may be that in the use of ketamine to treat addictive disorders, multiple sessions are needed, especially for treatment refractory patients. There is some evidence to support this. In a randomized trial of 59 detoxified heroin dependent subjects, subjects who received three sessions of ketamine administration as part of KPT, at monthly intervals had higher abstinence rates at 1-year follow up compared to those who only had one initial ketamine experience, this amounting to 50% versus 22% (P<.05).75 It has been reported that after the use of certain hallucinogens (both serotonergic and NMDA antagonist types), there is a “psychedelic afterglow” inducing positive psychological changes that can last for days to weeks.76 It may be necessary to repeat the experience in a controlled carefully prepared environment to consolidate the new changes/learning. Furthermore, the dose of the experience needs to be sufficiently intense or of a “peak” quality to have a higher likelihood of effecting change. Prior and current research with serotonergic hallucinogens has shown a clear relationship between attaining “peak” or “transcendental mystical” states and resulting in positive and lasting changes.77,78

 

Conclusion

In the US, ketamine administration in humans has almost exclusively been used in psychiatric research as a psychopharmacologic probe to understand the neurobiology of psychiatric disorders, in particular the glutamate hypothesis of schizophrenia, and the effects of drugs of abuse, in particular alcohol. A unique aspect of ketamine, unlike all of the serotonergic hallucinogens, is that it is a schedule III drug, currently available for off-label purposes other than for anesthesia (Table 2). As such, it is currently available in the US for legal use in the treatment of addiction, pain syndromes, and MDD where its ability to induce immediate antidepressant effects seems most promising and may constitute a truly novel psychopharmacologic property.79 However, the data to support the use of ketamine to treat addictive disorders does not currently rise to the level of unequivocally justifying its use as off-label treatment in clinical settings. More research would be needed, ultimately with phase III trials, demonstrating a clear and sufficient treatment effect. Its use would be similar to the current use of g-hydroxybutyrate, another schedule III “club drug” with addictive liability but one with therapeutic utility—treatment of cataplexy associated with narcolepsy and other sleep disorders in this case.1 If the application of ketamine, in conjunction with addiction psychotherapy, turns out to be an effective and reliable treatment for SUDs, it would constitute a novel psychopharmacologic/psychosocial paradigm of care for addicted individuals, although one where the risks of addiction to the substance itself would have to be carefully considered. PP

 

 

 

 

References

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2.    Krupitsky E. Kolp E. Ketamine psychedelic psychotherapy. In: Winkelman MJ, Roberts TB, eds. Psychedelic Medicine: New Evidence for Hallucinogenic Substances as Treatments. Westport, CT: Greenwood Publishing Group, Inc.; 2007:67-85.
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4.    Siegal RK. Phencyclidine and ketamine intoxication: a study of four populations of recreational users. NIDA Res Monogr. 1978;21:119-147.
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6.    Carpenter WT. The schizophrenia ketamine challenge study debate. Biol Psychiatry. 1999;46(8):1081-1091.
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11. Kiefer R, Rohr P, Unertl K, Altemeyer K, Grothusen J, Schwartzman RJ. Recovery from intractable complex regional pain syndrome type I (RSD) under high dose intravenous ketamine-midazolam sedation. Neurology. 2002;58A:475.
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15. Krystal JH, D’Souza DC, Mathalon D, Perry E, Belger A, Hoffman R. NMDA receptor antagonist effects, cortical glutamatergic function, and schizophrenia: toward a paradigm shift in medication development. Psychopharmacology (Berl). 2003;169(3-4):215-233.
16. Krystal JH, Karper LP, Seibyl JP, et al. Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans: psychotomimetic, perceptual, cognitive, and neuroendocrine responses. Arch Gen Psychiatry. 1994;51(3):199-214.
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19. Valentine G, Mason GF, Krystal JH, Sanacora G. The acute effects of ketamine on mood and occipital cortex amino acid neurotransmitter content. Biol Psychiatry. 2007;61(suppl 1):233.
20. Jansen KL. A review of the nonmedical uses of ketamine: use, users, and consequences. J Psychoactive Drugs. 1993;32(4):419-433.
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22. Lee SJ, Galanter M, Dermatis H, McDowell D. Circuit parties and patterns of drug use in a subset of gay men. J Addict Dis. 2003;22(4):47-60.
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24. Smith GS, Schloesser R, Brodie JD, et al. Glutamate modulation of dopamine measured in vivo with positron emission tomography (PET) and 11C-raclopride in normal human subjects. Neuropsychopharmacology. 1998;18(1):18-25.
25. Beardsley PM, Balster RL. Behavioral dependence upon phencyclidine and ketamine in the rat. J Pharmacol Exp Ther. 1987;242(1):203-212.
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27. Leccese AP, Marquis KL, Mattia A, Moreton JE. The anticonvulsant and behavioral effects of phencyclidine and ketamine following chronic treatment in rats. Behav Brain Res. 1986;22(3):257-264.
28. Benthuysen JL, Hance AJ, Quam DD, Winters WD. Comparison of isomers of ketamine on catalepsy in the rat and electrical activity of the brain and behavior in the cat. Neuropharmacology. 1989;28(10):1003-1009.
29. Jansen KL. Ketamine: can chronic use impair memory. Int J Addict. 1990;25(2):133-139.
30. Moore NN, Bostwick JM. Ketamine dependence in anesthesia providers. Psychosomatics. 1999;40(4):356-359.
31. Hampton RY, Medzihradsky F, Woods JH, Dahlstrom PJ. Stereospecific binding of 3H-phencyclidine in brain membranes. Life Sci. 1982;30(25):2147-2154.
32. Kornhuber J, Mack-Burkhardt F, Kornhuber ME, Riederer P. MK-801 binding sites in post-mortem human frontal cortex. Eur J Pharmacol. 1989;162(3):483-490.
33. Krystal JH et al. Dose-related ethanol-like effects of the NMDA antagonist, ketamine, in recently detoxified alcoholics. Arch Gen Psychiatry. 1998;55(4):354-360.
34. Smith DJ, Azzaro AJ, Zaldivar SB, Palmer S, Lee HS. Properties of the optical isomers and metabolites of ketamine on the high affinity transport and catabolism of monoamines. Neuropharmacology. 1981;20(4):391-396.
35. Leary T, Sirius RU. Design for Dying. New York, NY: HarperCollins Publishers; 1998.
36. Volkow ND, Wang GJ, Fowler JS, et al. Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects. Nature. 1997;386(6627):830-833.
37. Martin-Soelch C, Chevalley AF, Künig G. Changes in reward-induced brain activation in opiate addicts. Eur J Neurosci. 2001;14(8):1360-1368.
38. Kalivas PW, Volkow ND. The neural basis of addiction: a pathology of motivation and choice. Am J Psychiatry. 2005;162(8):1403-1413.
39. Yonezawa Y, Kuroki T, Kawahara T, Tashiro N, Uchimura H. Involvement of gamma-aminobutyric acid neurotransmission in phencyclidine-induced dopamine release in the medial prefrontal cortex. Eur J Pharmacol. 1998;341(1):45-56.
40. Moghaddam B, Adams BW. Reversal of phencyclidine effects by a group II metabotropic glutamate receptor agonist in rats. Science. 1998;281(5381):1349-1352.
41. Hoffer A, Osmond H. New Hope For Alcoholics. New Hyde Park, NY: University Books; 1968.
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43. O’Brien CP, Jones RT. Methodological Issues In the evaluation of a medication for its potential benefits in enhancing psychotherapy. In: Pletscher A, Ladewig D, eds. Fifty Years of LSD: Current Status and Perspectives of Hallucinogens (A Symposium of the Swiss Academy of Medical Sciences). Nashville, TN: Parthenon Publishing; 1994.
44. Greyson B. Varieties of near-death experience. Psychiatry. 1993;56(4):390-399.
45. Karasu TB. Spiritual psychotherapy. Am J Psychother. 1999;53(2):143-162.
46. Brady MJ, Peterman AH, Fitchett G, Mo M, Cella D. A case of including spirituality in quality of life measurement in oncology. Psychooncology. 1999;8(5):417-428.
47. Breitbart W. Spirituality and meaning in supportive care: spirituality- and meaning-centered group psychotherapy interventions in advanced cancer. Support Care Cancer. 2002;10(4):272-280.
48.    Krupitsky EM, Grinenko AY. Ketamine psychedelic therapy (KPT): a review of the results of ten years of research. J Psychoactive Drugs. 1997;29(2):165-183.
49. Krupitsky E, Burakov A, Romanova T, Dunaevsky I, Strassman R, Grinenko A. Ketamine psychotherapy for heroin addiction: immediate effects and two-year follow-up. J Substance Abuse Treat. 2002;23(4):273-283.
50. Collins ED, Ward AS, McDowell DM, Foltin RW, Fischman MW. The effects of memantine on the subjective, reinforcing and cardiovascular effects of cocaine in humans. Behav Pharmacol. 1998;9(7):587-598.
51.    Bisaga A, Evans SM. Acute effects of memantine in combination with alcohol in moderate drinkers. Psychopharmacology (Berl). 2004;172(1):16-24.
52. Krupitsky EM, Neznanova O, Masalov D, et al. Effect of memantine on cue-induced alcohol craving in recovering alcohol-dependent patients. Am J Psychiatry. 2007;164(3):519-523.
53. Comer SD, Sullivan MA. Memantine produces modest reductions in heroin-induced subjective responses in human research volunteers. Psychopharmacology (Berl). 2007;193(2):235-245.
54. Littleton JM. Acamprosate in alcohol dependence: implications of a unique mechanism of action. J Addict Med. 2007;1(3):115-125.
55. Alper KR, Lotsof HS, Frenken GM, Luciano DJ, Bastiaans J. Treatment of acute opioid withdrawal with ibogaine. Am J Addict. 1999;8(3):234-242.
56. Krupitsky EM, Rudenko AA, Burakov AM. Antiglutamatergic strategies for ethanol detoxification: comparison with placebo and diazepam. Alcohol Clin Exp Res. 2007;31(4):604-611.
57. Johnson BA, Rosenthal N, Capece JA, et al. Topiramate for treating alcohol dependence: a randomized controlled trial. JAMA. 2007;10;298(14):1641-1651.
58. Hoffman PL, Rabe CS, Grant KA, Valverius P, Hudspith M, Tabakoff B. Ethanol and the NMDA receptor. Alcohol. 1990;7(3):229-231.
59. Tsai GE, Ragan P, Chang R, Chen S, Linnoila VM, Coyle JT. Increased glutamatergic neurotransmission and oxidative stress after alcohol withdrawal. Am J Psychiatry. 1998;155(6):726-732.
60.    Krystal JH, Petrakis IL, Krupitsky E, Schutz C, Trevisan L, D’Souza DC. NMDA receptor antagonism and the ethanol intoxication signal: from alcoholism risk to pharmacotherapy. Ann NY Acad Sci. 2003;1003:176-184.
61. Gual A, Lehert P. Acamprosate during and after acute alcohol withdrawal: a double-blind placebo-controlled study in Spain. Alcohol Alcohol. 2001;36(5):413-418.
62. Hopkins JS, Garbutt JC, Poole CL, West SL, Carey TS. Naltrexone and acamprosate: meta-analysis of two medical treatments for alcoholism. Alcohol Clin Exp Res. 2002;26(suppl):130.
63.    Petrakis IL, Limoncelli D, Gueorguieva R, et al. Altered NMDA glutamate receptor antagonist response in individuals with a family vulnerability to alcoholism. Am J Psychiatry. 2004;161(10):1776-1782.
64.    Krystal JH, Petrakis IL, Limoncelli D, et al. Altered NMDA glutamate receptor antagonist response in recovering ethanol dependent patients. Neuropsychopharmacology. 2003;28(11):2020-2028.
65. Krystal JH, Petrakis IL, Webb E, et al. Dose-related ethanol-like effects of the NMDA antagonist, ketamine, in recently detoxified alcoholics. Arch Gen Psychiatry. 1998;55(4):354-360.
66. Krupitsky EM, Burakov AM, Romanova TN. Attenuation of ketamine effects by nimodipine in recently detoxified ethanol dependent men: psychopharmacologic implications of the interaction of the NMDA and L-type calcium channel antagonists. Neuropsychopharmacology. 2001;25(6):936-947.
67. Hirota K, Okawa H, Appadu BL, Grandy DK, Devi LA, Lambert DG. Sterioselective interaction of ketamine with recombinant mu, kappa, and delta opioid receptors expressed in Chinese hamster ovary cells. Anesthesiology. 1999;90(1):174-182.
68. Gorman AL, Elliott KJ, Inturrisi CE. The d- and l-isomers of methadone bind to the non-competitive site on the N-methyl-D-aspartate (NMDA) receptor in rat forebrain and spinal cord. Neurosci Lett. 1997;223(1):5-8.
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70. McGrath PJ, Nunes EV, Stewart JW, et al. Imipramine treatment of alcoholics with primary depression: a placebo-controlled clinical trial. Arch Gen Psychiatry. 1996;53(3):232-240.
71.    Nunes EV, Quitkin FM, Donovan SJ, et al. Imipramine treatment of opiate-dependent patients with depressive disorders. Arch of Gen Psychiatry. 1998;55(2):153-160.
72. Grof S. Spirituality, addiction, and western science. ReVision. 1987;10(2):5-21.
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79. Rot M, Charney DS, Mathew SJ. Intravenous ketamine for treatment-resistant major depressive disorder. Primary Psychiatry. 2008;15(4):39-47.

 

Dr. Galanter is professor of psychiatry and director, Dr. Glickman is assistant clinical professor, Dr. Dermatis is research associate professor, Dr. Tracy is assistant professor, and Ms. McMahon is research assistant, all at the Division of Alcoholism and Drug Abuse of New York University School of Medicine and Bellevue Hospital Center in New York City. Drs. Galanter, Dermatis, and Glickman are also research scientists at the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, New York.

Disclosures: Drs. Galanter and Dermatis receive research support from the John Templeton Foundation. Dr. Glickman and Ms. McMahon report no affiliation with or financial interest in any organization that may pose a conflict of interest. Dr. Tracy receives grant support from the National Institute on Alcohol Abuse and Alcoholism.

Acknowledgments: The authors thank Hannah Barbash, BA, New York University Divisional research assistant, for assistance in the preparation of this article. The authors also thank Lynda Curtis, Drs. Eric Manheimer and Marc Gourevitch, and Irene Torres.

Please direct all correspondence to: Marc Galanter, MD, Professor of Psychiatry, NYU School of Medicine, 550 First Ave, Room NBV20N28, New York, NY 10016; Tel: 212-263-6960, Fax: 212-263-8285;
E-mail: marcgalanter@nyu.edu.

 


 

 

Focus Points

• Many patients have strong spiritually grounded feelings related to their ability to cope with illness.
• Addressing patients’ spiritual needs in the general medical setting can improve their satisfaction with caregivers and their adherence to treatment plans.
• There are emerging approaches to address this issue in the clinical setting.

Abstract

Medical care has long been associated with religion and spirituality, but in recent years a trend has arisen to introduce diverse spiritually oriented approaches in the context of empirically grounded practice. This article reviews the application of these approaches in contemporary medical practice. It highlights the relative utility of such applications, the use of spiritual assessment of the patient, and the role of the clergy and nursing in introducing spirituality into the clinical setting. It then presents findings from a program developed by the authors to employ spiritual support groups in the general hospital in order to aid patients in coping with illness, and to develop among them a more positive identification with their treatment providers.

Introduction

In the Western tradition, medicine and religion have always been linked—sometimes closely and sometimes farther apart—and religious influences on medical practice and on the profession’s ethics are longstanding.1-3 The growth of interest in the interaction of medical practitioners with religion and spirituality over recent years has paralleled similar developments in the larger society, as many healthcare providers with a strong spiritual orientation have sought to bring this spiritual aspect of their personal lives more into their clinical work. A major aspect of this movement has involved legitimating the positive relationship between religious involvement, spirituality, and health in many publications in the professional literature.4 Of comparable importance has been the growing recognition that spirituality and religion permeate the lives of patients as well as many medical encounters. A question to be considered has become not only how to deal with the religious and spiritual aspects of health care, but how they can be introduced into the treatment context. This article focuses on recent attempts to establish the utility of such interventions, and provides by way of illustration such a program that the authors have developed and implemented in the general hospital setting.

The distinction between religion and spirituality is important to this work, though it is not without controversy. Spiritual or religious choices often reflect a very personal and private aspect of a person’s life, which makes any definition subject to intense scrutiny. It is counterproductive to the purposes of research to settle on a definition of spirituality that is either too broad and vague or too individualized.5 There is, however, general agreement on a fundamental level that both religion and spirituality are related to a search for the sacred or transcendental.6,7 This commonality has led to divergent notions of how spirituality and religion are related. According to the theoretical framework posited by Pargament,8 spirituality and religion are inextricably intertwined. Spirituality is viewed as a core component of the more “broadband concept” of religion.8 However, an increasingly widely held view is more in line with Koenig and colleagues’4 contrasting definitions. He casts religion as “an organized system of beliefs, practices, rituals, and symbols” in relation to the sacred, as opposed to the “personal quest for understanding” of spirituality.5 These conceptualizations of religion and spirituality allow for the option of being religious but not spiritual, spiritual but not religious, both, or neither. In this article, spirituality is defined as that which gives people meaning and purpose in life.9 It can be achieved through participation in a religion but can be much broader than that, such as involvement in family, humanism, or the arts.10 In much of the literature and in American culture, spirituality has come to be seen as a human dimension particularly useful in bridging sectarian divisions common to religion.

 

The Spiritual Assessment

A key technique for addressing spirituality in clinical practice is the spiritual assessment.9 Spiritual assessments focus on learning whether the patient is part of a supportive faith community, ascertaining unmet spiritual needs that should be addressed in the course of treatment, identifying religious beliefs that might influence medical treatment decisions, and identifying potentially harmful spiritual practices such as spiritual struggles that patients associate with their illness. Spiritual struggles are defined as “efforts to conserve or transform a spirituality that has been threatened or harmed” and are expressed in terms of conflict and questioning of one’s spiritual/religious convictions.11 With a patient who professes neither to be religious nor spiritual, the physician can still inquire into what they are doing to cope with their illness. Puchalski9 has developed an approach adapted to general clinical settings she terms FICA, involving inquiry into “F”aith and healing, “I”mportance of faith in the patient’s life, “C”ommunities of faith and healing they may be part of, and “A”ddressing unmet needs.

Practitioners developing long-term relationships with dying patients have developed questions probing deeper into their sense of how their illnesses relate to “what it all means” to aid patients in identifying spiritual interventions that might benefit them.10 Spiritual interventions refer to therapeutic strategies that are designed with a spiritual or religious dimension as their central component12 and include but are not limited to spiritual assessments.

Kristeller and colleagues13 designed an intervention to improve patients’ well being and adjustment to cancer and showed that a 5–7-minute patient-centered intervention by an oncologist made a small contribution in patient well being. Patients included in the intervention were recruited at random from the waiting rooms of oncologists’ offices, as were controls who received usual care. The short intervention introduced the topic of spiritual or religious beliefs and encouraged patients to identify ways they used spiritual or religious resources. Questioned after 3 weeks, 33% said they thought the intervention would influence how they coped with cancer, while >40% thought it made them more satisfied with their overall care. Improvement after 3 weeks in quality-of-life measures among patients in the study group compared to those in the control group reached levels associated with clinically meaningful impacts in drug or other behavioral trials. Improvements were most pronounced among those scoring low on a spiritual well-being scale at baseline. Spiritual well being was assessed by the Functional Assessment of Chronic Illness Therapy–Spiritual Well-Being Scale. This scale consists of two subscales, namely, meaning/peace and faith.14 The spiritual well-being composite score combining both subscale scores was moderately correlated with measures of emotional and functional well being (r=.58 for each) suggesting that it was an empirically distinct dimension. This study provides support for the benefit of a short, nondenominational empathic intervention in physicians’ offices, even absent a physician’s incorporating the acquired information into treatment. Attention, however, should be paid to whether any aspect of the intervention produces distress in the patient and/or clinician. How often spiritual interventions are conducted, and to what effect, remains unknown.

 

The Clergy

Approximately 85% of all United States hospitals employ chaplains, while an estimated 20% of all hospitalized patients receive a chaplain’s visit.15 The growing professionalization of chaplains within a medical model, however, has contributed to their acceptance as members of a supportive care and palliative medicine team in the intensive care unit of a large trauma hospital, a team including physicians, advanced practice nurses specializing in pain, intensive care unit and palliative care, social workers, pharmacists, and music therapists. Chaplains provide spiritual support to patients who are dealing with issues related to finding meaning in life and coping with suffering, and help patients utilize their beliefs in coping with illness.9

Major barriers identified by chaplains included inadequate staffing, inability of healthcare providers to identify patients’ spiritual needs, and being called in too late to provide proper care to families.16 Physicians are often advised to refer serious spiritually-related problems to clergy or a chaplain affiliated with their hospital; some advocates of greater inclusion of spiritual matters within medicine consider the lack of such appropriate referrals to be a form of negligence.17 Shadowing a chaplain can be a key component of the spiritual education program for many palliative care fellows.

More recently, at Memorial Sloan-Kettering Cancer Center in New York City, approximately 20% of all chaplain interventions came as a result of a referral, mostly from nurses; 33% of the interventions involved working with family and friends.18 A similar survey at a suburban community hospital found that nurses made >50% of referrals to chaplains; 75% of all referrals were to see patients and the remainder were to see friends and family.19 Although referrals by nurses to chaplains most often come in times of crisis, some nursing leaders see a need to develop more ongoing collaboration to address a wider range of situations.20,21 Patients are frequent sources of requests for pastoral care—more frequent than nursing referrals in a study of adolescent inpatients in a pediatric tertiary care hospital.20

 

Nursing

Studies of self-reported spiritual nursing interventions and ideal, complex spiritual nursing competencies shed some light on the vast range of activities nurses see as falling under this rubric to address the spiritual needs of their patients.22,23 Such research stems from the desire to capture the considerable spiritual care delivered by nurses that goes undocumented. Prayer and active listening are the most commonly reported nursing interventions.24 Other commonly reported interventions include conveying acceptance, being present with a patient, therapeutic touch, and instilling hope. Presence as an intervention refers to both being physically present without expecting interactional responses and a psychological component wherein the nurse is attentive and demonstrates an understanding of the patient’s experiences.24

Narayanasamy and Owens25 identified different patterns of nurses’ responses to critical incidents they regard as involving spirituality. In the personal approach, nurses, using counseling, become involved in a mutual sharing of spiritual concerns, usually framed in nonreligious terms. In the procedural approach, the nurse sticks to standard routines, often referring to the expert, the chaplain, or colluding with the patient’s relatives, often without the patient’s involvement. In the evangelical approach, nurses, often sharing the same religious background with patients, attempt to rekindle the patient’s faith. Ethical concerns that arise relate to the potential for nursing staff to impose their specific spiritual/religious beliefs on the patient and/or family and to blur the boundary between nurse professional and clergy.9

 

Incorporating Spirituality in Psychosocial Treatment

One approach to incorporating spirituality in treatment involves integrating a spirituality dimension into an established treatment modality such as psychotherapy. Various attempts have been made to develop psychotherapeutic approaches to accommodate Christian values, including prayer and religious materials. Results of an early study26 showed that although cognitive-behavioral therapy (CBT) and a modified CBT with religious content resulted in improvement among depressed patients, improvement was greatest among depressed patients in the religiously modified program. A small meta-analysis, however, found that religion-accommodative approaches to counseling depressed patients had essentially the same overall efficacy as non-religious approaches.27

Another approach involves integrating spirituality in an existing psychosocial rehabilitation program. A small study among patients with serious psychiatric disabilities in an inner-city community program found that all participants receiving a spiritually oriented support group intervention to improve program functioning met their treatment goals related to symptom management, community integration, and improvement in overall quality of life as opposed to only 50% in the standard rehabilitation program.28 A study by Worthington and Sandage29 included patients with depression who were assigned either to a Beck-oriented CBT program or a Christian accommodative one. Both approaches were found to be equally effective in reducing depression, while the religiously oriented program was associated with greater improvement in spiritual well being.

A recent review12 of the worldwide literature on spiritually modified cognitive therapy in the Islamic, Taoist, and Christian traditions classified these treatments as experimental for anxiety disorder, neurosis, obsessive-compulsive disorder, and other conditions except for depression, which was considered to meet American Psychological Association criteria for a well-established intervention.

 

Models for Intervention

Pargament and colleagues30 and McConnell and colleagues31 have conducted a substantial body of research supporting the view that some forms of spiritual struggles are linked to psychopathology, and that a spiritually integrated psychotherapy can effectively address this problem and others. They have developed interventions based on these ideas, including a short intervention with an individual therapist for female survivors of sexual abuse with spiritual struggles designed to improve spiritual well being.32 A group intervention for people with serious mental illness following Pargament’s theory of positive and negative implications of religious coping33 incorporated issues such as spiritual striving, spiritual struggles, and hope.

Cole and Pargament34 also developed a group psychotherapy program for cancer patients, “Re-Creating Your Life: During and After Cancer,” combining concern with core existential issues and positive religious coping. Numerous models of group psychotherapy have been developed for work with cancer patients.35,36 Although most such groups focus on providing education, a forum for emotional expression, and strengthening coping skills as elements of overall support, spiritual and religious issues are often raised as well directed at reducing spiritual suffering and distress at end of life.

The field of palliative medicine, with its focus on end-of-life care, has been a source of considerable innovation in connecting spiritual issues to its form of medical practice. One such program developed by Breitbart35 at Memorial Sloan-Kettering Cancer Center employs a meaning-centered approach, drawing on the logotherapy developed by Frankl, to develop an eight-session program that explicitly addresses issues of meaning, peace, and ultimate purpose.35,37 Participants, all with advanced cancer and a limited prognosis, are given assigned readings and homework related to group session topics such as “Meaning and Historical Context of Life,” “Cancer and Meaning,” and “Limitations and Finiteness of Life.” The goal here is to help strengthen patients’ sense of being at peace with themselves in the face of the spiritual suffering and hopelessness they often experience.

A more extensive three-level program to enhance patients’ level of spirituality, mood, and self-efficacy for patients with a range of cancer diagnoses and severity was implemented in a metropolitan cancer hospital in Toronto, Canada.38 Level 1 consists of four group sessions dealing with cancer stress; level 2 is comprised of eight group sessions on skills for coping by drawing on the “Inner Healer” through meditation and other modalities. Meditative techniques are not the core of the intervention. Rather, meditative chanting is done for the first few minutes of all the sessions before the main topics are covered. The third level consists of eight sessions on spiritual healing, with a follow-up program of twice-monthly groups available to all who complete the program. This multi-staged model allows patients to decide for themselves which level of spiritual involvement is comfortable for them. In an exploratory study to assess the efficacy of this program, a battery of psychometric tests was administered at entry, 8 weeks, and 6 months, and written homework assignments were completed by study participants. Ninety-seven patients completing the third level showed significant improvement in mood, self-efficacy, and spirituality over the 8-week intervention period. After 6 months, only improvement in spirituality remained significant. Based on the written assignments which showed patients struggling with their spiritual issues, the investigator suggested that this model can provide advanced spiritual training to highly motivated individuals within a resource-constrained environment.

Randomized controlled trials can help assess the relative value of spiritually oriented interventions compared to standard interventions and can also help identify subgroups for which they may be most helpful. A recent clinical trial39 conducted at the Mayo Clinic points in a direction this area is likely to go, namely, integrating spiritual concerns into multidimensional and multidisciplinary interventions with the goal being to improve the overall quality of life of cancer patients. In this trial, advanced cancer patients set to undergo radiation therapy participated in a manualized 3-week program consisting of eight sessions each with a cognitive, emotional, physical, social, and spiritual interventional component. Sessions were lead by a psychiatrist or psychologist, with a chaplain, social worker, and advanced practice nurse as co-facilitator, depending on the session’s content. Quality of life at 4 weeks and 6 months following the intervention was compared with patients receiving standard care supervised by their radiation oncologist. Compared to the controls, the intervention group experienced a significantly better quality of life at 4 weeks; however, at 6 months this difference largely disappeared. The major benefit of the intervention appeared to be averting the sharp decline in quality of life during and shortly after the radiation treatment.

Stefanik and colleagues40 caution against concluding that religion and spirituality affect treatment outcomes in cancer due to methodologic weaknesses in much of the research, including the preponderance of cross-sectional studies, use of small samples sizes and samples of convenience, lack of correction for multiple statistical comparisons, failure to control for confounding variables, and questionable reliability and validity of study instruments.

 

HIV/AIDS

Efforts to include spiritual and religious concerns in the treatment of HIV/AIDS take many forms, but most of them have not been evaluated. Community health workers in one innovative outpatient HIV Palliative Care Program in the Bronx, New York, provided material resources and a dialogic partner in the search for meaning for patients undergoing the process of dying and bereavement and their families.41 In another study, Pargament and colleagues42 developed an eight-session nondenominational group program tailored for urban black women with HIV/AIDS. The program uses exercises such as writing a letter to God about guilt and shame, and identifying dreams still possible despite their illness, to encourage participants to acquire spiritual resources that may contribute to their health and well being while living with illness.

Another intervention designed to improve quality of life is exemplified in a randomized controlled pilot study43 of patients at an AIDS-dedicated skilled nursing facility. The independent and additive effects of meditation and massage on spirituality and quality of life were examined. Patients in a program that combined both modalities showed substantially greater improvement on measures of overall and spiritual quality of life than patients receiving either a meditation or a massage intervention alone or patients receiving standard care. Interventions designed to reduce HIV/AIDS risk combining spirituality and cognitively-based approaches include a nontheistic Buddhist-based program targeting risk behaviors among inner city methadone patients and a spiritual coping group for patients with HIV.44-46

A recent study47 which has implications for the value of spirituality based interventions among people receiving a potentially life-altering diagnosis examined whether changes in spirituality occur after receiving an HIV diagnosis and whether changes are related to disease progression as reflected in CD4 cell counts and viral load. People who had an increase in spirituality/religiousness showed less disease progression on both measures even after controlling for church attendance and initial disease status. These findings support continued efforts to develop spirituality based interventions for people diagnosed with HIV.

Numerous concerns have been reported regarding implementing spiritual interventions in medical and psychiatric treatment settings. Healthcare professionals may feel they lack sufficient expertise to discuss spirituality, are uncertain as to what their role is in relation to that of the chaplain, or construe such inquiries as intruding into the patient’s private life.17 When patient spirituality is addressed within the physician-patient relationship there is the possibility that certain beliefs held by the patient may undermine the physician’s treatment plan resulting in treatment refusal or futile requests for treatment.17 Another issue relates to whether the spirituality intervention is designed to meet the needs of the patients. Healthcare professionals and patients may not agree on what dimensions of spirituality are needed in the care of patients. In a review of nursing research papers published on spiritual care, Ross21 reported that there appears to be a discrepancy between provider and patient understanding of spirituality and the nature of spiritual care desired by patients.

 

A Program for Spiritually Oriented Support Groups

Despite impressive advances in the technology of acute care in general hospitals, the limited adherence by many patients to medical treatment plans regularly compromises their clinical outcome. This results in recidivism, increased morbidity, and undue cost to the healthcare system. In relation to primary care, for example, the World Health Organization has estimated that no more than 50% of patients with hypertension adhere to their prescribed medication regimens.48 Much of this is due to a limited sense of mutuality and trust felt by patients toward their caregivers as well as the impersonal quality perceived in their medical encounters.49

This need has been operationalized by the Joint Commission of Accreditation of Health Care Organizations, the principal certifying body for American hospitals. Its requirements stipulate that, “spiritual and cultural values [should] be gathered during the initial assessment of patients,” and that “Each patient has the right to have his or her . . . spiritual and personal values and beliefs, and preferences respected.”50 Importantly, however, there is little if any programmatic experience published on how spiritually grounded values and beliefs can be effectively addressed in hospital settings.

In order to address this need, the authors of this article conducted focus groups with patients at Bellevue Hospital Center, New York University’s principal teaching hospital, and found that one issue that contributes to this problem is that many patients feel that their core personal and spiritual beliefs are neither recognized nor addressed by hospital personnel. In previous research, staff and patients rated the importance of spiritually related resources relative to medical and material ones in addiction recovery.51,52 Staff rated the spiritual resources lowest, while patients rated them highest. Furthermore, when staff gave ratings to how they thought the patients would respond, they erroneously scored spiritual resources lowest, not recognizing the importance of spirituality to patients’ understanding of how they achieve recovery from their illness.53 Staff underestimated the importance patients placed on spirituality focused groups in the recovery process.51,52 Given this experience, the authors developed a pilot clinical program to determine if patients would discuss how they can draw on their spiritual resources and strengths to enhance their recovery and rehabilitation with support of hospital staff. The authors drew on experience54-56 in related clinical and research projects on the feasibility of such discussion groups in diverse clinical settings, and established groups for patients in a primary care clinic setting and on units dedicated to the treatment of comorbid general psychiatric disorders and substance abuse.

All groups were facilitated by volunteer medical or allied professional staff who have given their time because of their appreciation of the value of this effort, with the goal being to elicit feedback from all participants concerning how their spiritual attitudes, beliefs, and behaviors can help to promote health and cope with illness. The tone of the groups has reflected a mutual respect for each other’s religious (or non-religious) orientations. It would emerge that an underlying spiritual orientation was the primary focus of exchanges. The format of the group meetings is outlined in Table 1.

 

 

The groups were established in a primary care clinic setting in which 221 patients participated in one or more group meetings. The authors chose the primary care clinic to ascertain the applicability of this approach in a general medical population. They were also established in three inpatient (131 participants) and two outpatient (48 participants) psychiatry units. There were six different facilitators, each dedicated to his or her respective unit. The psychiatric patients were chosen to compare singly diagnosed psychiatric patients to those with comorbid substance use disorder; a report on the psychiatric patients will appear elsewhere. In the primary care clinic reception area, posters were prominently displayed and flyers were distributed to patients containing information concerning the group meetings and inviting all patients to attend. On the psychiatry units all patients were invited to attend the discussion groups by staff. This would usually occur at the beginning of the weekly community meeting. Participation in the spirituality discussion groups was completely voluntary and did not in any way affect the medical or psychiatric services received by patients. For purposes of the present report, only participant data collected in the medical outpatient setting will be presented.

In the medical outpatient setting a survey assessing spiritual orientation to life using the Spirituality Self-Rating Scale (SSRS)53 was administered to 52 consecutive patients at their first group session. These patients had as high a mean SSRS score, as did the addiction inpatients, but significantly higher than medical students. In a subsequent survey again administered to consecutive attendees at their first group session, 113 participants were asked items assessing their spiritual and religious views and practices concerning worship service participation. These items had been used in previous national probability surveys.57 The sample was predominantly female (64%) with a mean age of 53 (SD 14). Ethnicity included 27% African-American, 25% Hispanic, 25% White, and 23% other designation which was mainly multiracial. Patients varied with regard to religious preference with 31% Catholic, 15% Protestant, 10% Muslim, 6% Jewish, 28% other religious preference such as “higher power,” and 10% no preference. The results indicated that a greater percentage of the medical outpatients described themselves as being both religious and spiritual and report a higher frequency of spiritual-related practices involving worship service attendance compared to national samples (Table 2).57 These findings suggest that primary care patients perceive spirituality to be important to them and are as active, if not more so, than the general population.

 

 

Feedback from patients attending the group indicate that they value the opportunity to discuss their spiritual experiences with professional healthcare staff in the primary care setting, they feel more positively connected to treatment, and they endorse treatment’s integration in the formal healthcare system. In order to document themes that were discussed during the group sessions, a project assistant had recorded the comments made by the medical outpatients. Patient responses over the course of the sessions have been categorized, and numerous themes emerge prominently.

 

The Meaning of Spirituality

When participants were asked whether they considered themselves to be spiritual, the most common response was belief in a higher power which embodied a connection to God or a higher power. The diversity of the participants’ backgrounds was reflected in the different forms of this higher power, eg, Christian participants spoke of praying to Jesus and God; others, for example, self-identified as Buddhists, believed that this higher power was present in everyday objects.

 

Comparing Spirituality and Religion

Some participants discussed certain aspects of their spirituality in terms of their specific religious practices (eg, prayer, reading of scriptures, rituals) but also articulated distinctions between religion and spirituality.

 

Resources They Draw On

Participants described numerous aspects of their spirituality that reinforced their belief in a higher power, including prayer, recitation of religious or personal mantras, direct communication with the external force (eg, singing), scripture reading, and meditation. These served to calm them, combat depression or discontent, and alleviate physical pain or emotional suffering.

 

Some Personal Experiences

Some participants described their spirituality in terms of internal processes that served to instill hope, empowerment, and general well being. They referred to transformative experiences including revelations, miracles, or rebirth.

 

Quest for Spiritual Fulfillment

Some participants described themselves as emotionally drained and in search of a spiritual connection. Many of these individuals recalled being more spiritual when they were younger, but due to their illness and the physical changes accompanying aging, they became more cynical and spiritually detached.

 

Alienation from the Bellevue Physicians

Some patients were disenchanted with the medical staff. As one said, “All they do is give you pills, and when they do not work they just give you more pills.” Some spoke of “student doctors,” who “do not have time to listen to my story.”

 

Relationship to Treatment and Recovery

Participants discussed various aspects of their spirituality relating to connections with others based on trust, as with a family physician, or a group such as a 12-step fellowship. Many shared their spiritual experiences as a means of helping others to cope with their illness and better adhere to treatment. To a lesser extent, patients expressed the view that their spiritual beliefs could provide a means to a cure for their physical ailments not available through modern medicine, although they rarely endorsed refusal of all medical recommendations.

 

Conclusion

This article highlights progress that has been made in translating a growing interest in the medical field in spirituality and religion into interventions that may be effective and possibly become part of standard medical care. One notable aspect of this development is how spiritually and religiously based interventions have been adapted to diverse forms of clinical practice. Uncontrolled clinical trials have provided most of the information required to describe the complex dynamics involved in the relationship between spiritual interventions and medical care. One approach, developed at New York University and Bellevue Hospital in New York City, illustrates some of the particulars of helping patients to draw on their spiritual resources in order to cope with illness.

Spiritually oriented programs may pose ethical issues like those that have been raised regarding interventions that are specifically religiously oriented. By broadening the scope of discussion to include the many interests subsumed under the rubric of spirituality, however, concerns over sectarianism and religiously grounded bias are mitigated. Given this, diversity of commitment and affiliation among participants in spiritually oriented groups should be accepted and respected. With this proviso in mind, such interventions may be effective in improving patients’ outlook on their medical care as well as their ability to identify with the mission of hospital staff, thereby promoting greater compliance with the treatment regimens proposed. PP

 

References

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Dr. Basson is clinical professor and director of the Sexual Medicine Program in the Department of Psychiatry at the University of British Columbia in Vancouver, Canada.

Disclosures: Dr. Basson reports no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Rosemary Basson, MD, British Columbia Centre for Sexual Medicine, General Hospital, 855 W 12th Ave, Vancouver, BC, Canada, V5Z 1M9; Tel: 604-875-8254; Fax: 604-875-8249; E-mail: bassonrees@telus.net.

 

 
 

Abstract

Current conceptualization of women’s sexual response recognizes overlapping phases of variable order. Even without their sensing sexual desire at a particular moment, women initiate or agree to a sexual encounter for numerous reasons. Provided there is adequate attention to appropriate sexual stimulation and an ability to remain focused, subjective arousal follows. That arousal is often poorly correlated with typically prompt reflexive genital congestion. If this complex state of arousal is accompanied by positive emotions and thoughts, then sexual desire, along with further arousal, is triggered. Positive sexual experiences provide further motivation to be sexual again. Understanding this cycle allows patients and clinicians to identify points of interruption, guiding traditional and recently adopted forms of psychosexual therapy for problematic desire and arousal. Given the strong correlation between women’s sexual function and their mental and relationship health, it is necessary to first address these parameters. Recommendations to change official definitions of women’s sexual disorders have been published. Pharmacologic and hormonal therapies for sexual disorders are currently under investigation. There are numerous gaps in present knowledge regarding the need and safety of any testosterone supplementation.

 

Introduction

Problematic low sexual desire and arousal is reported by approximately 33% of women.1-3 Sexual dissatisfaction or distress does not necessarily follow,1,4 but when it does and is ongoing, the diagnoses of sexual desire and arousal disorders are considered. Prevalence figures from recent nationally representative surveys of women in the United States suggest a prevalence of desire disorder of 8.3% and 9.5% with minimal variation across ages until a drop in women >60 years of age.2,5 Prevalence may generally reach 12.5% for surgically menopausal women, and 19.9% for women <45 years of age.5 Of women living in the US, the prevalence of dysfunction was higher in those of Japanese and Chinese backgrounds and lower in African-American women.6

 

Currently recommended definitions of disorder reflect the complexities of desire and arousal. Importantly, desire (ie, “drive,” “lust,” “sexual need”) may not be present initially, but it can be triggered during the sexual encounter along with arousal. Secondly, arousal itself includes numerous aspects, notably subjective excitement/sexual pleasure and physical genital and non-genital changes. That the mental and physical aspects are frequently poorly correlated has been repeatedly documented. Therefore, currently recommended definitions of disorder identify the different dysfunctional components of arousal.

This article describes current conceptualization and supporting evidence of women’s sexual response as well as recently recommended definitions of disorder. The main correlates of desire and arousal that guide the assessment and treatment of desire arousal disorders are outlined. Standard and recent additions to psychosexual therapy are clarified prior to mention of investigational medical treatments, including testosterone supplementation.

 

Current Conceptualization of Women’s Sexual Response

A variety of reasons prompt women (and men) to initiate or agree to sex. A recent study identified 235 discrete reasons that were divided into four domains, namely love and intimacy, physical pleasure and stress relief, goal attainment, and protection of the relationship/“mate guarding.” Evaluating 1,500 undergraduate psychology students, the majority of both men and women were mostly motivated for reasons related to attraction, pleasure, affection, love, romance, and emotional closeness. However, women exceeded men in their reporting emotional motivations.7 Although these motivations were not mutually exclusive, the results support the concept that even if drive is initially absent, there are numerous other reasons to engage in sexual activity.8 That women’s desire can be triggered subsequently during the sexual encounter also has empirical support. Data from 125 women 20–70 years of age showed that regardless of their reporting or not reporting sexual dysfunction, all women identified triggers of sexual desire.9 These triggers were in the domains of emotional bonding, erotica, romance and physical proximity. An absence of any initial desire was shown in the baseline Study of Women Across the Nation (SWAN), wherein the majority of 3,250 multi-ethnic middle-aged women in North America indicated that while they were moderately or extremely satisfied with their physical sexual pleasure, they never or very infrequently sensed desire.6 The highest figures were for Chinese and Japanese women (61.4% and 67.8%). If further equally large multi-ethnic studies confirm these findings, it can be concluded that beginning a rewarding sexual experience without desire is at least as common for mid-life women as beginning one with a definite sense of desire.

Consistent anticipatory sexual desire is more typical of new relationships, and it may be a major reason for sexual engagement. However, that phase may be brief; one study suggests it may last only 1 year for some women.10 Current conceptualization of women’s sexual response allows for the possibility that initially there is a willingness to become aroused and sense desire subsequently (Figure 1).8,11 Though the potential absence of initial desire in sexually satisfied women is now documented, the validated questionnaires used to assess sexual function are based on models of sexual response wherein desire was taken as necessary to the outset of engagement. This is unfortunately acknowledged as a serious limitation.12

 

 

It is important to note that qualitative research has shown that numerous women cannot clearly distinguish between desire and arousal.13 Some women refer to genital and non-genital physical sensations as components of their desire, which is especially true of younger women. The discrepancy between subjective sexual arousal and any measurement of the genital congestion has been frequently identified (Table 1).14-19

 

 

The genital response appears to be a reflex automatic entity that can be elicited in response to a stimulus deemed sexual but not erotic or potentially arousing (eg, viewing a video of primates mating).18,19 Moreover, women’s assessment of their genital congestion is inaccurate. Thus, it is clear that women’s arousal cannot be measured by their “report of genital swelling lubrication response.”20 Recently recommended definitions of disordered arousal include the different components of arousal, particularly genital and subjective excitement.21,22

To summarize the current understanding of sexual response, desire may or may not be present at outset.6,7,8 Even when desire is absent, the woman can choose to deliberately attend to sexual stimulation and remain focused for a sufficient amount of time to allow subjective arousal. The type of stimulation, the context, her ability to attend, the number of distractions, and the expected outcome influence the likelihood of her becoming aroused. When arousal follows and the stimulation continues sufficiently long, its intensity can increase and trigger desire. At that point, her focus becomes her need for sexual satisfaction. The latter may or may not include orgasm(s) but usually requires freedom from any pain or partner dysfunction or negative emotional conclusion. Positive experiences reinforce subsequent sexual motivation. The cycle shown in Figure 1 may be cycled many times during one encounter. This cyclicity and phase overlap predicts the well-documented comorbidity of desire and arousal disorders.2,3 This conceptualization includes and expands on those of Masters and Johnson23 and Kaplan.24 The latter described the phase of desire, mentioning both “intrinsic/ biologic” and “extrinsic/responsive” types, that add to the linear sequence of arousal/excitement, orgasm and resolution described by Masters and Johnson.23 Although after the publication of Human Sex Response Cycle by Masters and Johnson,23 the arousal phase in women often became equated to genital events (lubrication and swelling); the original description included both genital and subjective arousal. The focus on the mind’s processing of stimuli is derived from Janssen and colleagues’25 information processing model in addition to the concept of sexual excitation versus sexual inhibition as explored by Sanders and Graham.26 The circular model depicted in Figure 1 is composite, but it allows for the marked variability of response among women who consider their sexual lives as rewarding and functional.

  

Current Recommendations for Definitions of Disorder

Women’s sexual function is highly contextual, and when that context is problematic such that she reports sexual dysfunction it is questionable whether the term “sexual disorder” is truly appropriate. Frequently there is no evidence of innate disruption of her sexual response. Rather, a problematic sexual environment, including lack of emotional closeness or inadequate stimuli, underlies her problematic experiences. Therefore, current contextual factors, factors from the developmental or medical history, should be documented with any diagnosis of sexual disorder/dysfunction.21 Management of “her dysfunction” may well focus on correcting an unhealthy sexual context. It is important to note that women rate relationship difficulties as a major cause of sexual dysfunction.27

Table 28,20-22,28 outlines the recently recommended definitions of dysfunction from an international consensus committee organized by the American Urological Association Foundation.21 Subsequent to this consensus document, other colleagues made further recommendations that uphold the basic principles, including that desire may normally be limited to a “triggered” type, that subjective arousal must be addressed, that the entity of genital sexual arousal disorder should be included, and that the degree of distress must be assessed.22 These definitions have not been accepted by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision20 or International Classification of Diseases, Tenth Edition29 committees. However, the former is currently beginning extensive research in order to provide official revisions in 2010.

 

 

Psychological Factors Predisposing Arousal and Desire Dysfunction

The major risk factor documented in the literature is poor mental health.1,4 Even a history of major depressive disorder (MDD) without current depression or antidepressant therapy proved a risk factor for low arousal and physical pleasure in the SWAN study.30 In a recent study,31 successful antidepressant therapy improved sexual dysfunction that was initially present in 80% of 445 women with MDD, whereas dysfunction worsened if the depression continued. Even when clinical depression is formally excluded, women complaining of low desire still have lower self-esteem, more mood variability, and more anxious and depressed thoughts than control women.32

The second robust correlation with sexual arousal and desire disorders is relationship difficulties and negative feelings toward the current partner. Indeed, positive past sexual experiences and positive feelings for the partner appear to protect middle-aged women from dysfunction associated with their marked hormonal changes.33 Major factors protecting women from sexual distress have been found to be positive feelings for the partner generally and specifically at the time of sexual engagement.4 Even when medical factors are pertinent (eg, among breast cancer survivors), important predictors of their sexual satisfaction include relationship quality and mental health.34 Partner sexual dysfunction is also a major risk factor for a woman’s subsequent dysfunctions that typically improve with successful treatment of her partner.35

 

Biologic Risk Factors

The importance of biologic factors is less clear. Regarding estrogen, the vast majority of untreated postmenopausal women will show signs of vulvovaginal atrophy36 that can reduce sexual motivation, but dyspareunia is by no means universal and most epidemiologic studies show little increase in dyspareunia with age. The (albeit diminishing) intracellular production of estrogen from adrenal and ovarian prohormones, including dihydroepiandrosterone (DHEA) and DHEA sulphate, may be sufficient for some women. Rather than amounts of substrate (ie, prohormones), the activity of the various steroidogenic enzymes including aromatase in the different peripheral tissues may be the key factor. Variations in estrogen receptor numbers and sensitivities may also be relevant.

Regarding lack of androgen, this too is far from straightforward. Surgical menopause has been cited as an example of an androgen-deplete state. However, the prevalence of subsequent desire or arousal dysfunction is unknown. Elective bilateral oophorectomy along with required simple hysterectomy apparently may not lead to sexual dysfunction. This has been confirmed recently in three different studies.37-39 This seems to be in conflict with cross-sectional studies of women with surgical menopause who appear to have more distressing low desire and low satisfaction than naturally post-menopausal women.2,3 However, these latter studies give no details on the degree of choice the women had regarding the bilateral oophorectomy.

The complexities of the intracellular production of sex hormones is an area of active research.40 Adrenal production of precursors is said to decrease by 66% between late 30s and early 60s, but the amount of variation among individual women is unknown. Moreover, the decreased production may still be sufficient if the necessary enzymes in the cells to convert the precursors to testosterone and estrogen remain active.40 However, there are other complexities, including sensitivity of androgen receptors and availability and numbers of cofactors. Moreover, the brain can synthesize sex hormones from the basic building block of cholesterol.41 There is early evidence that with menopause this intracerebral production of neurosteroids increases.42 There is little research into how that production might be modulated with exogenous sex hormone supplementation.

There is consensus43 that the large studies exploring any correlation between (physiologic) serum levels of testosterone and women’s sexual function have been negative.44,45 Though studies are in process, whether a measure of total androgen production via androgen metabolites will show any such correlation remains to be seen. Benefit has been shown in the recent transdermal testosterone supplementation randomized controlled trials (RCTs),8 but the evidence of benefit is limited. This may be partially due to the fact that the women recruited for these studies were already having on average of three sexually satisfying events per month at baseline. In view of recently recommended definitions of disorder, it is questionable whether these women had any sexual disorder. Nevertheless, their arousal and orgasm scores on the questionnaires used in the study improved with testosterone compared to placebo. An important question is, would benefit have been greater if women unable to have any sexually satisfying events had been recruited?46 There is need to study benefits of testosterone supplementation for loss of response and, therefore, absence of triggered desire.

 

Assessment of Desire and Arousal Disorders

Assessment involves evaluating the stages in the woman’s sex response cycle (Figure 1). Involving both partners and seeing them both together and separately are advocated. The woman’s reasons or motivations to be sexual are assessed along with the suitability of the context (ie, circumstances, timing, interpersonal context). Further, her intrapersonal context, in terms of self-image, past sexual experiences, and mood, require careful examination. The variety and usefulness of the stimuli are assessed as is her proneness to distract. The nature of any distractions is clarified. These distractions might concern the sexual experience and the outcome or, more commonly, non-sexual issues. The actual sexual details are then assessed such as the extent to which intercourse is the focus, its timing, her need or experience of orgasm, any discomfort with sexual stimulation or intercourse, and any partner dysfunction. In addition, the emotional outcome both immediately and over the next few hours or days are noted.

While the couple is together, the evolution of their sexual difficulties and each partner’s reaction to them can be evaluated. Then, when the couple is separated, inquiry as to the woman’s own sexual experience with self-stimulation and further details she would like to add is possible now that she is alone. Her past sexual experiences, developmental history, and past and present medical details are also needed. The same information can be obtained from the partner when he or she is seen alone.

The rather simplistic “A–G” guide to sexual assessment is offered at least to screen and decide whether referral or care within one’s own practice is most appropriate (Table 3).47,48

 

 

 

Laboratory Investigations

Laboratory investigations are of limited use for sexual assessment. When there are other symptoms of, for example, thyroid disease or hyperprolactinemia (eg, galactorrhea, irregular menses, infertility), appropriate testing is conducted.

 

Physical Examination

The physical examination is of major importance when there is comorbid dyspareunia. In the context of chronic medical disease (eg, neurologic disease where there may be sensory loss in the genitalia, renal disease where there may be anemia and vulvovaginal atrophy, states of hyperprolactinemia where there may be galactorrhea and in hypoadrenal states where there may be loss of pubic hair), an examination is necessary. Genital examination is necessary when there is lost genital sexual sensitivity to exclude conditions such as lichen sclerosis. In addition, genital and pelvic examination is often used for reasons of reassurance and as a means to encourage the woman to consider what is going in her mind when she is sexual rather than believing the etiology of her arousal dysfunction is confined to her genitalia. In these situations, a psychiatrist not focusing his or her practice on sexual medicine may consider it more appropriate to have a colleague perform the physical examination.

 

Validated Questionnaires

Validated questionnaires are available but are best considered as survey instruments, for example in epidemiologic studies, since they provide only a cursory picture of sexual functioning and are not intended for use to make diagnoses. The algorithms in Figure 2 show how the diagnostic label stems from the assessment questions.28,48

 

 

 

Management of Disordered Sexual Arousal and Desire

The approach is to address the problematic areas in a woman’s sex response cycle that have been identified during the detailed assessment. It is guided by the documented robust correlations between women’s sexual satisfaction and their mental health, including self-image and their emotional intimacy with their partner. It is important to note that assessment typically continues throughout treatment as new information emerges.

 

Psychosexual Therapy

Figure 3 outlines the progression through psychosexual therapy options, initially addressing any mood disorder or interpersonal difficulties.48 Psychosexual education is often therapeutic. The couple is informed about women’s (and men’s) sexual response cycles, clarifying that suitable context and sexual stimuli are needed by all women to trigger desire on many, if not all, occasions. Cognitive-behavioral therapy (CBT) techniques clarify and challenge inaccurate thoughts, beliefs, and myths about the woman’s sexual response, herself, and frequently, misunderstandings about her partner. Behavioral therapy includes sensate focus treatment that targets anticipatory anxiety and performance anxiety about sexual activity. Briefly, these exercises involve the partners taking turns in providing pleasurable low-key sensual and then sexual stimulation to each other, with the recipient guiding as to the type of stimulation they would like. Once the couple has practiced with the low-key types of stimulation, more areas of the body are included, but intercourse itself is still “off-limits.” Focusing on the moment, guiding the partner, finding the pace at which she is more comfortable to progress with sexual activity, and realizing that sexual times can be planned in advance are all potential benefits of sensate focus therapy. When distractions are a difficulty, discussion of the mindfulness technique is warranted. Relevant literature or preferably classes can be suggested. Initially, mindfulness practice in non-sexual everyday life is encouraged and only later guidance on how to specifically use this skill during sexual activity is given.

 

Psychotherapy can include either psychodynamic treatment or psychoanalysis. The latter would be prescribed when there was belief that the sexual dysfunction is at least partially due to pathologic processes in personality development. To help the woman relate intimately to her partner, she works through conflicts from the past that were present in non-sexual relationships. While psychotherapy is supported by the clinical literature, there is minimal empirical support.49

In practice, commonly these methods are mixed. For example, “psychoeducational therapy” can involve CBT techniques, sexual information, sex therapy, and mindfulness practice. It has proven beneficial for women with desire and arousal disorders particularly if they have a history of sexual abuse50 as well as for women with genital sexual arousal disorder due to gynecologic cancer.51 Larger studies with wait-list controls are in process.

 

Hormonal Therapy

Estrogen-related dryness and dyspareunia improve with topical/local or systemic estrogen supplementation. Indirectly, sexual motivation may be improved. Although less well studied, genital sexual sensitivity may also respond to estrogen in the postmenopausal woman.

Supplemental testosterone for postmenopausal women is not approved in the US, but it has been prescribed since the 1930s, off-label, using formulations approved for men or using compounded creams. The previously mentioned recent RCTs8 of transdermal testosterone to surgically (four studies) and naturally (one study) menopausal estrogen supplemented women all by the same sponsor and using the same protocol showed modest benefit from the 300 mcg/day but not the 450 mcg/day dose. At recruitment, the women on average reported three sexually satisfying events each month and these increased to approximately five with active drug and to four with placebo.8 On the basis of this documented benefit, transdermal testosterone has been approved by the European Union for surgically menopausal women. More recently, minimal or no benefit was seen from transdermal testosterone in estrogen-deficient women.52 In pre-menopausal women only one of three doses aimed to increase pre-testosterone levels to the high normal range proved beneficial, and that benefit was in the order of 0.8 more sexually satisfying events per month and was not associated with any improvements beyond placebo as measured by a validated sexual function and satisfaction questionnaire.53 However, consistently, the focus has been on increasing the sexual frequency, recruiting women with satisfactory sexual experiences.

Numerous unresolved issues are shown in Table 4.8,37-39,52,53 A major concern is lack of long-term safety data. Recent reviews of potentially increased risk of breast cancer,54 metabolic syndrome,55 and cardiovascular disease clarify the current clinical dilemma. Testosterone supplementation requires co-administration of estrogen, which presents further difficulty. Despite cardiovascular benefit identified in non-randomized prospective trials of systemic estrogen initiated at menopause, women are currently advised against on-going systemic estrogen on the basis of cardiovascular harm shown in RCTs of women beginning estrogen supplementation many years post menopause.56 A 2006 guideline42 reviews some of these complexities underlying the American Endocrine Society’s advising against testosterone supplementation.

 

 

Identification of Women with “Androgen Deficiency”

Identifying women with “androgen deficiency” is currently not possible.43 The hypopituitary state would be a clear indication of androgen deficiency, but there is little clarity beyond that. Intracellular production of testosterone continues indefinitely as some supply of prohormones from adrenal glands (and ovaries in some women) continues indefinitely. Loss of ovarian androgens from surgery may not amount to androgen deficiency; note the studies showing elective bilateral oophorectomy at the time of perimenopausal hysterectomy does not lead to sexual dysfunction.37-39 As previously mentioned, serum levels of testosterone do not correlate with sexual function and androgen metabolites have not yet been shown to correlate with sexual function.

 

Investigational Therapy

Table 5 outlines some investigational drugs.57-68 The ongoing interest in addressing deficient genital congestion with various drugs, including phosphodiesterase inhibitors, alpha blockers, selective estrogen receptor modulators, and peptidase inhibitors is somewhat puzzling given the documented lack of correlation between women’s sexual symptoms and any measurable deficit in genital congestion. However, these drugs might benefit women with deficient congestion due to, for example, non-nerve-sparing radical hysterectomies.

 

 

 

Conclusion

Current understanding of women’s sex response cycle allows patients and clinicians to consider the points of interruption when difficulties with arousal and desire are reported. Women’s sexual motivation is broad such that interpersonal or personal psychological issues can readily deter women from instigating or accepting sex. Sexual stimuli in appropriate contexts are needed for the sexual response to unfold and trigger arousal and desire. Commonly, these are lacking or problematic. Distractions, low self-image, and difficulties with trust may preclude sufficient arousal to allow pleasure and more intense arousal along with desire. Concern about a negative outcome physically or emotionally may similarly lessen arousal. Having first addressed any mental health or interpersonal issues, combinations of psychoeducation, CBT, and sex therapy are the mainstay of therapy. Teaching mindfulness techniques appears to be a promising addition. Identifying women whose sexual disorder is based on deficiency of sex hormone activity remains challenging. Testosterone supplementation for loss of both initial and triggered desire requires investigation. Pharmacologic adjuncts are being investigated and may have a role especially for genital sexual arousal disorder. PP

 

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34. Ganz PA, Desmond KA, Belin TR, Meyerowitz BE, Rowland JH. Predictors of sexual health in women after a breast cancer diagnosis. J Clin Oncol. 1999;17(8):2371-2380.
35. Cayan S, Bozlu M, Canpolat B, Akbay E. The assessment of sexual functions in women with male partners complaining of erectile dysfunction: does treatment of male sexual dysfunction improve female partner’s sexual functions? J Sex Marital Ther. 2004;30(5):333-341.
36. Freedman MA. Estrogen, vaginal pH, and genital atrophy. Menopause. 2006;13(6):987.
37. Aziz A, Brannstrom M, Bergquist C, et al. Perimenopausal androgen decline after oophorectomy does not influence sexuality or psychological well-being. Fertil Steril. 2005;83(4):1021-1028.
38. Farquar CM, Harvey SA, Yu Y, et al. A prospective study of three years of outcomes after hysterectomy with and without oophorectomy. Am J Obstet Gynecol. 2006;194(3):714-717.
39. Teplin V, Vittinghoff E, Lin F, et al. Oophorectomy in premenopausal women: health-related quality of life and sexual functioning. Obstet Gynecol. 2007;109(2 pt 1):347-354.
40. Labrie F, Bélanger A, Bélanger P, et al. Androgen glucuronides, instead of testosterone, as the new markers of androgenic activity in women. J Steroid Biochem Mol Biol. 2006;99(4-5):182-188.
41. Melcangi RC, Panzica GC. Neuroactive steroids: old players in a new game. Neuroscience. 2006;138(3):733-739.
42. Ishunina TA, Swaab DF. Alterations in the human brain in menopause. Maturitas. 2007;57(1):20-22.
43. Wierman ME, Basson R, Davis SR, et al. Androgen therapy in women: an Endocrine Society Clinical Practice Guideline. J Clin Enocrinol Metab. 2006;91(10):3697-3710.
44. Davis SR, Davison SL, Donath S, Bell RJ. Circulating androgen levels in self-reported sexual function in women. JAMA. 2005;294(1):91-96.
45. Santoro A, Torrens J, Crawford S, et al. Correlates of circulating androgens in midlife women: the study of women’s health across the nation. J Clin Endocrinol Metab. 2005;90(8):2004-2063.
46. Basson R. Testosterone supplementation to improve women’s sexual satisfaction: complexities and unknowns. Ann Intern Med. 2008;148(8):620-621.
47. Basson R. Recent conceptualization of women’s sexual response. Menopause. 2007;16(3):16-28.
48. Young C, Tovey D, Martin A, et al. Congestive heart failure. BMJ. Point-of-Care. 2008. Available at: www.pointofcare.bmj.com. Accessed August 7, 2008.
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54. Schover LR. Androgen therapy for loss of desire in women: is the benefit worth the breast cancer risk? Fertil Steril. 2008;90(1):129-140.
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56. Stevenson JC. HRT and the primary prevention of cardiovascular disease. Maturitas. 2007;57(1):31-34.
57. Diamond LE, Earle DC, Heiman JR, Rosen RC, Perelman MA, Harning R. An effect on the subjective sexual response in premenopausal women with sexual arousal disorder by bremelanotide (PT-141), a melanocortin receptor agonist. J Sex Med. 2006;3(4):626-683.
58. Safarinejad MR. Evaluation of the safety and efficacy of bremelanotide, a melanocortin receptor agonist, in female subjects with arousal disorder: a double-blind placebo-controlled, fixed dose, randomized study. J Sex Med. 2008;5(4):887-897.
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68. Basson R. Women’s sexual function and dysfunction; current uncertainties future directions. Int J Impot Res. 2008. Epub ahead of print.

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Dr. Basson is clinical professor and director of the Sexual Medicine Program in the Department of Psychiatry at the University of British Columbia in Vancouver, Canada.

Disclosures: Dr. Basson reports no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Rosemary Basson, MD, British Columbia Centre for Sexual Medicine, General Hospital, 855 W 12th Ave, Vancouver, BC, Canada, V5Z 1M9; Tel: 604-875-8254; Fax: 604-875-8249; E-mail: bassonrees@telus.net.

 

 
 

Abstract

Current conceptualization of women’s sexual response recognizes overlapping phases of variable order. Even without their sensing sexual desire at a particular moment, women initiate or agree to a sexual encounter for numerous reasons. Provided there is adequate attention to appropriate sexual stimulation and an ability to remain focused, subjective arousal follows. That arousal is often poorly correlated with typically prompt reflexive genital congestion. If this complex state of arousal is accompanied by positive emotions and thoughts, then sexual desire, along with further arousal, is triggered. Positive sexual experiences provide further motivation to be sexual again. Understanding this cycle allows patients and clinicians to identify points of interruption, guiding traditional and recently adopted forms of psychosexual therapy for problematic desire and arousal. Given the strong correlation between women’s sexual function and their mental and relationship health, it is necessary to first address these parameters. Recommendations to change official definitions of women’s sexual disorders have been published. Pharmacologic and hormonal therapies for sexual disorders are currently under investigation. There are numerous gaps in present knowledge regarding the need and safety of any testosterone supplementation.

 

Introduction

Problematic low sexual desire and arousal is reported by approximately 33% of women.1-3 Sexual dissatisfaction or distress does not necessarily follow,1,4 but when it does and is ongoing, the diagnoses of sexual desire and arousal disorders are considered. Prevalence figures from recent nationally representative surveys of women in the United States suggest a prevalence of desire disorder of 8.3% and 9.5% with minimal variation across ages until a drop in women >60 years of age.2,5 Prevalence may generally reach 12.5% for surgically menopausal women, and 19.9% for women <45 years of age.5 Of women living in the US, the prevalence of dysfunction was higher in those of Japanese and Chinese backgrounds and lower in African-American women.6

 

Currently recommended definitions of disorder reflect the complexities of desire and arousal. Importantly, desire (ie, “drive,” “lust,” “sexual need”) may not be present initially, but it can be triggered during the sexual encounter along with arousal. Secondly, arousal itself includes numerous aspects, notably subjective excitement/sexual pleasure and physical genital and non-genital changes. That the mental and physical aspects are frequently poorly correlated has been repeatedly documented. Therefore, currently recommended definitions of disorder identify the different dysfunctional components of arousal.

This article describes current conceptualization and supporting evidence of women’s sexual response as well as recently recommended definitions of disorder. The main correlates of desire and arousal that guide the assessment and treatment of desire arousal disorders are outlined. Standard and recent additions to psychosexual therapy are clarified prior to mention of investigational medical treatments, including testosterone supplementation.

 

Current Conceptualization of Women’s Sexual Response

A variety of reasons prompt women (and men) to initiate or agree to sex. A recent study identified 235 discrete reasons that were divided into four domains, namely love and intimacy, physical pleasure and stress relief, goal attainment, and protection of the relationship/“mate guarding.” Evaluating 1,500 undergraduate psychology students, the majority of both men and women were mostly motivated for reasons related to attraction, pleasure, affection, love, romance, and emotional closeness. However, women exceeded men in their reporting emotional motivations.7 Although these motivations were not mutually exclusive, the results support the concept that even if drive is initially absent, there are numerous other reasons to engage in sexual activity.8 That women’s desire can be triggered subsequently during the sexual encounter also has empirical support. Data from 125 women 20–70 years of age showed that regardless of their reporting or not reporting sexual dysfunction, all women identified triggers of sexual desire.9 These triggers were in the domains of emotional bonding, erotica, romance and physical proximity. An absence of any initial desire was shown in the baseline Study of Women Across the Nation (SWAN), wherein the majority of 3,250 multi-ethnic middle-aged women in North America indicated that while they were moderately or extremely satisfied with their physical sexual pleasure, they never or very infrequently sensed desire.6 The highest figures were for Chinese and Japanese women (61.4% and 67.8%). If further equally large multi-ethnic studies confirm these findings, it can be concluded that beginning a rewarding sexual experience without desire is at least as common for mid-life women as beginning one with a definite sense of desire.

Consistent anticipatory sexual desire is more typical of new relationships, and it may be a major reason for sexual engagement. However, that phase may be brief; one study suggests it may last only 1 year for some women.10 Current conceptualization of women’s sexual response allows for the possibility that initially there is a willingness to become aroused and sense desire subsequently (Figure 1).8,11 Though the potential absence of initial desire in sexually satisfied women is now documented, the validated questionnaires used to assess sexual function are based on models of sexual response wherein desire was taken as necessary to the outset of engagement. This is unfortunately acknowledged as a serious limitation.12

 

 

It is important to note that qualitative research has shown that numerous women cannot clearly distinguish between desire and arousal.13 Some women refer to genital and non-genital physical sensations as components of their desire, which is especially true of younger women. The discrepancy between subjective sexual arousal and any measurement of the genital congestion has been frequently identified (Table 1).14-19

 

 

The genital response appears to be a reflex automatic entity that can be elicited in response to a stimulus deemed sexual but not erotic or potentially arousing (eg, viewing a video of primates mating).18,19 Moreover, women’s assessment of their genital congestion is inaccurate. Thus, it is clear that women’s arousal cannot be measured by their “report of genital swelling lubrication response.”20 Recently recommended definitions of disordered arousal include the different components of arousal, particularly genital and subjective excitement.21,22

To summarize the current understanding of sexual response, desire may or may not be present at outset.6,7,8 Even when desire is absent, the woman can choose to deliberately attend to sexual stimulation and remain focused for a sufficient amount of time to allow subjective arousal. The type of stimulation, the context, her ability to attend, the number of distractions, and the expected outcome influence the likelihood of her becoming aroused. When arousal follows and the stimulation continues sufficiently long, its intensity can increase and trigger desire. At that point, her focus becomes her need for sexual satisfaction. The latter may or may not include orgasm(s) but usually requires freedom from any pain or partner dysfunction or negative emotional conclusion. Positive experiences reinforce subsequent sexual motivation. The cycle shown in Figure 1 may be cycled many times during one encounter. This cyclicity and phase overlap predicts the well-documented comorbidity of desire and arousal disorders.2,3 This conceptualization includes and expands on those of Masters and Johnson23 and Kaplan.24 The latter described the phase of desire, mentioning both “intrinsic/ biologic” and “extrinsic/responsive” types, that add to the linear sequence of arousal/excitement, orgasm and resolution described by Masters and Johnson.23 Although after the publication of Human Sex Response Cycle by Masters and Johnson,23 the arousal phase in women often became equated to genital events (lubrication and swelling); the original description included both genital and subjective arousal. The focus on the mind’s processing of stimuli is derived from Janssen and colleagues’25 information processing model in addition to the concept of sexual excitation versus sexual inhibition as explored by Sanders and Graham.26 The circular model depicted in Figure 1 is composite, but it allows for the marked variability of response among women who consider their sexual lives as rewarding and functional.

  

Current Recommendations for Definitions of Disorder

Women’s sexual function is highly contextual, and when that context is problematic such that she reports sexual dysfunction it is questionable whether the term “sexual disorder” is truly appropriate. Frequently there is no evidence of innate disruption of her sexual response. Rather, a problematic sexual environment, including lack of emotional closeness or inadequate stimuli, underlies her problematic experiences. Therefore, current contextual factors, factors from the developmental or medical history, should be documented with any diagnosis of sexual disorder/dysfunction.21 Management of “her dysfunction” may well focus on correcting an unhealthy sexual context. It is important to note that women rate relationship difficulties as a major cause of sexual dysfunction.27

Table 28,20-22,28 outlines the recently recommended definitions of dysfunction from an international consensus committee organized by the American Urological Association Foundation.21 Subsequent to this consensus document, other colleagues made further recommendations that uphold the basic principles, including that desire may normally be limited to a “triggered” type, that subjective arousal must be addressed, that the entity of genital sexual arousal disorder should be included, and that the degree of distress must be assessed.22 These definitions have not been accepted by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision20 or International Classification of Diseases, Tenth Edition29 committees. However, the former is currently beginning extensive research in order to provide official revisions in 2010.

 

 

Psychological Factors Predisposing Arousal and Desire Dysfunction

The major risk factor documented in the literature is poor mental health.1,4 Even a history of major depressive disorder (MDD) without current depression or antidepressant therapy proved a risk factor for low arousal and physical pleasure in the SWAN study.30 In a recent study,31 successful antidepressant therapy improved sexual dysfunction that was initially present in 80% of 445 women with MDD, whereas dysfunction worsened if the depression continued. Even when clinical depression is formally excluded, women complaining of low desire still have lower self-esteem, more mood variability, and more anxious and depressed thoughts than control women.32

The second robust correlation with sexual arousal and desire disorders is relationship difficulties and negative feelings toward the current partner. Indeed, positive past sexual experiences and positive feelings for the partner appear to protect middle-aged women from dysfunction associated with their marked hormonal changes.33 Major factors protecting women from sexual distress have been found to be positive feelings for the partner generally and specifically at the time of sexual engagement.4 Even when medical factors are pertinent (eg, among breast cancer survivors), important predictors of their sexual satisfaction include relationship quality and mental health.34 Partner sexual dysfunction is also a major risk factor for a woman’s subsequent dysfunctions that typically improve with successful treatment of her partner.35

 

Biologic Risk Factors

The importance of biologic factors is less clear. Regarding estrogen, the vast majority of untreated postmenopausal women will show signs of vulvovaginal atrophy36 that can reduce sexual motivation, but dyspareunia is by no means universal and most epidemiologic studies show little increase in dyspareunia with age. The (albeit diminishing) intracellular production of estrogen from adrenal and ovarian prohormones, including dihydroepiandrosterone (DHEA) and DHEA sulphate, may be sufficient for some women. Rather than amounts of substrate (ie, prohormones), the activity of the various steroidogenic enzymes including aromatase in the different peripheral tissues may be the key factor. Variations in estrogen receptor numbers and sensitivities may also be relevant.

Regarding lack of androgen, this too is far from straightforward. Surgical menopause has been cited as an example of an androgen-deplete state. However, the prevalence of subsequent desire or arousal dysfunction is unknown. Elective bilateral oophorectomy along with required simple hysterectomy apparently may not lead to sexual dysfunction. This has been confirmed recently in three different studies.37-39 This seems to be in conflict with cross-sectional studies of women with surgical menopause who appear to have more distressing low desire and low satisfaction than naturally post-menopausal women.2,3 However, these latter studies give no details on the degree of choice the women had regarding the bilateral oophorectomy.

The complexities of the intracellular production of sex hormones is an area of active research.40 Adrenal production of precursors is said to decrease by 66% between late 30s and early 60s, but the amount of variation among individual women is unknown. Moreover, the decreased production may still be sufficient if the necessary enzymes in the cells to convert the precursors to testosterone and estrogen remain active.40 However, there are other complexities, including sensitivity of androgen receptors and availability and numbers of cofactors. Moreover, the brain can synthesize sex hormones from the basic building block of cholesterol.41 There is early evidence that with menopause this intracerebral production of neurosteroids increases.42 There is little research into how that production might be modulated with exogenous sex hormone supplementation.

There is consensus43 that the large studies exploring any correlation between (physiologic) serum levels of testosterone and women’s sexual function have been negative.44,45 Though studies are in process, whether a measure of total androgen production via androgen metabolites will show any such correlation remains to be seen. Benefit has been shown in the recent transdermal testosterone supplementation randomized controlled trials (RCTs),8 but the evidence of benefit is limited. This may be partially due to the fact that the women recruited for these studies were already having on average of three sexually satisfying events per month at baseline. In view of recently recommended definitions of disorder, it is questionable whether these women had any sexual disorder. Nevertheless, their arousal and orgasm scores on the questionnaires used in the study improved with testosterone compared to placebo. An important question is, would benefit have been greater if women unable to have any sexually satisfying events had been recruited?46 There is need to study benefits of testosterone supplementation for loss of response and, therefore, absence of triggered desire.

 

Assessment of Desire and Arousal Disorders

Assessment involves evaluating the stages in the woman’s sex response cycle (Figure 1). Involving both partners and seeing them both together and separately are advocated. The woman’s reasons or motivations to be sexual are assessed along with the suitability of the context (ie, circumstances, timing, interpersonal context). Further, her intrapersonal context, in terms of self-image, past sexual experiences, and mood, require careful examination. The variety and usefulness of the stimuli are assessed as is her proneness to distract. The nature of any distractions is clarified. These distractions might concern the sexual experience and the outcome or, more commonly, non-sexual issues. The actual sexual details are then assessed such as the extent to which intercourse is the focus, its timing, her need or experience of orgasm, any discomfort with sexual stimulation or intercourse, and any partner dysfunction. In addition, the emotional outcome both immediately and over the next few hours or days are noted.

While the couple is together, the evolution of their sexual difficulties and each partner’s reaction to them can be evaluated. Then, when the couple is separated, inquiry as to the woman’s own sexual experience with self-stimulation and further details she would like to add is possible now that she is alone. Her past sexual experiences, developmental history, and past and present medical details are also needed. The same information can be obtained from the partner when he or she is seen alone.

The rather simplistic “A–G” guide to sexual assessment is offered at least to screen and decide whether referral or care within one’s own practice is most appropriate (Table 3).47,48

 

 

 

Laboratory Investigations

Laboratory investigations are of limited use for sexual assessment. When there are other symptoms of, for example, thyroid disease or hyperprolactinemia (eg, galactorrhea, irregular menses, infertility), appropriate testing is conducted.

 

Physical Examination

The physical examination is of major importance when there is comorbid dyspareunia. In the context of chronic medical disease (eg, neurologic disease where there may be sensory loss in the genitalia, renal disease where there may be anemia and vulvovaginal atrophy, states of hyperprolactinemia where there may be galactorrhea and in hypoadrenal states where there may be loss of pubic hair), an examination is necessary. Genital examination is necessary when there is lost genital sexual sensitivity to exclude conditions such as lichen sclerosis. In addition, genital and pelvic examination is often used for reasons of reassurance and as a means to encourage the woman to consider what is going in her mind when she is sexual rather than believing the etiology of her arousal dysfunction is confined to her genitalia. In these situations, a psychiatrist not focusing his or her practice on sexual medicine may consider it more appropriate to have a colleague perform the physical examination.

 

Validated Questionnaires

Validated questionnaires are available but are best considered as survey instruments, for example in epidemiologic studies, since they provide only a cursory picture of sexual functioning and are not intended for use to make diagnoses. The algorithms in Figure 2 show how the diagnostic label stems from the assessment questions.28,48

 

 

 

Management of Disordered Sexual Arousal and Desire

The approach is to address the problematic areas in a woman’s sex response cycle that have been identified during the detailed assessment. It is guided by the documented robust correlations between women’s sexual satisfaction and their mental health, including self-image and their emotional intimacy with their partner. It is important to note that assessment typically continues throughout treatment as new information emerges.

 

Psychosexual Therapy

Figure 3 outlines the progression through psychosexual therapy options, initially addressing any mood disorder or interpersonal difficulties.48 Psychosexual education is often therapeutic. The couple is informed about women’s (and men’s) sexual response cycles, clarifying that suitable context and sexual stimuli are needed by all women to trigger desire on many, if not all, occasions. Cognitive-behavioral therapy (CBT) techniques clarify and challenge inaccurate thoughts, beliefs, and myths about the woman’s sexual response, herself, and frequently, misunderstandings about her partner. Behavioral therapy includes sensate focus treatment that targets anticipatory anxiety and performance anxiety about sexual activity. Briefly, these exercises involve the partners taking turns in providing pleasurable low-key sensual and then sexual stimulation to each other, with the recipient guiding as to the type of stimulation they would like. Once the couple has practiced with the low-key types of stimulation, more areas of the body are included, but intercourse itself is still “off-limits.” Focusing on the moment, guiding the partner, finding the pace at which she is more comfortable to progress with sexual activity, and realizing that sexual times can be planned in advance are all potential benefits of sensate focus therapy. When distractions are a difficulty, discussion of the mindfulness technique is warranted. Relevant literature or preferably classes can be suggested. Initially, mindfulness practice in non-sexual everyday life is encouraged and only later guidance on how to specifically use this skill during sexual activity is given.

 

Psychotherapy can include either psychodynamic treatment or psychoanalysis. The latter would be prescribed when there was belief that the sexual dysfunction is at least partially due to pathologic processes in personality development. To help the woman relate intimately to her partner, she works through conflicts from the past that were present in non-sexual relationships. While psychotherapy is supported by the clinical literature, there is minimal empirical support.49

In practice, commonly these methods are mixed. For example, “psychoeducational therapy” can involve CBT techniques, sexual information, sex therapy, and mindfulness practice. It has proven beneficial for women with desire and arousal disorders particularly if they have a history of sexual abuse50 as well as for women with genital sexual arousal disorder due to gynecologic cancer.51 Larger studies with wait-list controls are in process.

 

Hormonal Therapy

Estrogen-related dryness and dyspareunia improve with topical/local or systemic estrogen supplementation. Indirectly, sexual motivation may be improved. Although less well studied, genital sexual sensitivity may also respond to estrogen in the postmenopausal woman.

Supplemental testosterone for postmenopausal women is not approved in the US, but it has been prescribed since the 1930s, off-label, using formulations approved for men or using compounded creams. The previously mentioned recent RCTs8 of transdermal testosterone to surgically (four studies) and naturally (one study) menopausal estrogen supplemented women all by the same sponsor and using the same protocol showed modest benefit from the 300 mcg/day but not the 450 mcg/day dose. At recruitment, the women on average reported three sexually satisfying events each month and these increased to approximately five with active drug and to four with placebo.8 On the basis of this documented benefit, transdermal testosterone has been approved by the European Union for surgically menopausal women. More recently, minimal or no benefit was seen from transdermal testosterone in estrogen-deficient women.52 In pre-menopausal women only one of three doses aimed to increase pre-testosterone levels to the high normal range proved beneficial, and that benefit was in the order of 0.8 more sexually satisfying events per month and was not associated with any improvements beyond placebo as measured by a validated sexual function and satisfaction questionnaire.53 However, consistently, the focus has been on increasing the sexual frequency, recruiting women with satisfactory sexual experiences.

Numerous unresolved issues are shown in Table 4.8,37-39,52,53 A major concern is lack of long-term safety data. Recent reviews of potentially increased risk of breast cancer,54 metabolic syndrome,55 and cardiovascular disease clarify the current clinical dilemma. Testosterone supplementation requires co-administration of estrogen, which presents further difficulty. Despite cardiovascular benefit identified in non-randomized prospective trials of systemic estrogen initiated at menopause, women are currently advised against on-going systemic estrogen on the basis of cardiovascular harm shown in RCTs of women beginning estrogen supplementation many years post menopause.56 A 2006 guideline42 reviews some of these complexities underlying the American Endocrine Society’s advising against testosterone supplementation.

 

 

Identification of Women with “Androgen Deficiency”

Identifying women with “androgen deficiency” is currently not possible.43 The hypopituitary state would be a clear indication of androgen deficiency, but there is little clarity beyond that. Intracellular production of testosterone continues indefinitely as some supply of prohormones from adrenal glands (and ovaries in some women) continues indefinitely. Loss of ovarian androgens from surgery may not amount to androgen deficiency; note the studies showing elective bilateral oophorectomy at the time of perimenopausal hysterectomy does not lead to sexual dysfunction.37-39 As previously mentioned, serum levels of testosterone do not correlate with sexual function and androgen metabolites have not yet been shown to correlate with sexual function.

 

Investigational Therapy

Table 5 outlines some investigational drugs.57-68 The ongoing interest in addressing deficient genital congestion with various drugs, including phosphodiesterase inhibitors, alpha blockers, selective estrogen receptor modulators, and peptidase inhibitors is somewhat puzzling given the documented lack of correlation between women’s sexual symptoms and any measurable deficit in genital congestion. However, these drugs might benefit women with deficient congestion due to, for example, non-nerve-sparing radical hysterectomies.

 

 

 

Conclusion

Current understanding of women’s sex response cycle allows patients and clinicians to consider the points of interruption when difficulties with arousal and desire are reported. Women’s sexual motivation is broad such that interpersonal or personal psychological issues can readily deter women from instigating or accepting sex. Sexual stimuli in appropriate contexts are needed for the sexual response to unfold and trigger arousal and desire. Commonly, these are lacking or problematic. Distractions, low self-image, and difficulties with trust may preclude sufficient arousal to allow pleasure and more intense arousal along with desire. Concern about a negative outcome physically or emotionally may similarly lessen arousal. Having first addressed any mental health or interpersonal issues, combinations of psychoeducation, CBT, and sex therapy are the mainstay of therapy. Teaching mindfulness techniques appears to be a promising addition. Identifying women whose sexual disorder is based on deficiency of sex hormone activity remains challenging. Testosterone supplementation for loss of both initial and triggered desire requires investigation. Pharmacologic adjuncts are being investigated and may have a role especially for genital sexual arousal disorder. PP

 

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This interview took place on August 6, 2008, and was conducted by Norman Sussman, MD.

 

This interview is also available as an audio PsychCastTM at http://psychcast.mblcommunications.com.

 

Disclosure: Dr. Gandy is on the scientific advisory boards of and receives honoraria from Diagenic, Epix Pharmaceuticals, and SMART Pharmaceuticals; is on the Data and Safety Monitoring Board of  and receives honoraria from Elan/Wyeth; and receives grant support from Forest Research Institute.

 

Samuel Gandy, MD, PhD, is Mount Sinai Professor of Alzheimer’s Disease Research, professor of neurology and psychiatry, associate director of the Mount Sinai Alzheimer’s Disease Research Center in New York City, and past chair of the National Medical and Scientific Advisory Council of the Alzheimer’s Association. As an international expert in the metabolism of amyloid that clogs the brain in patients with Alzheimer’s disease, Dr. Gandy has written over 150 original papers, chapters, and reviews on this topic. In 1989, he and his colleagues discovered medications that could lower the formation of amyloid. He has received continuous National Institutes of Health funding for his research on amyloid metabolism since 1986.

 

 

 

What is Alzheimer’s disease?

Alzheimer’s disease is the most common cause of dementia, which is the loss of one’s ability to think. It involves changes in memory, executive function, ability to locate oneself in space, and personality. As a neurodegenerative disease, it is clearly related to aging. It is responsible for approximately 66% of all dementia.

 

Is there a way to distinguish age-related cognitive impairment from early Alzheimer’s disease?

Though there are other technologically advanced methods available, the best way to make a diagnosis of Alzheimer’s disease is to conduct a battery of neuropsychological tests. They can take several hours to administer, but they are the most sensitive way for physicians to diagnosis the condition.

While it is known that Alzheimer’s disease is associated with aging, it is also known that it is possible to live to 120 years of age and still be cognitively intact. Therefore, distinguishing age-associated cognitive impairment from early Alzheimer’s disease may be slightly artificial beyond that age. Since we know that it is possible to live to ≥100 years of age with completely intact cognition, we have taken that as our working definition of “successful aging,” and that is our goal.

 

Are imaging studies clinically useful?

Neuroimaging is important for excluding reversible causes of dementia, including hydrocephalous, brain tumors, and chronic neurologic infection. Currently, magnetic resonance imaging is the most popular imaging tool used for that purpose. The fluoride-oxyglucose positron emission tomography (PET) scan is useful in excluding the possibility of frontotemporal dementia (FTD), a rare disease formerly referred to as Pick’s disease and associated with approximately 15% to 33% of dementia. (Alzheimer’s disease is associated with the remaining percentage of all forms of dementia.) The fluoride-oxyglucose PET scan may help distinguish Alzheimer’s disease from FTD.

 

What is the clinical difference in presentation between Alzheimer’s disease and FTD?

FTD tends to occur earlier in life than Alzheimer’s disease. It is said to be the most common cause of new-onset psychosis between 40 and 60 years of age and may rival Alzheimer’s disease as the more common cause of dementia in that same young age group. The distinguishing features of FTD include disinhibition and development of especially inappropriate affect, sexual activity, and criminal activity. Further, prominent speech disturbance can lead to primary progressive aphasia. However, the underlying disease for speech disturbance is often FTD, as it affects the frontal and temporal poles of the brain wherein the personality and speech areas are prominent. PET scans have shown that Alzheimer’s disease tends to affect the occipital/posterior temporal and parietal lobes, which are involved in orientation in space, memory, and cognitive reasoning.

 

Are there genetic markers indicating Alzheimer’s disease and FTD?

The genetics of the rarer forms of these conditions are well configured. Approximately 3% of Alzheimer’s disease in early onset form usually occuring at ≤65 years of age is attributed to genetic makeup. In those cases, there are identified mutations causing a dominant, completely penetrant disease; that is, if a patient has a mutated gene, he or she is guaranteed to get the disease. The genes in which those mutations are located concern mistakes in amyloid metabolism, which are the strongest indicators available for identifying Alzheimer’s disease. Genetic tests predictive of early onset familial forms of Alzheimer’s disease can be conducted even from the time of conception.

FTD mutations are also identified in early onset forms of the disease. Unlike early onset Alzheimer’s disease wherein the mutations are in the amyloid protein, mutations in genetic makeup indicating FTD are in the tau protein that forms the tangles. The involvement of different proteins distinguishes Alzheimer’s disease from FTD pathologically. Alzheimer’s disease is an “amyloid plaque and tangle disease” while FTD is a “tangle-only” disease.

 

What is the prevalence of Alzheimer’s disease according to age group?

The prevalence of Alzheimer’s disease at 65 years of age is approximately 10%. At ≥85 years of age, the probability increases to  approximately 50%. On a physical basis, individuals ≥85 years of age have a dementia that is often categorized as Alzheimer’s disease. Statistically, it is a very common disease.

 

How effective are current treatments for Alzheimer’s disease?

Currently available medications fall into two classes. The first class consists of donepezil hydrochloride, rivastigmine tartrate, and galantamine hydrobromide. Though each medication has a slightly different dosing schedule than the others, all of them act on acetyl cholinesterase, an enzyme found in the synapses between nerve cells. Its job is to degrade excess acetylcholine after synapses have occurred and acetylcholine has been released. From the presynaptic neuron, acetylcholine diffuses across the synaptic cleft to the postsynaptic neurons and bound receptors where it leaves an excess. Acetyl cholinesterase helps degrade this excess to terminate neurotransmission. In Alzheimer’s disease, the presynaptic neurons making the acetylcholine eventually become sick and die. (The reasons for this occurrence have yet to be determined.) Once those presynaptic nerve cells are no longer able to make the acetylcholine, the treatment effects dissipate, as the acetylcholinesterase inhibitors require the integrity of the presynaptic neuron to create acetylcholine. In essence, the medications in the first class block the breakdown of the acetylcholine, offering patients modest, temporary relief that invariably wears off as time passes.

The second class of drugs is solely represented by memantine. While it is approved for moderate stages of Alzheimer’s disease, it is currently being tested in earlier stages of the disease and may eventually be tested for slowing the conversion of mild cognitive impairment to Alzheimer’s disease. Memantine blocks the receptor from glutamate, the most widely used neurotransmitter, particularly in the brain. However, excess amounts of glutamate can kill postsynaptic nerve cells. It has been shown in model systems, including nerve cells from a dish and animal models, that whenever amyloid plaques are present, nerve cells are more sensitive to glutamate than usual. Once amyloid plaque sufficiently accumulates, it begins exerting toxins on nerve cells. Memantine helps to block glutamate receptors (eg, N-methyl-d-aspartic acid), preventing them from their becoming too sensitive. The treatment helps preserve and protect the surviving nerve cells.

 

For how long does the treatment hinder the usual progression of the disease?

Cholinesterase inhibitors (ChEIs) “turn back the clock” (in terms of regaining lost function) for approximately 3–6 months, but “the clock keeps ticking” so that the rate of decline is unchanged with these drugs. The National Institute for Clinical Excellence study1 from the United Kingdom indicated that, after 18 months, patients treated with ChEIs and those who go untreated have roughly equivalent functional status. In other words, there is a brief improvement in functional status but since the ChEIs are not disease modifying, the benefit wears off after 1.5–2 years.

Are anti-inflammatory drugs helpful in treating Alzheimer’s disease?
The association of non-steroidal anti-inflammatory drugs (NSAIDs) has an interesting history. Pathologists noticed that people with chronic arthritis taking NSAIDs seemed to have lower burdens of plaque pathology in their brains. This observation formed the basis of numerous trials recently initiated on certain compounds. For example, a class of classical anti-inflammatories involving the enzyme cyclooxygenase-2 (COX-2) was tested and failed, as there was excess mortality in subjects taking the NSAIDs. Conventional NSAIDs seemed to have no place in slowing the progression of Alzheimer’s disease.

Approximately 5 years ago, an unusual property was discovered indicating certain subtypes of NSAIDs could modify the production of amyloid. On that basis, flurbiprofen, a fluoride derivative of ibuprofen, was synthesized to maximize anti-amyloid activity and completely ablate COX-2 activity, which is responsible for side effects accompanying NSAIDs such as gastrointestinal distress and hemorrhage. Flurbiprofen recently underwent a phase-3 trial to see if it would slow the progression of Alzheimer’s disease. It failed with no clear explanation for this failure despite new modalities of neuroimaging that make visualizing plaque build-up during life possible. For example, chemists and physicians at the University of Pittsburgh developed a compound called Pittsburgh Compound-B (PIB) that can show plaque burden when used in PET scans. When flurbiprofen was tested, PET scans using PIB were not employed, so we do not now know whether the flurbiprofen was ineffective in changing amyloid burden or whether amyloid burden was relieved but cognitive function remained poor.

Current knowledge of genetic forms notes amyloid build-up as one of the earliest indicators of Alzheimer’s disease. It is known from pathologic studies, and now from these PIB scans, that plaque begins to accumulate ≥10 years before the first clinical symptom or sign. Therefore, it is possible that patients suffering from mild Alzheimer’s disease may already have such a heavy plaque burden that it is basically too late for an anti-amyloid agent to have a meaningful impact. Another possibility is that there are several stages to the disease’s progression. First, there is the amyloid build-up. Second, the build-up triggers the formation of neurofibrillary tangles and an inflammatory response around the amyloid plaque. Once the amyloid build-up triggers these secondary effects, even the removal of the amyloid cannot stop the progression of the disease. The knowledge concerning genetic forms has been especially important in modeling the disease’s pathology in animals. However, much research must be conducted in order to translate those models  into meaningful therapy.

 

Do exercising and mental stimulation help prevent shrinkage in the brain?

The aforementioned cases were epidemiologic studies, and it is very difficult to show causality in these types of studies. However, it seems that the factors associated with cardiac health are also associated with brain health and dementia. For example, controlling body weight, blood sugar, cholesterol, blood pressure, and other activities associated with heart health are relevant for brain health as well.

Health risks applying to the heart (eg, diabetes, hypertension, hypercholesterolemia, obesity) also apply to Alzheimer’s disease. In terms of factors modulating the risk for Alzheimer’s disease, issues of fitness and mental stimulation are robust clinical associations. It is difficult to reduce an individual’s mental stimulation to a drug. It is difficult to both write patients prescriptions and tell them what to do so that they improve their condition. The challenge now is to determine whether it is possible to specify good physical and mental activities. It is important to test them the same way in which medications are tested; that is, the effects of physical and mental activity on the development and progression of Alzheimer’s disease should be evaluated in randomized clinical trials. That a patient’s starting a regimen of physical and mental activity will protect or delay him or her from onset of Alzheimer’s disease should be definitively determined, not supposed. Epidemiologic studies come with risk, as they may result in associations arising due to a possibility that was not initially considered. For example, there may be people who have better access to professional care or who take better care of themselves. These participants may be the ones who confound a study’s results. For this possibility, randomized clinical trials are the gold standard. However, maintaining a heart-healthy lifestyle and mental stimulation is beneficial to an individual. Physicians recommend them, as they are obviously good for the heart and do no harm to the brain. Though it is believed that such activities are helpful in the prevention of Alzheimer’s disease, such a belief cannot be completely proven that prescribing will be effective with the usual level of scientific rigor.

[Additional information on the topic of Alzheimer’s disease can be found by consulting references 2–15]. PP

 

References

1.    Loveman E, Green C, Kirby J, et al. The clinical and cost-effectiveness of donepezil, rivastigmine, galantamine and memantine for Alzheimer’s disease. Health Technol Assess. 2006;10(1):iii-iv,ix-xi,1-160.
2.    Qin W, Chachich M, Lane M, et al. Calorie restriction attenuates Alzheimer’s disease type brain amyloidosis in Squirrel monkeys (Saimiri sciureus). J Alzheimers Dis. 2006;10(4):417-422.
3.    Greenberg SM, Rosand J, Schneider AT, et al. A phase 2 study of tramiprosate for cerebral amyloid angiopathy. Alzheimer Dis Assoc Disord. 2006;20(4):269-274.
4.    Small SA, Gandy S. Sorting through the cell biology of Alzheimer’s disease: intracellular pathways to pathogenesis. Neuron. 2006;52(1):15-31.
5.    Martins IJ, Hone E, Foster JK, et al. Apolipoprotein E, cholesterol metabolism, diabetes, and the convergence of risk factors for Alzheimer’s disease and cardiovascular disease. Mol Psychiatry. 2006;11(8):721-736.
6.    Gandy S, Heppner FL. Breaking up (amyloid) is hard to do. PLoS Med. 2005;2(12):e417.
7.    Balakrishnan K, Verdile G, Mehta PD, et al. Plasma Abeta42 correlates positively with increased body fat in healthy individuals. J Alzheimers Dis. 2005;8(3):269-282.
8.    Lautenschlager NT, Wu JS, Laws SM, et al. Neurological soft signs are associated with APOE genotype, age and cognitive performance. J Alzheimers Dis. 2005 Aug;7(4):325-330.
9.    Gandy S, Heppner FL. Alzheimer’s amyloid immunotherapy: quo vadis? Lancet Neurol. 2005;4(8):452-453.
10.    Gandy S. The role of cerebral amyloid beta accumulation in common forms of Alzheimer disease.J Clin Invest. 2005;115(5):1121-9.
11.    Walker LC, Ibegbu CC, Todd CW, et al. Emerging prospects for the disease-modifying treatment of Alzheimer’s disease. Biochem Pharmacol. 2005;69(7):1001-1008.
12.    Gandy S, Walker L. Toward modeling hemorrhagic and encephalitic complications of Alzheimer amyloid-beta vaccination in nonhuman primates. Curr Opin Immunol. 2004;16(5):607-615.
13.    Heppner FL, Gandy S, McLaurin J. Current concepts and future prospects for Alzheimer disease vaccines. Alzheimer Dis Assoc Disord. 2004;18(1):38-43.
14.    Gandy S. Cerebral Abeta amyloidosis and postmenopausal hormone deficiency: roles in the genesis of Alzheimer’s disease. Hum Pathol. 2004;35(3):271-274.
15.    Gandy S, DeMattos RB, Lemere CA, et al. Alzheimer’s Abeta vaccination of rhesus monkeys (Macaca mulatta). Mech Ageing Dev. 2004;125(2):149-151.

 

Dr. Rao is associate professor and vice-chair in the Department of Psychiatry and Behavioral Neurosciences at Loyola University Medical Center in Maywood, Illinois.

Disclosures: Dr. Rao is on the speaker’s bureau of Forest.

Acknowledgments: The author thanks Maria Theodorou for her assistance in compiling the references used in this manuscript.

Please direct all correspondence to: Murali Rao, MD, DFAPA, FAPM, Associate Professor and Vice-Chair, Department of Psychiatry and Behavioral Neurosciences, Loyola University Medical Center, Maywood, IL 60153; Tel: 708-216-3276; Fax: 708-216-5885; E-mail: mrao1@lumc.edu.

 


 

Focus Points

• Depression should not be discounted as an inevitable natural consequence  to a serious medical illness.
• The utility of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, in diagnosing depression in the medially ill is limited.
• Aggressive treatment of depression utilizing all available modalities along with the treatment of comorbid medical illnesses is important as it affects not only the patient’s improved participation in the treatment but also decreased morbidity.
• The overall effect on the course of the disease itself and mortality needs to be further studied.

 

Abstract

As depression is strongly associated with physical illness, it can be a complex and challenging condition for the medically ill. Approximately 33% of physically ill patients have depressive symptoms, many of which are regarded as understandable responses or reactions to the physical illness. Depressive illness is often under-diagnosed and under-treated, particularly in those with coexisting physical illnesses. The assessment of both conditions and the interaction between them is critical in managing these patients. Studies have clearly established that these depressive disorders are amenable to psychological or pharmacologic treatments.

 

Introduction

Depressed patients are more likely than non-depressed patients to have longer hospital stays and more outpatient visits, suffer greater disability, suffer from poorer quality of life, and experience suicidal thoughts and even commit suicide.

Major depression is at least twice as common in hospitalized medical patients compared to depression in the general population. The prevalence of major depressive disorder (MDD) in patients with comorbid medical illness can be as high as 30% in the hospital setting.1 Presence of comorbid depression is predictive of worse outcomes of medical illness and increased mortality.2 It may be better to risk over diagnosing depression than to leave depression untreated. Studies have shown that treatment of even minor or sub-syndromal depression has beneficial effects on the overall functioning of the physically ill individual and enhances treatment compliance for the co-existing medical illness and the recovery and rehabilitation process. It has been well established that in patients with type-2 diabetes, MDD is both a precursor as well as a comorbid illness. This is also the case in cerebrovascular and cardiovascular diseases.

 

The Association of Depression and Physical Illness

The association of depression and physical illness can be best understood as follows. First, depression can be caused by an underlying physical illness or be an exacerbated response3 or a reaction to the illness. Second, depression can be a consequence of treatment of physical illness with medications (eg, antihypertensives, corticosteroids, and other immunosuppressants) or cancer treatments, especially with interferons.4 Third, depression may be a consequence of various medical illnesses. Depression occurs in approximately 30% to 40% of patients with acute stroke or myocardial infarction, and has been linked to poorer cognitive and physical recovery. Fourth, depression can be a complication.3 Depression should be considered a new strong risk factor among other pre-existing risk factors, especially anxiety or panic states, through increased sympathetic activity; mobilization of free fatty acid from adipose tissue; thrombogenicity and platelet activation, agglutination; thrombus formation; and inflammation, particularly in coronary and cerebrovascular disorders; and possibly in other conditions. Fifth, depression may be a co-existant, pre-existant, or coincidental association3 to a physical illness. Sixth, depression can be contextual; it may be an effect of illness and its impact on life situations (eg, personal, job, relationships, finances) or in the context of metabolic disturbances (eg, hypoactive delirium presenting as depression). Seventh, depression may be a cue or clue to an underlying illness or a prelude to yet to be diagnosed major illness, especially in those who have the first onset of depression in mid-life or later. Approximately 33% of Alzheimer’s patients experience depression in the prodromal and early stages of dementia.5 Last, depression may be a contributing factor to the prolongation of the distress of a physical illness.

 

Detection of Depression

Detection of depression in the medically ill can be difficult for the following reasons.6 First, it may be regarded as a “normal: reaction to physical illness. Second, common vegetative symptoms include weight loss, fatigue, weakness, and anorexia often due to the medical illness. Third, it is difficult to distinguish onset of a depressive syndrome from psychological reactions to life-threatening illness. Last, the effects of impaired cognitive functioning secondary to the medical illness itself may detract from the detection of depression. As a result, the symptom pattern cannot be relied upon to a make a definitive diagnosis.7

To quote Dr. Elizabeth Scott8:

The reason for these disorders largely being unrecognized is fairly complex. But, certainly the conventional classification systems that we use in psychiatry contribute to this. Those classification systems are often not helpful in patients with physical illness. That’s because these systems largely depend on vegetative symptoms, as part of their diagnostic criteria. Symptoms such as sleep or appetite disturbance, changes in weight, changes in neuro-cognitive status, short-term memory or concentration, or changes in energy level also are symptoms of the underlying physical illness itself and then it becomes hard to tease out what’s the underlying physical illness or the disease process and what’s the contribution of depression or anxiety and also it makes it hard to gauge the severity of depressive or anxiety symptoms. Psychiatrists generally have a lack of agreement or consensus about the appropriate diagnostic criteria or classification systems to use in these patients…Physicians and patients themselves often assume that these symptoms are a reaction to the underlying physical illness, or…part of the disease process itself, so they often feel that they don’t merit separate identification assessment or intervention.

Screening instruments such as the Beck Depression Inventory cannot replace clinical assessment. When usual resilience to illness is replaced by pervasive low mood, depression characterized by lack of interest in life should be strongly suspected; empirical trial of treatment should be considered, especially in view of newer, safer antidepressants and psychological treatments.4 Although depression associated with medical illness has been shown to increase mortality, the benefits of treating depression on medical morbidity and mortality have yet to be established.9

 

Alternative Approaches to Help Detect Comorbid Depression

The Inclusive Approach

Instead of excluding symptoms appearing to be caused by a medical condition (eg, fatigue), the inclusive approach considers all symptoms describing depression. The inclusive approach is easy to use and sensitive to functional impairment.10

 

Substituting the “Classic” Vegetative Symptoms

Classic vegetative symptoms include change in appetite and sleep, fatigue and loss of energy, diminished ability to think or concentrate, indecisiveness, psychomotor slowing, tearfulness, depressed appearance, social withdrawal and decreased talkativeness, brooding, self-pity, pessimism, lack of reactivity to environmental events, and latency in responses.11

 

Modifying DSM-IV Criteria

One alternative approach to help detect comorbid depression is to modify the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,12 to include the criteria in Table 1.13

 

 

Eliciting Positive Answers

Eliciting positive answers to the questions in Table 2 should raise awareness of the possibility of depression.

 

 

Asking Useful Questions

It is important to ask prime medical questions eliciting emotion and cognitive symptoms (Table 3).14 For example, during the past month, has the patient been frequently bothered by feeling down, depressed, or hopeless? During the past month, has he or she held little interest or experienced meager pleasure from certain activities? More simply, the patient could be directly asked if he or she felt sad or depressed, which seems to be the simplest and most yielding research question.

 

 

 

Prevalence Rates of Depression in Various Medical Conditions

As per the United States Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, the prevalence rates of depression in various medical conditions are listed in Table 4 and Figure 1.15-27

 

 

 

Cardiovascular System

According to Ginzburg, “the damage to the heart, with its symbolic meaning as the essence of the human being may shatter the patient’s sense of wholeness and safety.”28

Figure 2 shows cumulative mortality for depressed and non-depressed patients following a heart attack.29

 

As first reported by Frasure-Smith and colleagues,29 MDD in patients hospitalized following a myocardial infarction is an independent risk factor for mortality at 6 months and increases mortality 3–5 fold. Its impact is at least equivalent to that of left ventricular dysfunction and history of previous myocardial infarction.

A prospective cohort study by Surtees and colleagues30 found that MDD was associated with an increased risk of ischemic heart disease mortality. This association was independent of established risk factors for ischemic heart disease and remained undiminished several years after the original assessment.

One study31 has shown that, after acute coronary syndromes, depressed patients have elevated levels of inflammatory markers, thus suggesting chronic endothelial activation among these patients.

Depression may itself predispose to vascular disease. Mechanisms proposed for the linkage between depression and cardiovascular disease include the effects of hypercortisolemia (glucocorticoids inhibiting inflammation processes38 or by reducing glucocorticoid signaling leading to abnormal brain functioning32-24), immune activation, depression-related platelet aggregation leading to increased thrombosis, depression-induced impairment of arterial endothelial functioning, and abnormal folate or homocysteine metabolism. Although these mechanisms have been proposed to relate depression to cardiovascular diseases, depression could also be linked to cerebrovascular disease.32

 

Cerebrovascular System

Depression occurs in approximately 40% of patients with acute stroke and has been linked to poorer cognitive and physical recovery. An association between depressive symptoms and stroke mortality was reported by Morris and colleagues,35 who found that stroke patients with in-hospital depression were 3.5 times more likely to die during 10 years of follow up than patients without depression.

Treatment with fluoxetine or nortriptyline for 12 weeks during the first 6 months poststroke significantly increased the survival of both depressed and nondepressed patients. This finding suggests that the pathophysiologic processes determining the increased mortality risk associated with poststroke depression last longer than the depression itself and can be modified by antidepressants.36

Based on the above, one could wonder if depression is a “contributor or a consequence” of both cardiovascular and cerebrovasular pathologies (Figure 3).37,38 It remains possible that the high rate of depression in both conditions represents a common vascular mechanism.39

 

 

 

Cancer

The prevalence of depression among cancer patients ranges between 23% and 60%. Acute stress and anxiety and/or dysphoric states following discovery of cancer (a traumatic life event) are poorly understood in traditional medical settings. Pain and depression are the most common neuropsychiatric presentations, and they are followed by fatigue, distress, and various disabilities. As the disease progresses, immunologic changes and the effect of treatment could be an additional burden contributing to MDD. Increased levels of cytokines, (eg, interleukin) secreted by the immune system to fight cancer or infections could also result in “sickness behavior syndrome,” characterized by a depressed mood, sleepiness, and poor concentration (Figure 4).40 Higher than normal plasma IL-6 concentrations were associated with a diagnosis of MDD in cancer patients. IL-6 may contribute to sickness behavior that has overlapping symptoms with MDD.41

 

While helping to bolster the immunologic response, it is equally important to acknowledge the patient’s symptoms and treat them vigorously with cognitive-behavioral therapy, stress management, and antidepressant drug therapy.

 

Diabetes Mellitus

Depression as a precursor and as a consequence to type 2 diabetes has been studied. Prevalence of depression in adult diabetics is 3–5 times compared to prevalence in general population. Fourteen percent to 15% of patients diagnosed with type-2 diabetes have MDD. Thirty-three percent of all patients with neuropathy, retinopathy, and nephropathy are depressed. MDD in diabetes indicates poorer prognosis, worse glucose control, increased symptoms, decreased adherence to prescription plans, increased complications, decreased overall functional well being, and occasionally suicidality with complications.

Following a large population-based study in Norway, Engum and colleagues21 concluded that diabetes did not predict symptoms of depression or anxiety. Rather, symptoms of depression and anxiety emerged as significant risk factors for onset of type-2 diabetes independent of established risk factors for diabetes, such as socioeconomic factors, lifestyle factors, and markers of the metabolic syndrome.

The studies, presented at the meeting of the European Association for the Study of Diabetes,42 add to a growing body of evidence linking depression and other mental disorders to diabetes risk. Symptoms of depression or psychological stress were associated with increased risk of type-2 diabetes in men, but not in women, as per Swedish researchers.42 “People with diabetes had a higher prevalence of all mental illnesses compared with people without diabetes,” according to researchers from Canada.43 In particular, they noted that the rate of affective and anxiety disorders was >30% higher in people with diabetes who were <50 years of age. Other researchers have found hippocampal changes in patients with juvenile onset diabetes.

 

Neurologic Illnesses

Table 5 provides the rates of depression in neurologic illnesses.44

 

 

 

Aging, Frailty, and Alzheimer’s Disease

Physical frailty and need for assistance in daily living often causes dysphoria. However, depression should not be accepted as a normal part of aging, as untreated depression in the elderly causes needless suffering. Depression can render mild cognitive impairment to appear like dementia, thus confounding diagnosis and prognostication. A history of early onset depression increases the risk for Alzheimer’s disease compared to those with no history.45

 

HIV/AIDS

In addition to social stigma in the early stages, even when physically well, drug issues, HIV’s later physical effects of nausea and fatigue with anti-retro virals, HIV-related apathy, mood disorders, and cognitive impairments are seldom recognized early in the course of the disease. The cerebral events may remain compartmentalized and not necessarily reflected in the routine assessment of peripheral markers such as viral loads or T-cell counts.

 

Musculoskeletal Rehabilitation

See Table 6 for the prevalence of psychiatric disorders in musculoskeletal rehabilitation.46

 

 

 

Conclusion

In addition to the knowledge that depression contributes both to disability and diminished survival among medically ill, it is increasingly evident that MDD is a multi-systemic disorder that affects both brain and bodily functions.40

The inter-relationship between the two is rather complex. Inflammation could be the common link through neuro-immuno-endocrine mechanisms contributing to both psychological and somatic symptoms such as depression and cardiovascular diseases.27,47,48 As more evidence accumulates, it seems clear that late-onset depression in particular is not just a mood disorder but could be a warning signal of an impending major or catastrophic physical illness. It is well known that depression is a heralding symptom of undiagnosed medical conditions including multiple sclerosis, Parkinson’s disease, hypo- or hyperthyroidism, Cushing’s disease, and pancreatic cancer. The assessment of both conditions and the interaction between them is critical in managing these patients.1 When the medical illness is treated, the depression often gets better. While the importance of recognition and treatment of comorbid depression in helping reduce disability and suffering is very clear, the effect of treatment on the course of the comorbid illnesses themselves and the overall effect on survival need to be further studied. Also in need of further investigation are yet-to-be-discovered, non-antidepressant, disease-modifying effects of selective serotonin reuptake inhibitors or other newer agents on diabetes, stroke, multiple sclerosis, and Alzheimer’s disease (among other diseases).

Considering the available evidence, it is clearly prudent to include aggressive treatment of comorbid depression, utilizing all available modalities—including psychopharmacologic agents—in the management of all physical illnesses. PP

 

References

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2.    Goodnick PJ, Hernandez M. Treatment of depression in comorbid medical illness. Expert Opin Pharmacother. 2000;1(7):1367-1384.
3.    Peveler R, Carson A, Rodin G. Depression in medical patients. BMJ. 2002;325(7356):149-152.
4.    Rapp MA, Schnaider-Beeri M, Grossman HT, et al. Increased hippocampal plaques and tangles in patients with alzheimer disease with a lifetime history of major depression. Arch Gen Psychiatry. 2006;63(2):161-167.
5.    Wyszynski AA, Wyszynski B. Manual of Psychiatric Care for the Medically Ill. 1st ed. Washington, DC: American Psychiatric Publishing, Inc.; 2004.
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31.    Lesperance F, Frasure-Smith N, Theroux P, Irwin M. The association between major depression and levels of soluble intercellular adhesion molecule 1, interleukin-6, and C-reactive protein in patients with recent acute coronary syndromes. Am J Psychiatry. 2004;161(2):271-277.
32.    Kales HC, Maixner DF, Mellow AM. Cerebrovascular disease and late-life depression. Am J Geriatr Psychiatry. 2005;13(2):88-98.
33.    Pace TW, Hu F, Miller AH. Cytokine effects on glucocorticoid receptor function. Brain Behav Immun. 2007;21(1):9-19.
34.    Andrea Danese, Moffitt TE, Pariante CM, Ambler A, Poulton R, Caspi A. Elevated inflammation levels in depressed adults. Arch Gen Psychiatry. 2008;65(4):409-416.
35.    Morris PL, Robinson RG, Andrzejewski P, Samuels J, Price TR. Association of depression with 10-year poststroke mortality. Am J Psychiatry. 1993;150(1):124-129.
36.    Jorge RE, Robinson RG, Arndt S, Starkstein S. Mortality and poststroke depression: a placebo-controlled trial of antidepressants. Am J Psychiatry. 2003;160(10):1823-1829.
37.    Hays JC, Krishnan KR, George LK, Blazer DG. Age of first onset of bipolar disorder: demographic, family history, and psychosocial correlates. Depress Anxiety. 1998;7(2):76-82.
38.    Frasure-Smith N, Lesperance F. Depression and other psychological risks following myocardial infarction. Arch Gen Psychiatry. 2003;60(6):627-636.
39.    Aben I, Verhey F, Strik J, Lousberg R, Lodder J, Honig A. A comparative study into the one year cumula¬tive incidence of depression after stroke and myocardial infarction. J Neurol Neurosurg Psychiatry. 2003;74(5):581-585.
40.    Insel TR, Charney DS. Research on major depression: strategies and priorities. JAMA. 2003;289(23):3167-3168.
41.    Musselman DL, Miller AH, Porter MR, et al. Higher than normal plasma interleukin-6 concentrations in cancer patients with depression: preliminary findings. Am J Psychiatry. 2001;158(8):1252-1257.
42.    Östenson CG, Eriksson AK, Granath F, Hilding A, Efendic S, Ekbom A. Depressive symptoms and risk of type 2 diabetes and pre-diabetes in a prospective study of middle aged Swedish men and women. Paper presented at: 43rd Annual Meeting of the European Association for the Study of Diabetes; September 20, 2007; Amsterdam, Netherlands.
43.    Osterweil, N. Studies Link Depression and Type 2 Diabetes. EASD: European Association for the Study of Diabetes Meeting. MedPage Today. Reviewed by Agus, Z. Sept 21, 2007. Available at: www.medpagetoday.com/MeetingCoverage/EASD/tb/6752. Accessed August 7, 2008.
44.    Geerlings MI, den Heijer T, Koudstaal PJ, Hofman A, Breteler MM. History of Depression, depressive symptoms, and medial temporal lobe atrophy and the risk of Alzheimer disease. Neurology. 2008:70(15):1258-1264.
45.    Schiffer RB. Goldman consensus statement on depression in MS. Goldman Consensus Group. Multiple Sclerosis. 2005;11:328-337.
46.    Harter M, Reuter K, Weisser B, Schretzmann B, Aschenbrenner A, Bengel J. A descriptive study of psychiatric disorders and psychosocial burden in rehabilitation patients with musculoskeletal diseases. Arch Phys Med Rehabil. 2002;83(4):461-468.
47.    Evans DL, Charney DS, Lewis L, et al. Mood disorders in the medically ill: scientific review and recommendations. Biol Psychiatry. 2005;58(3):175-189.
48.    Berkman LF, Blumenthal J, Burg M, et al. Effects of treating depression and low perceived social support on clinical events after myocardial infarction: the enhancing recovery in coronary heart disease patients (ENRICHD) randomized trial. JAMA. 2003;289(23):3106-3116.

Letter to the Editor

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Adam Keller Ashton, MD
Primary Psychiatry. 2008;15(8)

 

To the Editor:              

I read Dr. Ginsberg’s comments in the August 2007 Primary Psychiatry1 on aripiprazole’s off-label use for augmentation of established therapy for the treatment of obsessive-compulsive disorder.2 I wanted to alert you that I had written what I believe was the first such report, at least according to the manufacturer Bristol-Myers Squibb (personal communication, September 7, 2007). In January 2005 I reported a woman who had failed trials of six adequately dosed selective serotonin reuptake inhibitors (SSRIs) and clomipramine, as well as having had a course of cognitive-behavioral psychotherapy.3 This patient subsequently improved to what she felt was “55% better” with a combination of sertraline 200 mg/day along with escitalopram 30 mg/day. However, she experienced the most improvement with aripiprazole augmentation using 30 mg/day in addition to her two SSRIs, stating she was now “70%” improved; she has maintained this improvement thus far for >2 years. This report was not referenced in the column1 as I have since discovered that the journal in which it was published does not subscribe to the larger medical reference services.

Case reports such as these are plagued by limitations including small sample size and the possibility of placebo response, although the latter would be unlikely after failing many prior agents as well as experiencing an enduring clinical improvement over the course of years. Nevertheless, I was encouraged to read of this latest example of aripiprazole augmentation as it reinforces what I, too, have seen on occasion, namely, the non-psychotic patient with refractory anxiety who seems to inexplicably respond to the addition of an atypical antipsychotic. Further research in this area will hopefully shed light on which patients may be good candidates for this kind of clinical approach. At the least, reports such as these stimulate academic dialogue and hopefully encourage clinicians to report their findings in peer-reviewed journals.

Sincerely,
Adam Keller Ashton, MD

Dr. Ashton is clinical professor of psychiatry at the State University of New York at Buffalo School of Medicine.

Disclosure: Dr. Ashton has been on the speaker’s bureaus of AstraZeneca, Bristol-Myers Squibb, Cephalon, Eli Lilly, Forest, GlaxoSmithKline, Pfizer, sanofi-aventis, Sepracor, Takeda, and Wyeth.

 

References

1. Ginsberg DL. Psychopharmacology reviews. Primary Psychiatry. 2007;14(8):19-20.
2. Friedman S, Abdallah TA, Oumaya M, Rouillon F, Guelfi JD. Aripiprazole augmentation of clomipramine-refractory obsessive-compulsive disorder. J Clin Psychiatry. 2007;68(6):972-973.
3. Ashton AK. Aripiprazole augmentation of combination escitalopram and sertraline in the treatment of refractory obsessive-compulsive disorder. Psychiatry. 2005;2(1):18-19.

 

Response

I extend my sincere thanks to Dr. Ashton for sharing with us his case report. I agree with his comment that gaining better insight into candidate selection for off-label approaches such as the one here is very important to pursue. Our patients’ needs demand it.

Sincerely,
David L. Ginsberg, MD

Dr. Ginsberg is Vice-chair of Clinical Affairs in the Department of Psychiatry at New York University Langone Medical Center in New York City, and author of the Primary Psychiatry column “Psychopharmacology Reviews.”

Disclosures: Dr. Ginsberg receives hororaria for lectures, papers, and/or teaching from AstraZeneca and GlaxoSmithKline; and receives research support from Cyberonics.

Please send letters to the editor to Primary Psychiatry, c/o Norman Sussman, MD, 333 Hudson St., 7th Floor, New York, NY 10013; E-mail: ns@mblcommunications.com.

 

Dr. Franks is associate professor in the Department of Psychiatry and Ms. Kaiser is doctoral candidate in health psychology at the University of North Texas Health Science Center in Fort Worth, Texas.

Disclosures: The authors report no affiliation with or financial interest in any organization that may pose a conflict of interest.
Please direct all correspondence to: Susan F. Franks, PhD, 3500 Camp Bowie Blvd, University of North Texas Health Science Center, Department of Psychiatry, Fort Worth, TX 76107; Tel: 817-735-5122; Fax: 817-735-0615; E-mail: franks@hsc.unt.edu.

 


 

Focus Points

• Bariatric surgery candidates are psychologically heterogeneous.
• The preoperative psychological evaluation provides recommendations for optimizing outcomes.
• Psychological risk factors reducing post-operative success must be uniquely considered for the individual patient.

 

Abstract

What are the psychological characteristics of bariatric surgery candidates? What components of the preoperative psychological evaluation are the most relevant to postsurgical outcomes? Bariatric surgery is a weight-loss tool that can resolve obesity-related comorbidities and improvements in quality of life. The degree of success experienced by patients depends largely on their ability to maintain postsurgical lifestyle changes affecting weight loss and maintenance. Understanding the psychological and behavioral issues unique to bariatric patients is important for primary care and mental health providers so that pre- and postsurgical treatment recommendations are developed to optimize outcomes.

 

Introduction

Bariatric surgery is more common in the United States due to the increasing rate of morbid obesity, advances in surgical techniques, and accessibility of the procedure.1,2 Based on the 1991 National Institutes of Health Consensus Development Panel recommendations3-5 and psychological and behavioral factors impacting obesity and weight loss in conventional programs, it has been widely believed that a presurgical psychological evaluation is valuable to bariatric surgery candidates. While initial hopes were to determine a clear set of prognostic indicators serving to screen those who would not be successful,6,7 it is increasingly clear that this oversimplifies a more complex phenomenon.8,9

Recently, there has been a conceptual shift in the role of the preoperative psychological evaluation.10 In addition to identifying patients who may clearly be unsuitable for the procedure, the preoperative evaluation can be designed to identify risk factors and formulate treatment plans to improve postsurgical outcomes.8 This article provides a clinical-educational review of published data regarding the crucial elements of the preoperative psychological evaluation, highlighting key risk factors of prognostic value that may be used to improve patient outcomes.

 

Methods

The relevant literature was identified through a search on PubMed, MedLine, and PsychInfo. Several reviews, published between 2003 and 2006,9,11-13 were identified that covered a scope similar to this article. To build on these reports, the authors performed a comprehensive review of empirical studies published from January 2003 to March 2008. Articles were excluded if they were in certain categories, including non-English language, adolescent samples, case or questionnaire validation studies, surgical technique, nursing concerns, general commentaries, or <1-year postsurgical follow up. In order to increase the likelihood of adequate statistical power, reports with total sample sizes of <50 were also excluded. Otherwise, articles published between January 2003 and March 2008 that meet the aforementioned criteria were included in this article.

The organization of this article is based on clinical utility. This method of presentation will allow the clinician to process multiple sources of information in a manner consistent with standard training and clinical practice. Elements of the preoperative evaluation are presented as they are customarily organized in a standard diagnostic intake. Table 1 provides commonly used acronyms and their definitions.

 

 

 

Results

Demographics

The most frequently examined demographic variables were age, gender, and race/ethnicity. Although studies were restricted to investigation of presurgical differences, the present article focuses on how select demographic differences may be related to postsurgical outcomes alone or in combination.

 

Gender

A recent study examining age and gender differences found that older males had the least percent excess weight loss (%EWL).14 Other studies comparing gender directly to postsurgical outcomes have not found a significant relationship.15,16 However, the low proportion of male subjects (16.9% to 24%) in these studies may have obscured the possible influence of gender.

Age
Age has been demonstrated to be a factor in weight-loss outcomes in three of the four studies reviewed.14,15,17,18 Based on a 50% EWL success criterion in a sample of 1,081 subjects followed for 2 years, significant odds ratios for failure were found for patients with higher age, higher initial body mass index (BMI), and lack of either recovery or increased levels of physical activity.17 Others found that while the older patients did not lose as much weight as their younger counterparts, their rates of comorbidity resolution were similar.18

Race/Ethnicity
In a recent study19 of 213 African American and Caucasian bariatric surgery candidates matched for age, gender, and presurgical BMI, a lower %EWL was found for African Americans at 3 years postsurgical follow up. Both groups had similar rates of comorbidity resolution. Others have found no difference in %EWL between African Americans and Caucasians. However, the low percentages of African Americans (5.5%) in this study may have interfered with the validity of the findings.20

 

Medical History

Existing medical factors in bariatric surgery candidates have been an important consideration in approval for surgery, surgical procedure selection, and medical management. Two studies21,22 indicated that diabetics were at greater risk for lower %EWL from 1–2 years post-surgery In one sample21 of 494 subjects, when controlling for age, gender, depression, and baseline weight, diabetes remained a significant predictor of lower %EWL. A review of insurance claims cases (N=1,760) indicated that preoperative sleep apnea or GERD were most predictive of postoperative complication risks.23

 

Psychiatric History

Recent studies utilizing the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (SCID) to examine a history of diagnosable psychiatric conditions have consistently estimated an approximately 37% lifetime prevalence rate for any Axis I disorder. However, there was less agreement regarding lifetime prevalence rates for specific disorders, even when utilizing the same methodology. Table 2 provides a summary of lifetime prevalence rates for Axis I disorders.24-29

 

 

Previous reviews of the literature resulted in slightly differing conclusions regarding the importance of psychiatric history on outcomes of bariatric surgery. While some concluded that a history of psychiatric inpatient admissions were related to postsurgical medical/psychological complications and poor patient satisfaction, the admission number was not related to weight loss.7,9 Prior outpatient treatment was not significantly related to any outcome variable studied. Others found that a history of psychiatric treatment or counseling for substance abuse was a positive predictor for postsurgical weight loss attributable to the development of adaptive lifestyle skills that may generalize to postoperative behavioral and psychological challenges.13

 

Psychosocial History

Aspects of the psychosocial history of bariatric surgery candidates have been examined for their prognostic role in postsurgical success. These have included childhood abuse and maltreatment, marital status, social support, and psychosocial stress.

Childhood Sexual Abuse and Maltreatment
Utilizing the Childhood Trauma Questionnaire (CTQ), approximately 65% to 69% of patients undergoing Roux-en-Y gastric bypass (RYGB) reported some form of childhood maltreatment estimated to be 2–3 times higher than that found in normative community samples.30,31 Estimated rates of childhood sexual abuse varied widely among studies. When responding to questioning, between 17% and 50% of RYGB candidates reported a history of sexual abuse.32,33 However, in response to the CTQ, approximately 30% of RYGB patients were found to have a childhood history of sexual abuse.30,31,34 Use of the CTQ also determined rates of approximately 47% for childhood emotional abuse, and 29% to 40% for physical abuse.30,31 Physical and emotional neglect were estimated at 32% and 49%, respectively.30 Although BMI in RYGB candidates has not been related to childhood maltreatment, the results of studies examining the relationship between childhood maltreatment and psychopathology have been conflicting.30,31

Specific forms of childhood maltreatment other than sexual abuse have not been studied with regard to bariatric surgery outcomes. Two articles9,13 differed in conclusion regarding the prognostic significance of childhood sexual abuse. Recent studies33,34 comparing patients with and without a history of childhood sexual abuse did not find it to be of prognostic significance at 12 and 24 months post-surgery. Table 3 provides a summary of recent articles related to childhood sexual abuse and postsurgical outcomes.21,33-38

 

 

Marital Satisfaction
Two recent reviews of the literature found conflicting results regarding the role of marital satisfaction on weight-loss outcomes in bariatric surgery patients. Herpertz and colleagues39 found that marital dissatisfaction was a positive predictor of weight loss. However, van Hout and colleagues9 suggested that marital satisfaction positively affected weight loss and that problematic marital relationships could potentially create challenges as the patient lost weight.

Support System
A previous review reported that social support in bariatric patients was an important determinant of adherence to postsurgical lifestyle modifications and may affect weight loss.13 However, others concluded that although low levels of social support were associated with postoperative medical and psychological complications, it had no bearing on weight loss.39

Psychosocial Stress
In comparison to treatment-seeking women with mild and moderate obesity, women with severe obesity seeking bariatric surgery reported experiencing higher levels of stress related to health, legal, or financial matters.40 High levels of preoperative life stress may be positively associated with weight loss, and patients have been found to experience the same positive physical and psychological well-being after surgery regardless of stress level.9,39

 

Other Issues

Body Dissatisfaction
According to a recent review,41 approximately 70% of patients reported body dissatisfaction prior to surgery. Limited research suggested patients with childhood-onset obesity showed less satisfaction with postsurgical weight and shape than patients whose obesity developed in adulthood.41 Although less presurgical body dissatisfaction has been correlated with greater weight loss, a causal relationship with postsurgical weight loss has not been established.

Self-Esteem
Studies utilizing self-esteem measures have reported lower self-esteem in bariatric surgery candidates than in normal weight reference groups.41 A comparison study of patients in different weight classification groups found that severely obese bariatric candidates were lower in self-esteem than patients in the lower-level obesity classifications.40 A previous review by van Hout and colleagues9 found conflicting results with regard to the impact of self-esteem on postsurgical weight loss.

Personality Traits
Herpertz and colleagues39 concluded that there was insufficient evidence to support the prognostic value of personality traits with regard to postsurgical weight loss or mental health outcomes. Van Hout and colleagues42 recently utilized a cluster analytic approach to investigate psychological profiles in 153 candidates for vertical banded gastroplasty (VBG). Results confirmed the heterogeneity of the group, indicating three distinct clusters ranging from high to low functioning on a variety of domains, including personality, coping, eating behavior, locus of control, body attitude, social functioning, and health-related quality of life (HRQOL). They suggested that the heterogeneity of bariatric surgery candidates and the reliance on psychological measures not specifically obesity-related may account for the inconsistent findings across studies.

 

Current Psychiatric Status

Current prevalence rates of specific Axis I pathologies varied widely across studies due to methodologic differences in determining diagnosis.27,40,43-45 For example, clinician-formulated impression determined major depressive disorder (MDD) as the most common Axis I diagnosis,27 whereas the use of the SCID ranked MDD as third most prevalent behind anxiety disorders and eating disorders.45 Recent data indicated that prevalence rates of psychiatric disorders based on the use of formal diagnostic criteria appear to match findings in the general population.45 However, studies of psychopathology have consistently found greater preoperative rates in severely obese patients seeking bariatric surgery as compared to the general population, non-treatment seeking obese individuals, and mild-to-moderately obese treatment-seeking patients.40,43,44 Furthermore, several studies reported sizable numbers of surgical candidates undergoing psychiatric treatment at the time of their evaluation, ranging from 38.9% to 47.7%.10,27 Table 2 provides a summary of prevalence rates for current Axis I disorders.

An absence of psychiatric problems and personality disorders has been associated with greater weight loss and positive postoperative psychosocial outcome.39 Although there has been little systematic study on clinical practice decisions based on preoperative psychological evaluations, Pawlow and colleagues10 reported that recommendations were made to defer surgery for 15.8% of their 449 patients based on a diagnosis of MDD, either as sole or primary psychiatric diagnosis. Sarwer and colleagues27 reported a psychiatric referral rate of 26.7% in their sample of 90 patients evaluated for RYGB and VGB. Slightly >50% of 58 patients diagnosed with a form of psychopathology were undergoing psychiatric treatment at the time of their presurgical evaluation.

Depression
The use of SCID-based DSM-IV criteria has yielded substantially lower estimates of MDD (3.4% to 10.4%)24,25,45 than the use of depression questionnaires21 or clinician-driven diagnostic determinations (31.1% to 44.9%; Table 2). Prevalence rates for dysthymia ranged between 1.1% and 5.7%.24,25,45 Based on available empirical evidence, it appears that depression does not prevent postsurgical success. An article by van Hout and colleagues9 found that in many studies, depression predicted less weight loss than in non-depressed patients but was not prognostic of overall failure or success. Rather, bariatric surgery in depressed patients generally appeared to result in significant treatment gains with respect to weight loss, psychosocial function, and quality of life.41,46 Recent follow up with preoperatively depressed patients found that depression was not a negative predictor for postoperative success based on %EWL or HRQOL,21 and in some patients it may promote greater weight loss over the short term.21,35 Table 3 provides a summary of articles related to depression and postsurgical outcomes.

It should be noted that approximately 33% to 50% of bariatric surgery candidates may already be taking antidepressants or be in some other form of psychological treatment prior to surgery, which was not accounted for in these studies.10,27 Pawlow and colleagues10 found antidepressants were the most commonly prescribed psychotropic medication in the 47.7% of 153 patients who were taking at least one psychotropic at the time of their evaluation.10 It was unclear whether these were prescribed for depression or other psychiatric reasons. However, these were most often prescribed by primary care physicians.27

Anxiety
Despite recent findings of considerable prevalence rates, anxiety appears to have been under-recognized in bariatric surgery candidates. There is disagreement between studies regarding rates for specific disorders (Table 2). The role of anxiety in postsurgical outcomes has not been well studied, perhaps due to the assumption that it is largely related to the societal stigma and bias experienced by obese people.24,28 Limited evidence suggested that the presence of anxiety as a correlate of psychosocial stress may be positively associated with weight loss.9,39 At 2-year follow up in the Swedish Obese Subjects study, declining levels of distress were found with increased weight loss.47

Binge Eating Disorder
Prevalence rates of binge eating disorder (BED) and binge eating of any kind in bariatric surgery candidates have been highly variable.25,27,29,36-38,45,48 Previous research has found that most studies reported significant postsurgical weight loss in bariatric patients with BED or binge eating behaviors, although some studies found a smaller percent weight loss for this group than patients without similarly disordered eating.9,13,39,49,50 Patients who develop or redevelop binge eating behaviors postsurgically were found to experience more weight regain at long-term follow up.9,39,50

Recent studies of RYGB and laparoscopic adjustable gastic banding (LAGB) patients have consistently found no significant differences in %EWL between BED and non-binge eating (NBE) for follow-up periods of 1–5 years.33,36,37 However, one prospective study found that patients with a presurgical diagnosis of BED or sub-clinical BED showed less %EWL than NBE at 2-year follow up.38 In a recent study of LAGB patients,37 those with a presurgical diagnosis of BED had a higher frequency of manageable postsurgical complications and underwent more band adjustments than their non eating-disordered counterparts. No differences in postsurgical medical complications between patients with and without BED have been reported for patients undergoing RYGB, suggesting that restrictive procedures hold particular challenges for patients who do not normalize their eating behavior postsurgically. Table 3 provides a summary of articles related to BED and postsurgical outcomes.

Somatization and Hypochondriasis
Only one study28 examining Axis I prevalence rates deteremined the presence of somatization disorder (29.3%) and hypochondriasis (15.0%) in a sample of 294 patients (RYGB candidates) who were evaluated with a screening questionnaire. These findings were attributed to characteristic obesity-related physical concerns and problems. Using the Minnesota Multiphasic Personality Inventory-2 (MMPI-2), higher presurgical elevations of the hypochondriasis and hysteria scales were found for RYGB patients with <50 %EWL as compared to those with >50 %EWL at 1-year follow up.51 However, neither of these two MMPI-2 scales were above the clinical cut off.51 Relationships have been found between the presence of at least one lifetime and current Axis I disorder with BMI, pain, and health-related role limitations.24 The propensity toward somatic focus is unclear as it relates to postoperative outcome.

Personality Disorder
Prevalence rates of Axis II pathologies were generally consistent across studies, ranging from 19.5% to 29%.24,25 The highest prevalence rates were found for Cluster C disorders at approximately 18%, with avoidant personality disorder at 6.8% to 17% and obsessive-compulsive personality disorder between 7.6% and 13.9%.25 Previous articles concluded poor postsurgical weight loss was likely for bariatric candidates with personality disorder due to poor adaptive skills and lack of insight.12,13 Concerns have also been raised regarding the ability of patients with borderline personality disorder to remain stable under the stress inherently associated with any major surgical procedure.13

 

Eating Patterns

Eating behaviors that have been the subject of recent empirical studies include grazing, night eating syndrome, and emotional eating. Grazing has been a factor in some patients both pre- and postoperatively,52 but the effect on weight loss has not been empirically studied. Table 4 provides a summary of recent studies on eating behavior and outcomes.53-57

 

 

Eating Behavior
Aside from the maladaptive eating patterns previously discussed, general eating behavior has been the subject of numerous measurement tools to determine increased risk for disordered eating or obesity (eg, Three-Factor Eating Questionnaire [Eating Inventory], Dutch Eating Behavior Questionnaire, Questionnaire on Eating and Weight Patterns-Revised, Eating Disorders Inventory, Weight and Lifestyle Inventory). Many of these tools have applied slightly different names for the same general constructs of cognitive restraint, disinhibition and hunger described by Stunkard and Messick.58 Bariatric surgery patients have been shown to fall anywhere in the spectrum of these factors. Data59,60 indicated that Eating Inventory scores for hunger and disinhibition drop to the “low-average” range up to 1-year post-LAGB, but whether these changes are stable is unknown.

Recent studies evaluating postsurgical weight loss as related to changes in eating behavior all highlight the importance of this component of postsurgical management.53,54,56,57,61,62 Patients have generally reported that they do not experience hunger in the early months following surgery. If patients are not prepared to cope with a return of hunger cues or a tendency to eat despite a lack of hunger cues, the efficacy of the surgery as a weight-loss tool may be diminished.

 

Discussion

Results of the present review highlight the heterogeneity of bariatric surgery candidates, resulting in inconsistent and often conflicting results between studies examining presurgical characteristics and postsurgical outcomes. However, patterns emerge of which the clinican should be alert. This will promote evidence-based decision making and treatment recommendations on behalf of bariatric surgery candidates.

Having reasonable expectations for weight loss is clearly important for diabetics and older patients, who are known to lose less weight than their healthier or younger counterparts. Similarly, patients with a childhood onset of obesity appear to be at risk for dissatisfaction with postsurgical weight and shape. These patients may need additional education and postsurgical support regarding expectations for outcomes. Patients with sleep apnea and GERD need to have an understanding of their postoperative complication risks to increase compliance.

A history of Axis I psychiatric disturbance appears to be important, but the associated positive or negative postsurgical outcomes appear to depend on the degree to which the person was able to benefit from psychological treatment. In addition, patients with psychologically unresolved histories of childhood sexual abuse may be at risk for negative psychological consequences after substantial weight loss and may require additional postsurgical support. Suggestions have been made to inquire about the patient’s attribution of their weight as a psychological “protective factor” to assist the patient in anticipating negative psychological consequences to significant weight loss.13

Based on reports of present practices, there is general agreement that current alcohol and/or illicit substance abuse, active psychosis, and inability to provide informed consent contraindicate surgery.6,10,63 Uncontrolled bipolar disorder and a history of suicide attempts receive similar concerns.6,63 It is also thought that patients with a personality disorder lack the adaptive skills, insight, and mental stability necessary to consistently comply with postoperative recommendations and long-term lifestyle changes. Because such patients are generally screened out in the preoperative evaluation phase, these various conditions have not been empirically studied.

A current diagnosis of depression or anxiety does not generally appear to negatively affect weight loss. However, the extent to which these are tied to the patient’s distress about being obese may be important with regard to psychosocial outcomes and postoperative compliance. Pre- and postsurgical intervention may be necessary for some patients to help increase postoperative compliance and improve quality of life.48 Collazo-Clavell and colleagues64 emphasized the serious effect that psychotropic medications may have on weight and recommended selection or modification of the medication regimen to promote weight loss. Thus, psychotropic medication regimens, regardless of the condition for which they are prescribed, should be evaluated for their efficacy and potential to adversely affect weight and should be monitored over the course of weight loss.

There has been disagreement among authors regarding recommendations for bariatric candidates with BED. Some suggested that significant binge eating should be treated prior to surgery,13 while others concluded that there is insufficient evidence to exclude such patients from bariatric surgery or provide preoperative care.9,37 Others have suggested that postsurgical success in BED patients requires continued postsurgical support and long-term follow up.49 The types of patients who may be at risk for less than optimum weight loss as a result of maintenance or development of binge eating behaviors is unclear and should be further studied. Because LAGB patients with postsurgical binge eating behaviors are at higher risk for medical complications, they should undergo psychological intervention and close postsurgical monitoring.

The quality of the marital relationship and extended social support appear to be important determinants of postsurgical medical and psychological complications. It has been suggested that patients should have an awareness of the impact that dramatic weight loss can have on relationships in order to prepare them for potential psychological challenges.13 Thus, a detailed inquiry regarding the quality of relationships and the patient’s psychological dependence on them is important to determine potential targets of clinical focus.

Findings regarding other demographic, psychiatric, behavioral, and psychosocial issues were either inconsistent or have not been studied well enough to draw conclusions. In addition, the use of a variety of different assessment approaches, often non-standardized, as well as differences in frequency and length of follow up make it difficult to compare studies. Numerous studies were excluded from this article because of small sample sizes that render results without adequate statistical power and subject to the errors of utilizing a non-representative sample from a highly heterogeneous population.

Despite the recognition that there are multiple outcomes by which to measure success, the search for factors predictive of postsurgical outcomes for bariatric patients has been predominantly focused on the 50% EWL criterion. This particular criterion is a statistically derived marker with no demonstrated clinical relevance and is subject to inconsistencies in ideal weight calculations. This asks the therapist to predict degrees of success in comparison to an arbitrary standard, instead of other more clinically relevant outcomes. Weight loss that is less than “ideal” may still represent a positive outcome with regard to reduced comorbidities, improved quality of life, and psychosocial functioning. Furthermore, a standard for postsurgical failure has yet to be defined, certainly a disconcerting fact since the initial purpose of the psychological evaluation was to identify high-risk patients. Since improved medical outcomes provides current justification for the surgery, perhaps postsurgical failure should be considered the point at which obesity-related comorbidities return or do not resolve.

 

Conclusion

Given the state of current knowledge regarding predictive factors for postsurgical outcomes, there is no empirical basis for widely accepted contraindications to bariatric surgery. Except for the psychopathologic states of patients who are clearly unable to be responsible for their health care, some psychological factors may predispose patients to more or less favorable outcomes. However, this is not to imply that they predict negative outcomes. Such conclusions need to be based on studies identifying patients whose obesity-related comorbidities return or do not resolve.

Furthermore, few preoperative characteristics have been consistently predictive of postoperative outcomes in the type of studies that have been performed. Rather than concluding that preoperative factors are of little utility for prognosis, the field should critically examine the methodologic approach taken to elucidate these relationships. Group-based statistical designs focusing on single, global psychological constructs can obscure results that may be meaningful in aggregate at the individual level. Studies that are designed to examine multiple psychological constructs may prove valuable for developing more sophisticated evidence-based guidelines for presurgical psychological evaluations, prognostic determinations, and treatment recommendations.

Bariatric surgery is currently the most effective treatment for obesity in terms of the amount of weight lost and, therefore, offers the best hope for resolution of the associated comorbidities. Future studies should also investigate the trajectory of biologic and psychological change over long-term follow up, in order to determine a true marker by which success and failure can be explored. Until then, a clinician in the preoperative psychological evaluation must converge multiple factors at the individual level in order to determine pre- and post-treatment recommendations that will maximize an individual patient’s chances for optimal postsurgical outcomes. PP

 

References

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2.     Nguyen NT, Root J, Zainabadi K, et al. Accelerated growth of bariatric surgery with the introduction of minimally invasive surgery. Arch Surg. 2005;140(12):1198-1202.
3.    NIH Consensus Development Conference. Gastrointestinal Surgery for Severe Obesity. National Library of Medicine 1991. Available at: http://consensus.nih.gov/1991/1991GISurgeryObesity084PDF.pdf. Accessed May 5, 2008.
4.    Buddeberg-Fischer B, Klaghofer R, Sigrist S, Buddeberg C. Impact of psychosocial stress and symptoms on indication for bariatric surgery and outcome in morbidly obese patients. Obes Surg. 2004;14(3):361-369.
5.    Buchwald H. Consensus conference statement bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payers. Surg Obes Relat Dis. 2005;1(3):371-381.
6.    Bauchowitz AU, Gonder-Frederick LA, Olbrisch ME, et al. Psychosocial evaluation of bariatric surgery candidates: a survey of present practices. Psychosom Med. 2005;67(5):825-832.
7.    Ashton D, Favretti F, Segato G. Preoperative psychological testing-another form of prejudice. Obes Surg. 2008. Epub ahead of print.
8.    O’Neil PM. Editorial: lessons from, and on, the psychological assessment of bariatric surgery patients. Surg Obes Relat Dis. 2006;2(2):133-135.
9.    van Hout GC, Verschure SK, van Heck GL. Psychosocial predictors of success following bariatric surgery. Obes Surg. 2005;15(4):552-560.
10.    Pawlow LA, O’Neil PM, White MA, Byrne TK. Findings and outcomes of psychological evaluations of gastric bypass applicants. Surg Obes Relat Dis. 2005;1(6):523-527.
11.    Greenberg I. Psychological aspects of bariatric surgery. Nutr Clin Pract. 2003;18(2):124-130.
12.    Herpertz S, Kielmann R, Wolf AM, Langkafel M, Senf W, Hebebrand J. Does obesity surgery improve psychosocial functioning? A systematic review. Int J Obes Relat Metab Disord. 2003;27(11):1300-1314.
13. Grothe KB, Dubbert PM, O’Jile JR. Psychological assessment and management of the weight loss surgery patient. Am J Med Sci. 2006;331(4):201-206.
14. Branson R, Potoczna N, Brunotte R, et al. Impact of age, sex and body mass index on outcomes at four years after gastric banding. Obes Surg. 2005;15(6):834-842.
15.    Dallal RM, Bailey L. Outcomes with the adjustable gastric band. Surgery. 2008;143(3):329-333.
16.    Tymitz K, Kerlakian G, Engel A, Bollmer C. Gender differences in early outcomes following hand-assisted laparoscopic Roux-en-Y gastric bypass surgery: gender differences in bariatric surgery. Obes Surg. 2007;17(12):1588-1591.
17.    Chevallier JM, Paita M, Rodde-Dunet MH, et al. Predictive factors of outcome after gastric banding: a nationwide survey on the role of center activity and patients’ behavior. Ann Surg. 2007;246(6):1034-1039.
18.    Frutos MD, Lujan J, Hernandez Q, Valero G, Parrilla P. Results of laparoscopic gastric bypass in patients > or =55 years old. Obes Surg. 2006;16(4):461-464.
19.    Parikh M, Lo H, Chang C, Collings D, Fielding G, Ren C. Comparison of outcomes after laparoscopic adjustable gastric banding in African-Americans and whites. Surg Obes Relat Dis. 2006;2(6):607-610.
20.    Lutfi R, Torquati A, Sekhar N, Richards WO. Predictors of success after laparoscopic gastric bypass: a multivariate analysis of socioeconomic factors. Surg Endosc. 2006;20(6):864-867.
21.    Ma Y, Pagoto SL, Olendzki BC, et al. Predictors of weight status following laparoscopic gastric bypass. Obes Surg. 2006;16(9):1227-1231.
22.    Melton GB, Steele KE, Schweitzer MA, Lidor AO, Magnuson TH. Suboptimal weight loss after gastric bypass surgery: correlation of demographics, comorbidities, and insurance status with outcomes. J Gastrointest Surg. 2008;12(2):250-255.
23.    Cawley J, Sweeney MJ, Kurian M, Beane S. Predicting complications after bariatric surgery using obesity-related co-morbidities. Obes Surg. 2007;17(11):1451-1456.
24.    Kalarchian MA, Marcus MD, Levine MD, et al. Psychiatric disorders among bariatric surgery candidates: relationship to obesity and functional health status. Am J Psychiatry. 2007;164(2):328-334.
25.    Mauri M, Rucci P, Calderone A, et al. Axis I and II disorders and quality of life in bariatric surgery candidates. J Clin Psychiatry. 2008;69(2):295-301.
26.    Rosenberger PH, Henderson KE, Grilo CM. Correlates of body image dissatisfaction in extremely obese female bariatric surgery candidates. Obes Surg. 2006;16(10):1331-1336.
27.    Sarwer DB, Cohn NI, Gibbons LM, et al. Psychiatric diagnoses and psychiatric treatment among bariatric surgery candidates. Obes Surg. 2004;14(9):1148-1156.
28.    Rosik CH. Psychiatric symptoms among prospective bariatric surgery patients: rates of prevalence and their relation to social desirability, pursuit of surgery, and follow-up attendance. Obes Surg. 2005;15(5):677-683.
29.    de Zwaan M, Mitchell JE, Howell LM, et al. Characteristics of morbidly obese patients before gastric bypass surgery. Compr Psychiatry. 2003;44(5):428-434.
30.    Grilo CM, Masheb RM, Brody M, Toth C, Burke-Martindale CH, Rothschild BS. Childhood maltreatment in extremely obese male and female bariatric surgery candidates. Obes Res. 2005;13(1):123-130.
31.    Wildes JE, Kalarchian MA, Marcus MD, Levine MD, Courcoulas AP. Childhood maltreatment and psychiatric morbidity in bariatric surgery candidates. Obes Surg. 2008;18(3):306-313.
32.    Buser A, Dymek-Valentine M, Hilburger J, Alverdy J. Outcome following gastric bypass surgery: impact of past sexual abuse. Obes Surg. 2004;14(2):170-174.
33.    Fujioka K, Yan E, Wang HJ, Li Z. Evaluating preoperative weight loss, binge eating disorder, and sexual abuse history on Roux-en-Y gastric bypass outcome. Surg Obes Relat Dis. 2008;4(2):137-143.
34.    Grilo CM, White MA, Masheb RM, Rothschild BS, Burke-Martindale CH. Relation of childhood sexual abuse and other forms of maltreatment to 12-month postoperative outcomes in extremely obese gastric bypass patients. Obes Surg. 2006;16(4):454-460.
35.    Averbukh Y, Heshka S, El-Shoreya H, et al. Depression score predicts weight loss following Roux-en-Y gastric bypass. Obes Surg. 2003;13(6):833-836.
36.    Bocchieri-Ricciardi LE, Chen EY, Munoz D, et al. Pre-surgery binge eating status: effect on eating behavior and weight outcome after gastric bypass. Obes Surg. 2006;16(9):1198-1204.
37.    Busetto L, Segato G, De LM, et al. Weight loss and postoperative complications in morbidly obese patients with binge eating disorder treated by laparoscopic adjustable gastric banding. Obes Surg. 2005;15(2):195-201.
38.    Sallet PC, Sallet JA, Dixon JB, et al. Eating behavior as a prognostic factor for weight loss after gastric bypass. Obes Surg. 2007;17(4):445-451.
39.    Herpertz S, Kielmann R, Wolf AM, Hebebrand J, Senf W. Do psychosocial variables predict weight loss or mental health after obesity surgery? A systematic review. Obes Res. 2004;12(10):1554-1569.
40.    Wadden TA, Butryn ML, Sarwer DB, et al. Comparison of psychosocial status in treatment-seeking women with class III vs. class I-II obesity. Surg Obes Relat Dis. 2006;2(2):138-145.
41.    Swan-Kremeier LA. Psychosocial Outcome of Bariatric Surgery. In: Mitchell JE, deZwaan M, eds. Bariatric Surgery: A Guide for Mental Health Professionals. New York, NY: Taylor & Francis Group; 2005:101-118.
42.    Van Hout GC, Van Oudheusden I, Krasuska AT, van Heck GL. Psychological profile of candidates for vertical banded gastroplasty. Obes Surg. 2006;16(1):67-74.
43.    Maddi SR, Fox SR, Khoshaba DM, Harvey RH, Lu JL, Persico M. Reduction in psychopathology following bariatric surgery for morbid obesity. Obes Surg. 2001;11(6):680-685.
44.    Mathus-Vliegen EM, de Weerd S, de Wit LT. Health-related quality-of-life in patients with morbid obesity after gastric banding for surgically induced weight loss. Surgery. 2004;135(5):489-497.
45.    Rosenberger PH, Henderson KE, Grilo CM. Psychiatric disorder comorbidity and association with eating disorders in bariatric surgery patients: a cross-sectional study using structured interview-based diagnosis. J Clin Psychiatry. 2006;67(7):1080-1085.
46.    Kalarchian MA, Marcus MD. Bariatric Surgery and Psychopathology. In: Mitchell JE, deZwaan M, eds. Bariatric Surgery: A Guide for Mental Health Professionals. New York: Taylor & Francis Group; 2005:59-76.
47.    Ryden A, Karlsson J, Sullivan M, Torgerson JS, Taft C. Coping and distress: what happens after intervention? A 2-year follow-up from the Swedish Obese Subjects (SOS) study. Psychosom Med. 2003;65(3):435-442.
48.    Dymek-Valentine M, Rienecke-Hoste R, Alverdy J. Assessment of binge eating disorder in morbidly obese patients evaluated for gastric bypass: SCID versus QEWP-R. Eat Weight Disord. 2004;9(3):211-216.
49.    Greenberg I, Perna F, Kaplan M, Sullivan MA. Behavioral and psychological factors in the assessment and treatment of obesity surgery patients. Obes Res. 2005;13(2):244-249.
50.    Niego SH, Kofman MD, Weiss JJ, Geliebter A. Binge eating in the bariatric surgery population: a review of the literature. Int J Eat Disord. 2007;40(4):349-359.
51.    Tsushima WT, Bridenstine MP, Balfour JF. MMPI-2 scores in the outcome prediction of gastric bypass surgery. Obes Surg. 2004;14(4):528-532.
52.    Saunders R. “Grazing”: a high-risk behavior. Obes Surg. 2004;14(1):98-102.
53.    Hotter A, Mangweth B, Kemmler G, Fiala M, Kinzl J, Biebl W. Therapeutic outcome of adjustable gastric banding in morbid obese patients. Eat Weight Disord. 2003;8(3):218-224.
54.    Colles SL, Dixon JB, O’Brien PE. Grazing and loss of control related to eating: two high-risk factors following bariatric surgery. Obesity (Silver Spring). 2008;16(3):615-622.
55.    Zijlstra H, Larsen JK, van Ramshorst B, Geenen R. The association between weight loss and self-regulation cognitions before and after laparoscopic adjustable gastric banding for obesity: a longitudinal study. Surgery. 2006;139(3):334-339.
56.    Colles SL, Dixon JB, O’Brien PE. Hunger control and regular physical activity facilitate weight loss after laparoscopic adjustable gastric banding. Obes Surg. 2008. Epub ahead of print.
57.    van Hout GC, Jakimowicz JJ, Fortuin FA, Pelle AJ, van Heck GL. Weight loss and eating behavior following vertical banded gastroplasty. Obes Surg. 2007;17(9):1226-1234.
58.    Stunkard AJ, Messick S. The three-factor eating questionnaire to measure dietary restraint, disinhibition and hunger. J Psychosom Res. 1985;29(1):71-83.
59.    Kaiser KA, Franks SF, Hall JR, McGill JC, Berbel G, Smith AB. Changes in psychological dimensions of eating behavior after laparoscopic banding: a preliminary analysis. Ob Res. 2004;12:353-P, A91.
60.    Smith, AB, Franks, SF, Kaiser, KA, Carroll, JF. Eating behavior patterns and weight loss one year after laparoscopic banding surgery. Paper presented at: 25th Annual Meeting of the American Society for Metabolic and Bariatric Surgery; June 15-20, 2008; Washington, DC.
61.    Guerdjikova AI, West-Smith L, McElroy SL, Sonnanstine T, Stanford K, Keck PE Jr. Emotional eating and emotional eating alternatives in subjects undergoing bariatric surgery. Obes Surg. 2007;17(8):1091-1096.
62.    Fischer S, Chen E, Katterman S, et al. Emotional eating in a morbidly obese bariatric surgery-seeking population. Obes Surg. 2007;17(6):778-784.
63.    Walfish S, Vance D, Fabricatore AN. Psychological evaluation of bariatric surgery applicants: procedures and reasons for delay or denial of surgery. Obes Surg. 2007;17(12):1578-1583.
64.    Collazo-Clavell ML, Clark MM, McAlpine DE, Jensen MD. Assessment and preparation of patients for bariatric surgery. Mayo Clin Proc. 2006;81(10 suppl):11-17.

 

Needs Assessment: Methods of pre-surgical psychological evaluation, post-operative psychological support, and common psychological issues are presented to mental health professionals following patients’ surgery. As the field of bariatric surgery grows rapidly, it is necessary to be familiar with these issues to provide adequate care.

Learning Objectives:
• Understand the various roles mental health professionals play in a multidisciplinary team of a surgical weight-loss program.
• List the objectives of a pre-surgical weight-loss evaluation.
• Recognize common psychological issues patients face at various stages after bariatric surgery.

Target Audience: Primary care physicians and psychiatrists.

CME Accreditation Statement: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the Mount Sinai School of Medicine and MBL Communications, Inc. The Mount Sinai School of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Credit Designation: The Mount Sinai School of Medicine designates this educational activity for a maximum of 3 AMA PRA Category 1 Credit(s)TM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Faculty Disclosure Policy Statement: It is the policy of the Mount Sinai School of Medicine to ensure objectivity, balance, independence, transparency, and scientific rigor in all CME-sponsored educational activities. All faculty participating in the planning or implementation of a sponsored activity are expected to disclose to the audience any relevant financial relationships and to assist in resolving any conflict of interest that may arise from the relationship. Presenters must also make a meaningful disclosure to the audience of their discussions of unlabeled or unapproved drugs or devices. This information will be available as part of the course material.

This activity has been peer-reviewed and approved by Eric Hollander, MD, chair and professor of psychiatry at the Mount Sinai School of Medicine, and Norman Sussman, MD, editor of Primary Psychiatry and professor of psychiatry at New York University School of Medicine. Review Date: June 23, 2008.

Drs. Hollander and Sussman report no affiliation with or financial interest in any organization that may pose a conflict of interest.

To receive credit for this activity: Read this article and the two CME-designated accompanying articles, reflect on the information presented, and then complete the CME posttest and evaluation. To obtain credits, you should score 70% or better. Early submission of this posttest is encouraged: please submit this posttest by August 1, 2010 to be eligible for credit. Release date: August 1, 2008. Termination date: August 31, 2010. The estimated time to complete all three articles and the posttest is 3 hours.

Primary Psychiatry. 2008;15(8):42-47

 

Dr. Huberman is clinical instructor in the Department of Psychiatry at New York University School of Medicine and in private practice in New York City.

Disclosure: Dr. Huberman reports no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Warren L. Huberman, PhD, 104 East 40th St, Suite 206, New York, NY 10016; Tel: 212-983-6225; Fax: 212-692-9305; E-mail: whuberman@verizon.net.

 


 

Abstract

The role of a mental health professional working with surgical weight-loss patients is diverse. Primary responsibilities include the provision of patients’ evaluations prior to surgery and either individual or group counseling after surgery. Consultation with the surgeon at various points of patient care is also common. While there is no consensus regarding the content of pre-surgical evaluations or the criteria used to exclude patients from surgery, it is generally accepted that the evaluation is necessary and beneficial. Research supports the benefits of post-surgical mental health services as well. This article suggests pre-surgical evaluations should not primarily focus on psychopathology but on patient expectations and preparedness for the behavioral and emotional changes following surgery. Common reasons patients present for post-operative psychotherapy are reviewed and a stage model of psychological change following surgery is presented.

 

Introduction

It is a pleasure to contribute to this issue on psychological considerations of bariatric surgery. I began working as the consulting psychologist to the New York University (NYU) Program for Surgical Weight Loss in 2000 and have had the good fortune of working with Christine Ren Fielding, MD, George Fielding, MD, and Marina Kurian, MD. The field has changed in numerous ways since 2000, and the knowledge base regarding the psychological impact of weight-loss surgery has grown considerably.

When I was first introduced to bariatric surgery, I was quite skeptical. Having worked extensively as a cognitive-behavioral psychologist focusing on health-behavior change, I was leery that bariatric surgery was another hoax or quick fix for obesity. After having the privilege to work with >5,000 patients, I think that bariatric surgery may represent the only empirically valid treatment for morbid obesity.

In recent years, the use of bariatric surgery as a treatment for obesity has increased significantly, a trend that will grow as obesity rates continue to climb.1 The number of patients presenting for surgery may also increase, as research continues to demonstrate the benefits to both physical health2 and various aspects of psychological well-being and quality of life (QOL).3 The objective of this article is to overview the role of the mental health professional working with surgical weight-loss patients both before and after surgery and to share observations based on my experience with this population.

 

The Role of the Mental Health Professional

Most surgical weight-loss practices adopt a multidisciplinary approach and have accepted that this is needed to help patients achieve success from bariatric surgery.4 The definition of “success” from weight-loss surgery should extend beyond weight loss per se and include improvements in patients’ QOL as well. A mental health professional is typically a member of the team along with nurses, a nutritionist, surgeons, and other clinical staff.

Common responsibilities of a mental health professional in a bariatric surgery program include conducting pre-surgical psychological evaluations, running support groups, and providing individual psychological services to patients before and after surgery. However, there is much variability from program to program. Some programs require pre-surgical psychological evaluations of all patients while others do not.5-10 Numerous programs offer support groups while others do not. This author is unaware of any program that requires patients to participate in ongoing psychological counseling following surgery although some may recommend this practice and make such services available. At least one study has demonstrated that participation in psychotherapy can result in increased weight loss following surgery.11

 

Pre-surgical Evaluations

Both the Surgical Review Corporation and the American College of Surgeons require the involvement of mental health experts in screening bariatric patients for their respective accreditation processes. Numerous experts agree that psychopathology and a number of pre-morbid psychological difficulties can have an effect on post-operative success.12-13 However, findings of studies investigating underlying psychopathology or other emotional obstacles in the bariatric population have yielded inconsistent results. Early studies seemed to suggest there was no greater incidence of psychopathology among the morbidly obese.

Recent studies suggest that morbidly obese patients may have significant symptoms of depression, eating disorders, poor body image, low QOL, and other coexisting mental disorders.5,14-20 In addition to attempting to avoid post-operative psychiatric crises, there is also a strong desire for surgical weight-loss practices to avoid legal proceedings in the event of an adverse surgical outcome. For example, a surgeon would have difficulty defending him- or herself against a legal proceeding from a patient with poorly controlled bipolar disorder who experienced an adverse surgical outcome if the surgeon made little effort to identify and evaluate that such a pre-morbid psychiatric history was present. Such occurrences are commonly reviewed at bariatric conferences and in the general literature.21-26

Interestingly, there is still little consensus as to what the contents of a psychological evaluation should be. Some professionals use structured inventories and psychological instruments such as the Minnesota Multiphasic Personality Inventory-2, Medical Outcomes Study 36-item short form health survey, and a variety of instruments that assess the presence and severity of eating disorders while other professionals rely primarily on a structured clinical interview.27 There is little evidence that any method or instrument of assessment is superior in either identifying inappropriate candidates for surgery or predicting long-term success from surgery.

There is also little consensus as to what specific psychological factors predict outcome, despite the increased focus on inventories or structured tests to identify such variables (GM Boulton-Lewis, unpublished material, 2008).6,10 Numerous variables, including age, gender, socioeconomic status, comorbidities, pre-operative body mass index, prior weight-loss attempts, eating disorders, disordered eating, personality disorders, motivational factors, history of sexual abuse, and social support, among others, have all received some investigation into their effect on surgical outcome, yet none have demonstrated any consistent effects (GM Boulton-Lewis, unpublished material, 2008).

 

Post-Operative Care and Support

Mental health services can be provided as either a prophylaxis against the occurrence of difficulties or a way to address them as they occur. When patients struggle to achieve satisfactory weight loss and medical explanations are inadequate, it is reasonable to consider that psychological variables may be involved. At these times, the surgeon can consult with the mental health professional regarding a difficult case or could refer the patient for psychotherapy.

In addition, several weight-loss surgery programs offer post-operative support groups. These groups may be run by a professional or by patients themselves. There is some debate as to whether support groups or therapy groups are more appropriate28; however, there is little debate that such groups are helpful and desirable. Studies have demonstrated that patients who attended support groups following surgery lost more weight than those who did not attend.29,30 Another study noted that the most highly valued aspect of overall treatment was the provision of continuing care followed by group supports.31

 

Personal Experience

Pre-surgical Evaluations

My initial role as the consulting psychologist to the NYU Program for Surgical Weight Loss was to conduct pre-surgical psychological evaluations. I was familiarized with the types of surgeries, current literature, and nature of the information she wanted me to acquire through the evaluation. My objective in conducting the evaluations was to follow generally accepted practices and to address particular questions and concerns. My objectives for the pre-surgical evaluations have evolved to include the following, as shown in Table 1.

 

 

I created a questionnaire that assesses eating habits, social support, weight-loss history, and mental health history among other areas and have revised it over the years. The questionnaire serves as a template that would enable me to take the patient through a structured yet simple process that is more like a conversation than a clinical interview.

Patients are often anxious about the evaluation because they either have never met with a mental health professional or fear that they will disclose information that will disqualify them from surgery. Patients who have never met with a mental health professional will often ask where the couch is, which is a prompt to explain the objectives of this meeting.

The majority of patients with anxiety fear they may disclose something that will disqualify them from having surgery. I inform patients that this is rare and would most likely be their decision. I have recommended that a surgeon deny surgery to a patient in only a few cases. I can generally explain to the patient why I believe he or she is not presently suitable for surgery and have him or her take steps to address my concerns before moving forward.

It is important to understand the context in which the patient is seeking surgery. One may ask how they learned about it, why they have chosen the present time to pursue surgery, and what the “tipping point” was. The latter question often indicates the patient’s primary objective in having surgery and what his or her expectations are from surgery. It is the opinion of this author that patients do not have surgery simply to lose weight but to accomplish what they believe “thinnerness” will provide. Some patients have dieted for so long that they forgot that weight loss in and of itself is not the final objective. Such patients may not be psychologically prepared for surgery. For most patients, goals include improvements in physical functioning, improved esteem, improved health, and improved interpersonal relationships.

Interestingly, a primary objective in having surgery cited by an overwhelming number of patients is to end the psychological exhaustion from dieting and chronic feelings of failure for their inability to lose weight. Most patients that present for surgery have successfully lost weight before and many have lost >50 pounds on more than one occasion. Unfortunately, most patients believe that maintaining such weight loss with diet and exercise is commonplace and indicate that their family and friends believe this as well, although virtually all clinical research suggests this is hardly the case. For this reason, many patients report feeling guilt and shame over their resorting to surgery as opposed to losing weight the “normal” way. I commonly dispute this notion and refer patients to the clinical literature on this subject.32-34

When patients recognize that the objective is not to try to disqualify them, the assessment becomes a conversation more than an evaluation. For many, this meeting will be their only interaction with a mental health professional, and it is my responsibility that they leave the meeting with a favorable impression of our profession. In doing so, I believe that patients may be more willing to seek out help should the need arise in the future.

The evaluation is as much educational as it is an assessment. In past years, I spent a great deal of time evaluating psychopathology. Colleagues indicated their practice of disqualifying candidates if they expressed a history of major depressive disorder (MDD), suicidality, substance abuse, eating disorders, and other issues. I have since worked with individuals who have had histories of numerous diagnoses and many have done well in terms of both weight loss and improvements in QOL. I continue to assess the presence of Axis I and II pathology but move on to other areas if these issues are absent or are well controlled. This focus on areas beyond psychopathology during the pre-surgical evaluation is receiving further support.35

In the experience of myself and colleagues at NYU, patients with histories of psychopathology, if appropriately managed in follow-up care, can react well. In fact, one study found that patients who met criteria for MDD before surgery did better than non-depressed patients in terms of total weight loss.36 It does not appear that the presence of any particular personality type, trait, or characteristic assures an unsatisfactory outcome from surgery.

Another objective is to encourage the patient to think about life beyond surgery. I ask patients to consider the issues they believe cause behavioral and emotional difficulties after surgery and how they would address them should they occur. Most patients understand the rationale for seeking help if they struggle to lose weight. Fewer patients understand why I ask about potential emotional difficulties that could arise should they be successful in losing weight. Most cannot see weight loss as anything other than desirable, but for patients who see beyond that particular end, they understand completely.

Patients who have been sexually abused or who are socially anxious are often aware of, and have reservations about, making their body more appealing to others. Such patients often report feeling “invisible” in their obesity and are concerned about becoming more “visible” to others following surgery. Numerous morbidly obese patients report that others have ignored them, failed to make eye contact, or rolled their eyes and sighed when they came near. They anticipate that social interactions will change considerably when they begin to lose weight and some have anxiety about these changes.

Patients also express concern that the expectations they have of themselves and that others have of them will change. Such patients acknowledge their weight as a “grand excuse” for shortcomings in various areas of their lives and recognize that improvements in these areas will be expected as they lose weight. For example, many patients fear that they will feel pressure to begin dating now that they are thinner or to begin interviewing for a new job now that concern about weight discrimination has diminished.

It has been my experience that most morbidly obese patients either are, or can become, suitable candidates for surgery. If a patient appears unsuitable, it is likely that he or she is simply not ready at that time. Many patients have presented for surgery in the midst of other issues (ie, divorce, recent loss of a loved one), and when I suggest that they wait until such issues are resolved, it is generally well received. For the vast majority of patients, the medical and psychological benefits of bariatric surgery significantly outweigh its potential consequences so much that there must be an extraordinary reason to deny a patient this opportunity. For this reason, it is imperative that the pre-surgical evaluation is conducted by a clinician who has expertise in the field, so that patients are not inappropriately screened out of surgery, and that those who are allowed to proceed are fully educated and emotionally prepared to do so.

 

Surgical Weight-Loss Patients in Follow Up

Almost all patients who have followed up with me after surgery have been successful from the perspective of weight loss. Most are seeking assistance in making the emotional and behavioral adjustments in their personal and social lives that their weight loss has necessitated. I have yet to speak to a patient who has expressed regret with his or her decision to have surgery. Most patients express satisfaction with the outcome of their surgery, including many who have experienced complications related to surgery. Weight-loss surgery is a powerful tool that enables dramatic weight loss and helps patients to make significant life changes. Therefore, weight-loss surgery should be made available to the majority of patients unless extraordinary circumstances suggest otherwise.

Interestingly, some of the issues that have received significant media coverage have not been common concerns among my patients. I have yet to work with a patient complaining of “food mourning,” wherein one experiences the loss of eating as a primary mechanism to cope with negative emotions because they cannot eat in the manner they did before surgery. Similarly, I have seen only one or two patients who reported increased consumption of alcohol or other substances following surgery (ie, “addiction transfer”). Much has been discussed on this topic and more research is required37 before any conclusions are drawn. In circumstances where my patients have reported increased alcohol consumption following surgery, it has generally been a natural consequence of becoming more socially active after losing weight and not a cause for alarm. However, there are physiologic changes in the way alcohol is absorbed and metabolized, particularly following gastric bypass and other malabsorptive surgeries, and patients need to be aware of the potential problems associated with this phenomenon.

I have seen numerous people who continued to have issues with emotional eating and binge eating following surgery, but many of these patients achieved expected weight loss and did not report dissatisfaction from surgery. These eating issues can continue to be addressed during follow-up but do not necessarily need to be “cured” before surgery is indicated.

 

A Stage Model of Psychological Change Following Bariatric Surgery

In my experience, patients who present for bariatric surgery can be viewed as being in one of two groups: those who are generally satisfied with their lives and those who are not. Those in the former group generally want to lose weight to address health concerns or to stop their weight from interfering with their ability to enjoy their lives as they are. Such patients usually adjust well after surgery, as their primary objective is to lose weight to better enjoy what is already present in their lives.

Those in the latter group are typically the patients who present for post-operative psychotherapy; their lives remain unsatisfying despite the weight loss. Such patients often have impaired esteem, poor body image, unsatisfying or non-existent intimate relationships, minimal or unsatisfying social contacts, and other issues that need to be addressed. For these patients, losing weight may be the easy part. I often tell patients that “fat body goes away faster than fat brain,” explaining that losing the weight takes less time than making the psychological adjustments to the weight loss. Many continue to emotionally feel like their formerly obese selves long after the weight has been lost. Making the life changes that enable them to achieve a greater QOL, the true “success” that I referred to earlier is a more difficult and time-consuming task.

By my observation, many patients go through a series of four stages in making the psychological adjustments to dramatic weight loss following bariatric surgery (Table 2). During the first stage, the focus is on maintaining compliance with dietary rules and on losing weight. Choosing the right foods and learning how to eat properly are of primary concern. Emotionally, there can be excitement from losing weight or apprehension if complications are experienced and weight loss is slow.

 

 

During the second stage, patients may begin to incorporate other tools such as dietary change and exercise and are trying to achieve weight-loss goals whether measured by pounds or by sizes. Rudimentary psychological changes occur such as learning to accept compliments and adjusting to changes in social interactions. Patients are in pursuit of their weight-loss goal and the changes they anticipate will occur when that goal is reached.

During the third stage, patients have achieved or approximated major milestones such as losing 75 or 100 pounds or achieving a desired size. Many will punctuate their accomplishment through a physical achievement or by taking a major step in their personal lives. I have had numerous patients run a marathon or take a physically demanding vacation while others will post their profile on an Internet dating site or begin attending social events. This stage involves experimentation and risk taking as if to demonstrate to themselves and others that they are truly a new person.

The fourth stage can be the most enduring and difficult. It is the stage during which depression and other emotional difficulties are most likely to occur. In this stage, patients begin to adjust to life after weight loss. The life-long objective to defeat obesity in terms of numerical weight may have been accomplished. Friends and family are no longer cheering and the weight loss has become old news. The focus of their life needs to transition from losing weight to adjusting to life in a thinner body and moving beyond weight-related objectives. This is the stage during which changes in one’s personal, social, and professional lives are to occur and is thus ongoing. Success in working through this stage will define overall success from bariatric surgery for many patients.

 

Conclusion

There is a significant contribution that mental health professionals can and do make to bariatric surgery patients and surgeons alike. They play a vital role in patient selection, preparation, and education before surgery and inpatient care following surgery. In many regards, the treatment of morbid obesity through bariatric surgery is as much psychological as it is physical. The work is rich and extremely gratifying; it can have a great impact on patient outcomes. In addition, as the field is growing with the rising number of patients undergoing bariatric surgery, familiarity with the issues faced by these patients is necessary.

There is a unique quality in working with bariatric surgery patients as well. When Dr. Ren Fielding and I met 7 years ago, I asked her what motivated her to work with the morbidly obese. I was touched by her reply and have since adopted it as my own. Her reply was that “surgery is generally about saving lives…weight-loss surgery is often about giving life.” PP

 

References

1.    Steinbrook R. Surgery for severe obesity. N Engl J Med. 2004;350(11):1075-1079.
2.    Maggard MA, Shugarman LR, Suttorp M, et al. Meta-analysis: surgical treatment of obesity. Ann Intern Med. 2005;142(7):547-559.
3.    Wadden TA, Sarwer DB, Fabricatore AN, Jones L, Stack R, Williams NS. Psychosocial and behavioral status of patients undergoing bariatric surgery: what to expect before and after surgery. Med Clin North Am. 2007;91(3):451-469.
4.    Buchwald H. Bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payers. J Am Coll Surg. 2005;200(4):593-604.    
5.    Greenburg I, Perna F, Kaplan M, Sullivan MA. Behavioral and psychological factors in the assessment and treatment of obesity surgery patients. Obes Res. 2005;13(2):244-249.
6.    Lemont D, Moorehead MK, Parish MS, Reto CS, Ritz SJ. Suggestions for the pre-surgical psychological assessment of bariatric surgery candidates. Gainesville, FL: American Society for Metabolic and Bariatric Surgery; 2004.
7.    Sogg S, Mori DL. The Boston interview for gastric bypass: determining the psychological suitability of surgical candidates. Obes Surg. 2004;14(3):370-380.
8.    Fabricatore AN, Crerand CE, Wadden TA, Sarwer DB, Krasucki JL. How do mental health professionals evaluate candidates for bariatric surgery? Survey results. Obes Surg. 2006;16(5):567-573.
9.    Buchwald H. Bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payers. J Am Coll Surg. 2005;200(4):593-604.
10.    Wadden TA, Sarwer DB. Behavioral assessment of candidates for bariatric surgery: a patient-oriented approach. Surg Obes Rel Dis. 2006;2(2):171-179.
11.    Nicolai A, Ippoliti C, Petrelli MD. Laparoscopic adjustable gastric banding: essential role of psychological support. Obes Surg. 2002;12(6):857-863.
12.    Simon GE, Von Korff M, Saunder K, et al. Association between obesity and psychiatric disorders in the US adult population. Arch Gen Psychiatry. 2006;63(7):824-830.
13.    Herpertz S, Kielmann R, Wolf AM, Hebebrand J, Senf W. Do psychosocial variables predict weight loss or mental health after obesity surgery? A systematic review. Obes Res. 2004;12(10):1554-1569.
14.    Larsen JK, van Ramshorst B, Geenen R, Brand N, Stroebe W, van Doornen LJ. Binge eating and its relationship to outcome after laparoscopic adjustable gastric banding. Obes Surg. 2004;14(8):1111-1117.
15.    Kinzl JF, Schrattenecker M, Traweger C, Mattesich M, Fiala M, Biebl W. Psychosocial predictors of weight loss after bariatric surgery. Obes Surg. 2006;16(12):1609-1614.
16.    Carpenter KM, Hasin DS, Allison DB. Relationships between obesity and DSM-IV major depressive disorder, suicide ideation, and suicide attempts: results from a general population study. Am J Public Health. 2000;90(2):251-257.
17.    Onyike CU, Crum RM, Lee HB, Lyketsos CG, Eaton WW. Is obesity associated with major depression? Results from the Third National Health and Nutrition Examination Survey. Am J Epidemiol. 2003;158(12):1139-1147.
18.    Allison KC, Stunkard AJ. Obesity and eating disorders. Psychiatr Clin North Am. 2005;28(1):55-67.
19.    Berkowitz RI, Fabricatore AN. Obesity, psychiatric status, and psychiatric medications. Psychiatr Clin North Am. 2005;28(1):39-54.
20.    Wadden TA, Butryn ML, Sarwer BD, et al. Comparison of psychosocial status in treatment-seeking women with class III vs. class I-II obesity. Surg Obes Rel Dis. 2006;2(2):138-145.
21.    Lindstrom W. Professional liability and risk management. Presented at: 19th Annual Meeting of the American Society for Metabolic and Bariatric Surgery; June 24-28, 2002; Las Vegas, NV.
22.    Saxton J, Corboy PH, Sheldon A. Bariatric surgery: what the plaintiff’s lawyers think, the defense lawyers, and most importantly the jurors! Presented at: 23rd Annual Meeting of the American Society for Metabolic and Bariatric Surgery; June 26-July 1, 2006; San Francisco, CA.
23.    Saxton JW. Reducing your bariatric risk while enhancing your program. Presented at: Adding, Updating, and Expanding Bariatric Surgery Centers of Excellence Hospitals and Health Systems Conference; March 8, 2007; San Francisco, CA.
24.    Wittgrove AC. An interview with Alan C. Wittgrove, MD. Bariatric Times. 2007;4(3):13-16.
25.    Wong-Swartz E. Minimizing risk exposure in bariatric surgery. Bariatric Times. 2006;3(5):42-44.
26.    Eagan MC. Bariatric surgery: malpractice risks and risk management guidelines. Am Surg. 2005;71(5):369-375.
27.    Wadden TA, Sarwer DB, Womble LG, Foster GD, McGuckin BG, Schimmel A. Psychosocial aspects of obesity and obesity surgery. Surg Clin North Am. 2001;81(5):1001-1024.
28.    Janeway JM, Sparks K. Support versus therapy: have you got it right? Bariatric Times. 2007;4(9):1,14-17.
29.    Elakkary E, Elhorr A, Aziz F, Gazayerli MM, Silva YJ. Do support groups play a role in weight loss after laparoscopic adjustable gastric banding? Obes Surg. 2006;6(3):331-334.
30.    Latner JD, Stunkard AJ, Wilson GT, Jackson ML. The perceived effectiveness of continuing care and group support in the long-term self-help treatment of obesity. Obesity (Silver Spring). 2006;14(3):464-471.
31.    Song Z, Reinhardt K, Buzdon M, Liao P. Association between support group attendance and weight loss after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2008;4(2):100-103.
32.    Brownell KD. Obesity: understanding and treating a serious, prevalent, and refractory disorder. J Consult Clin Psychol. 1982;50(6):820-840.
33.    Tsai AG, Wadden TA. Systematic review: an evaluation of commercial weight loss programs in the United States. Ann Intern Med. 2005;142(1):56-66.
34.    Mann T, Tomiyama AJ, Westling E, Lew AM, Samuels B, Chatman J. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol. 2007;62(3):220-233.
35.    Bauchowitz A, Azarbad L, Day K, Gonder-Frederick L. Evaluation of expectations and knowledge in bariatric surgery patients. Surg Obes Rel Dis. 2007;3(5):554-558.
36.    Averbukh Y, Heshka S, El-Shoreya H, et al. Depression score predicts weight loss following Roux-en-Y Gastric Bypass. Obes Surg. 2003;13(6):833-836.
37.    Sogg S. Alcohol misuse after bariatric surgery: epiphenomenon or “Oprah” phenomenon? Surg Obes Rel Dis. 2007;3(3):366-368.

 

Needs Assessment: Weight-loss surgery patients present with issues specific to the weight-loss surgery experience and substantial weight loss. Awareness of the challenges these patients typically face will enable physicians to provide appropriate health and mental health care.


Learning Objectives:

• Identify at least four positive interpersonal changes likely to occur after weight-loss surgery.
• Identify at least four potential interpersonal challenges arising after weight-loss surgery.
• Provide medical or mental health care sensitive to interpersonal changes after weight-loss surgery.


Target Audience:
Primary care physicians and psychiatrists.

CME Accreditation Statement: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the Mount Sinai School of Medicine and MBL Communications, Inc. The Mount Sinai School of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Credit Designation: The Mount Sinai School of Medicine designates this educational activity for a maximum of 3 AMA PRA Category 1 Credit(s)TM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Faculty Disclosure Policy Statement: It is the policy of the Mount Sinai School of Medicine to ensure objectivity, balance, independence, transparency, and scientific rigor in all CME-sponsored educational activities. All faculty participating in the planning or implementation of a sponsored activity are expected to disclose to the audience any relevant financial relationships and to assist in resolving any conflict of interest that may arise from the relationship. Presenters must also make a meaningful disclosure to the audience of their discussions of unlabeled or unapproved drugs or devices. This information will be available as part of the course material.

This activity has been peer-reviewed and approved by Eric Hollander, MD, chair and professor of psychiatry at the Mount Sinai School of Medicine, and Norman Sussman, MD, editor of Primary Psychiatry and professor of psychiatry at New York University School of Medicine. Review Date: June 23, 2008.

Drs. Hollander and Sussman report no affiliation with or financial interest in any organization that may pose a conflict of interest.

To receive credit for this activity: Read this article and the two CME-designated accompanying articles, reflect on the information presented, and then complete the CME posttest and evaluation. To obtain credits, you should score 70% or better. Early submission of this posttest is encouraged: please submit this posttest by August 1, 2010 to be eligible for credit. Release date: August 1, 2008. Termination date: August 31, 2010. The estimated time to complete all three articles and the posttest is 3 hours.

Primary Psychiatry. 2008;15(8):61-66

 

Drs. Sogg and Gorman are staff psychologists at the Massachusetts General Hospital Weight Center and instructors in psychology at the Harvard University School of Medicine in Boston, MA.

Disclosure: Drs. Sogg and Gorman report no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Stephanie Sogg, PhD, MGH Weight Center, 50 Staniford St, 4th Fl, Boston, MA 02114; Tel: 617-726-6761; Fax: 617-724-6565; E-mail: ssogg@partners.org.

 


 

 

Abstract

Weight-loss surgery literature suggests that the majority of patients experience the changes that occur as a result of dramatic weight loss after weight-loss surgery as being overwhelmingly positive. However, even positive change may pose a variety of psychosocial challenges. In the case of weight-loss surgery, these changes and challenges often manifest themselves in a variety of interpersonal realms, including everyday social interactions and relationships with close friends and loved ones. In addition, patients must learn to function in certain interpersonal situations they may not have had to navigate in years or have never encountered before. This article examines some of the interpersonal changes and challenges arising after weight-loss surgery, with a brief review of empirical literature on this topic. It concludes with a discussion of the ways healthcare providers can facilitate smooth adjustment to interpersonal changes after weight-loss surgery.

 

Introduction

Due to the rapidly increasing prevalence of weight-loss surgery in recent years,1-4 healthcare professionals of all disciplines are more likely to encounter weight-loss surgery patients in their clinical practices. Therefore, it is important for clinicians who do not specialize with this population to become knowledgeable about weight-loss surgery and the common post-operative experiences patients face to ensure the provision of appropriate care and referrals.

A growing body of empirical literature suggests that after weight-loss surgery, the majority of patients experience overwhelmingly positive changes,5-10 including dramatic improvements in medical comorbidities2,11-16; enhanced energy, mobility, mood, and self-esteem; and increased desire and ability to engage in a variety of activities.5,6,8,11,17 However, even positive change may pose a variety of psychosocial challenges.5

For weight-loss surgery patients, these changes and challenges often manifest themselves in a variety of interpersonal realms. Weight-loss surgery may affect spheres ranging from everyday social interactions to relationships with close friends and loved ones. In addition, patients must learn to function in certain interpersonal situations they may not have had to navigate in years or have never encountered before. This article examines some of the interpersonal changes and challenges arising after weight-loss surgery, including a brief review of empirical literature on this topic. Ways to facilitate smooth adjustment to interpersonal changes after weight-loss surgery are discussed as well.

It should be noted that there is a relative dearth of empirical literature examining this topic6; many of these studies were published decades ago, involve small samples, and pertain to bariatric procedures that are now rarely performed. Examination of interpersonal outcomes tends to be done in broad strokes,6 with patients rating general satisfaction or improvement, rather than focusing on specific types or mechanisms of change. Thus, patient report and clinical experience must often be used to inform the effect of weight-loss surgery on interpersonal functioning.

 

Everyday Social Interactions

Positive Changes

Almost immediately after surgery, patients report receiving increased attention from supportive family and friends around taking an important step in addressing their health risks. As patients lose weight, positive attention often takes the form of compliments, which many patients report finding pleasurable and gratifying. In addition, patients frequently report that both strangers and acquaintances tend to be more likely to approach and generally act more positively toward them. Patients typically attribute these changes directly to improved appearance. Though this may be the case, it is likely that this change is partly attributable to changes in the way the patients interact with others. As their mood, self-confidence, and self-esteem improve, patients may approach others more often and more positively, effecting a change in how others respond to them.

 

Challenges

While receiving compliments is pleasurable for most people, it is not uncommon for weight-loss surgery patients to feel uncomfortable when this occurs, especially if they were not accustomed to receiving compliments in the past. Numerous patients express concern that they will appear conceited if they do not downplay or reject compliments. Frequently, it takes some time before a patient’s self-concept becomes consistent with his or her changed outward appearance.18 Therefore, compliments may be perceived as uncomfortably discordant with the patient’s self-image; one patient described the experience of receiving a compliment as causing “a short-circuit in my brain.” In other cases, patients simply have not developed the basic skill of responding to a compliment by merely saying, “Thank you.” Fortunately, this skill can be developed through a very brief intervention of guided role-playing (and some practice), greatly easing this type of social transaction.

For some patients, changes in the way others respond to them can be experienced as insulting. Some patients report feeling resentful about being treated better by other people simply because they lost weight.5,6 Patients may interpret a sudden increase in compliments to mean that before surgery, people found them unappealing; one patient reported responding to enthusiastic compliments with the thought, “Wow, what must they have thought of me before?”

Before weight-loss surgery, patients frequently report experiencing significant stigma and discrimination related to their weight.6,19-23 Numerous patients complain about bias at work, within their families, and from strangers; empirical investigations substantiate the reality of widespread prejudice and discrimination against individuals with obesity.21,22,24-30 It has been found that medical professionals,18,25,31-35 even those who specialize in studying and treating obesity,29,36 hold such prejudices. It has been noted that obesity is “one of the last acceptable forms of prejudice” in our society.37 Further, unlike members of other stigmatized groups, it has been found that people with obesity tend to internalize these biases.20,22,25,28,38,39 Because of the stigma related to obesity, research has demonstrated that people with obesity are more susceptible to depression and lowered self-esteem.40-46 Fortunately, after weight-loss surgery, as patients lose weight, they encounter fewer of these experiences.23 However, they often remain acutely aware of and troubled by the prejudice that exists toward individuals with obesity in Western culture.5 It can be particularly uncomfortable when patients catch themselves engaging in this type of stigmatizing behavior. One patient described feeling horrified and saddened when, having just been cut off by another driver in a parking lot, she found herself making disparaging observations about that driver’s being overweight.

Weight-loss surgery may also lead to unwanted inquiries by others. For many reasons, the topic of weight-loss surgery seems to be quite interesting to the lay public, and weight-loss surgery patients often find themselves reluctantly assuming the role of “weight-loss surgery ambassador” to their family and friends. Patients report being subjected to frequent questions about the surgery and post-operative regimen. Although patients often report being enthusiastic about their experiences and wanting to share them with others, some patients find it tiresome to answer repetitive questions about weight-loss surgery or find that conversations with others too frequently focus on this topic. In addition, patients sometimes report being asked intrusive personal questions, such as “How much weight have you lost?” or “What did you weigh before?” Patients also often report that others appear to be inordinately curious about what, how much, and how fast they can eat.

One of the more distressing challenges that weight-loss surgery patients sometimes face is being subjected to the opinions of people who mistakenly believe that weight-loss surgery is somehow “cheating” or “taking the easy way out,” when the patient “should have been able to lose the weight on his or her own.” This is yet another expression of the bias and misapprehensions about obesity among the general public, and it leaves the patient in an unpleasant position of having to justify his or her decision to have surgery. Unfortunately, in Western society, obesity is often believed to be the result of a psychiatric or behavioral disorder, laziness, or failure of will power.24-26 However, a growing body of research strongly indicates that biologic factors are very powerful in determining body weight.26,47 In fact, it has been estimated that 40% to 85% of the individual variation in obesity may be attributable to genetic factors.48,49 In addition, once it has developed, obesity is notoriously resistant to nonsurgical treatments such as lifestyle change or weight-loss medications regardless of etiology,12,50-56 leaving weight-loss surgery as most patients’ best hope for improvement or reversal of the dangerous comorbidities of obesity.1,12,14,15,57-59 It is often incumbent upon weight-loss surgery patients to explain these facts to others, which can be tedious at best and, at worst, demoralizing.

 

Intimate Relationships

Positive Changes

Another realm of interpersonal changes after weight-loss surgery is in the sphere of intimate relationships: close friendships, family relationships, and romantic partnerships. Before surgery, patients frequently report that their weight diminishes both the ability and the desire to engage in a variety of activities.42,60,61 After weight-loss surgery, improvements in health, mobility, energy, mood, and self-confidence render patients more able and eager to engage in a wider spectrum of activities.5,6,10,11,18,62 This can translate into more enjoyable time spent with friends and loved ones and participation in or rediscovery of activities and hobbies that had been abandoned in the past. Patients report being able to take long walks with their spouses or chase their grandchildren around the backyard. One patient reported feeling elated by the simple pleasure of being able to cook a meal for her spouse, an activity that was impossible before weight-loss surgery, as she could not stand at the stove for more than a few minutes at a time.

Additionally, improved mood and self-confidence make social situations more enjoyable after weight-loss surgery. Patients report that after weight-loss surgery, they appreciate becoming free of the constant awareness of their size; the fear of being evaluated negatively by others diminishes.6,11,18,62,63 Patients who, before surgery, tended to avoid parties and other social situations because they were self-conscious about their appearance no longer feel they have to refuse invitations.

The vast majority of weight-loss surgery patients report that having surgery has affected their romantic relationships in a positive way.8,62,64-69 As noted above, weight-loss surgery offers patients the opportunity to engage in more shared activities with their partners62,68 or to resume a larger share of household responsibilities. Additionally, weight-loss surgery appears to lead to significant improvements in most patients’ sexual functioning.62,64,67,70,71 Patients often report that improved mood, body image, and self-confidence significantly increase their sexual desire and level of comfort with physical intimacy.8,66,70 Sexual activity becomes mechanically easier due to increased endurance, improved mobility, and smaller body size.5,66,70 Some patients report that their partners show a renewed or increased sexual interest toward them as they lose weight.62 One study70 found that patients’ partners reported being even more satisfied with sexual changes after weight-loss surgery than the patients themselves.

 

Challenges

Despite the positive changes described, challenges may arise in close relationships after weight-loss surgery. As the patient loses weight, friends or family members may become envious or competitive.5,6,72 It is not uncommon for patients to report that a close friend or relative has commented, “Wow, you are getting close to my size, now–I should go on a diet!” In some cases, the weight-loss surgery patient was part of a friendship, family, or social group in which he or she played the role of “the fat one,” someone who was less assertive or posed less of a threat or competition for the opposite sex. As the patient loses weight after surgery, this dynamic may be changed, disrupting the equilibrium of the friendship, family, or social group.

Relationships that in the past had centered around eating, cooking, or visiting restaurants may have to undergo some adjustments after the patient undergoes weight-loss surgery, and friends and family members may also be concerned about losing an “eating buddy.” In Western culture, it can be difficult to find opportunities for socialization that do not focus on food or drink.6 In addition, as patients create healthier eating patterns for themselves, eating in the entire household is likely to be affected. In some cases, patients may feel guilty about the possibility that family meals will be disrupted or worry that loved ones will feel deprived of certain favorite foods. Conversely, some weight-loss surgery patients find that friends or family begin to act as the “food police,” monitoring and commenting on each bite the patient eats. Although this behavior may reflect genuine caring and concern on the part of the friend or family member, it can be quite aversive to the patient.

Another potential challenge is possible sabotage by a friend or family member in the form of exhortations to eat more or expressions of concern about the patient losing too much weight. This type of behavior may be either intentional or unintentional, driven by envy, insecurity, or a lack of knowledge of the post-operative regimen. Examples of this type of challenge can range from a concerned relative repeatedly asking, “Is that all you’re going to eat?” or serving the patient too much at family dinners, to a partner complaining because there is no longer any ice cream in the house or refusing to buy healthier foods for the home.

Although the effect of weight-loss surgery on romantic relationships tends to be overwhelmingly positive, some patients report significant disruption in their romantic relationships. Family systems theory holds that a homeostatic balance is established and maintained within relationships by each member fulfilling his or her specific role in relation to the other. When one person in a relationship changes, this disrupts homeostasis, and if the relationship does not change accordingly, balance will not be re-established and destabilization will occur.73 Empirical investigation of marital changes after weight-loss surgery suggests that relationships that were strong before surgery tend to stay that way, while relationships that were less healthy originally are more likely to be destabilized.17,62,64,66 For example, an improved self-image and feelings of self-worth may make a patient less willing to tolerate a relationship in which he or she is not treated with kindness and respect.5 In one study, wives rated themselves as more sociable and interesting after surgery, while rating their husbands as less sociable and interesting than they did before surgery.63 As the patient develops a stronger sense of self-worth, the balance of power may shift in a friendship or romantic relationship.5 In a healthy relationship, a new, positive equilibrium is reached, while in an unhealthy one, this shift in power may lead to the dissolution of the relationship. Similarly, because of the disability and ill-health that may accompany severe obesity, some patients may have become reliant on their partners in a variety of ways. As health improves and autonomy grows, the relationship may be disrupted if, as the patient asserts newfound independence, his or her partner feels that he or she has lost an important role or is no longer needed.5,62,63,72 In addition, some patients report that their partners become jealous, or express anxiety about patients leaving the relationship as they lose weight and become more attractive to others.5,66,72

It is worth noting that although patients commonly report improvements in their sexual functioning and sexual relationships after weight-loss surgery, a significant minority of patients report a negative impact on their sex lives.66 For some, wound complications or other early surgical sequelae interfere with sexual functioning.62,70 Some patients may experience a short-term decrease in sex drive after weight-loss surgery5,62,66 Though most patients experience improvement in their body image and improvements in their sexual functioning, for some patients, excess skin, which can develop after a significant weight loss, may actually worsen body image10 and increase inhibitions toward sexual intimacy.66

 

New Experiences

As weight-loss surgery patients lose weight and regain energy, mobility, and self-confidence, they may begin to find themselves in a variety of situations that they have not encountered in the past, or which they had avoided for some time because of the functional or psychological impact of their obesity.5,74 For example, before surgery many patients find that because of their obesity people do not really see or pay attention to them. After losing weight, however, weight-loss surgery patients sometimes note that they are no longer “invisible.”5 Although in general this is likely to be a positive change, it can be uncomfortable and it may take patients time to become accustomed to being “visible” again.

This newfound visibility may lead to increased romantic or sexual attention, which is welcome and exciting for most patients and contributes to improved confidence, mood, self-esteem, and body image. However, for others, this type of attention may be disruptive. Some patients with a history of sexual abuse may find increased sexual or romantic attention to be threatening.5,17 It has been hypothesized that these patients may experience their extra weight as a defense or protective factor that minimizes the risk of receiving sexual attention or finding themselves in sexual situations,41,75,76 and losing this buffer may lead to feelings of vulnerability.5,17 One study found that patients with a history of sexual abuse lost less weight at 12 months post-surgery.71 Another77 found that while there was no difference in weight loss 2 years after surgery between patients with and without a history of sexual abuse, those with an abuse history were significantly more likely to report having had a psychiatric hospitalization in the first 2 post-operative years. However, it is important to note that a history of sexual abuse is not considered to be a contraindication for weight-loss surgery, and research studies have typically found that such a history has no impact on post-surgical weight loss or psychosocial adjustment in the long term.78-81

Even for those patients for whom an increase in romantic opportunities is a welcome change, this new situation may still pose challenges. Some patients, particularly those who are younger at the time of surgery, report that they had never been involved in romantic relationships before and may never have grown accustomed to dating or developed necessary dating “skills.”5 Learning how to navigate the world of romantic relationships can be a complicated experience, even if it is an enjoyable one. For other patients, it may have been years since they were involved in dating, and they may find that their skills are “rusty,” or that the norms in the dating world have changed. For example, expectations about which party asks or pays for the date, or how quickly sexual activity is introduced, may be quite different now than they were when the patient last dated. For some patients, vigilance about sexually transmitted diseases is a new development that requires some consideration. Those whose fertility may have been impaired by their obesity may not appreciate the increased need for protection against unplanned pregnancy. This is particularly problematic, since there is risk for birth defects in pregnancies occurring within the first 12–18 months after weight-loss surgery.82,83

 

Conclusion

Although patients presenting for weight-loss surgery are highly motivated to achieve and maintain significant weight loss, they may not anticipate the impact the surgery could have on their interpersonal functioning. Weight-loss surgery typically results in changes experienced as extremely positive and enriching, especially in the interpersonal realm. However, these changes may also present significant challenges. Clinicians caring for weight-loss surgery patients must be aware of the significant changes and challenges that may arise. As noted above, these may include changes in everyday social interactions and close interpersonal relationships, and facing situations with which the patient had little experience before losing weight. There are numerous opportunities for healthcare providers to facilitate successful adjustment to weight-loss surgery.

This may begin even before surgery, with the pre-operative psychosocial evaluation. This evaluation serves the function of identifying potential post-surgical challenges and affords the opportunity to help the patient to proactively formulate appropriate coping strategies. Educating the patient about potential challenges is an important and powerful tool for enhancing adjustment after surgery.84 Further, the evaluating clinician need not be relegated to the role of “gatekeeper”; a mental health practitioner can also serve as the facilitator of whatever intervention is needed to clear the patient’s path to surgery and increase the safety and efficacy of this important medical procedure.45,84-87

During the perioperative and early adjustment period, clinicians who are mindful of the potential changes and challenges discussed above can provide appropriate psychosocial intervention; this may be done within the surgical program itself or, if no appropriate clinician is on staff, referrals can be made to clinicians in the community who have experience working with weight-loss surgery patients.

It is also important that ongoing psychosocial support is available in the long term after weight-loss surgery.17,84,86,88 It is recommended that routine follow-up visits extend beyond the first 6–12 months after surgery, as many of the challenges described above may emerge at a longer latency after surgery.88 Regular, long-term follow up fosters working relationships in which the patient feels comfortable discussing any challenges that may arise, as well as increasing opportunities for doing so. Programs that incorporate or have a close association with mental health providers can provide appropriate referrals for patients to receive assistance in coping with adjustment to life after weight-loss surgery. In addition, other healthcare providers can be helpful to patients navigating the interpersonal challenges that may arise after weight-loss surgery by being aware of the common issues. Sensitivity to these issues will allow medical and mental health providers to provide better care, make sensitive inquiries during routine visits, and make the appropriate referrals when necessary. PP

 

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18.    Ogden J, Clementi C, Aylwin S. The impact of obesity surgery and the paradox of control: a qualitative study. Psychol Health. 2006;21(2):273-293.
19.    Ashmore JA, Friedman KE, Reichmann SK, Musante GJ. Weight-based stigmatization, psychological distress, & binge eating behavior among obese treatment-seeking adults. Eat Behav. 2008;9(2):203-209.
20.    Friedman KE, Reichmann SK, Costanzo PR, Zelli A, Ashmore JA, Musante GJ. Weight stigmatization and ideological beliefs: relation to psychological functioning in obese adults. Obes Res. 2005;13(5):907-916.
21.    Puhl RM, Andreyeva T, Brownell KD. Perceptions of weight discrimination: prevalence and comparison to race and gender discrimination in America. Int J Obes. 2008;32:992-1000.
22.    Puhl RM, Moss-Racusin CA, Schwartz MB, Brownell KD. Weight stigmatization and bias reduction: perspectives of overweight and obese adults. Health Educ Res. 2008;23(2):347-358.
23.    Rand CS, Macgregor AM. Successful weight loss following obesity surgery and the perceived liability of morbid obesity. Int J Obes. 1991;15(9):577-579.
24.    Andreyeva T, Puhl RM, Brownell KD. Changes in perceived weight discrimination among Americans, 1995-1996 through 2004-2006. Obesity. 2008;16(5):1129-1134.
25.    Crandall CS. Prejudice against fat people: ideology and self-interest. J Pers Soc Psychol. 1994;66(5):882-894.
26.    Friedman JM. Modern science versus the stigma of obesity. Nat Med. 2004;10(6):563-569.
27.    Puhl R, Brownell KD. Bias, discrimination, and obesity. Obes Res. 2001;9(12):788-805.
28.    Schwartz MB, Vartanian LR, Nosek BA, Brownell KD. The influence of one’s own body weight on implicit and explicit anti-fat bias. Obesity (Silver Spring). 2006;14(3):440-447.
29.    Teachman BA, Brownell KD. Implicit anti-fat bias among health professionals: is anyone immune? Int J Obes Relat Metab Disord. 2001;25(10):1525-1531.
30.    Teachman BA, Gapinski KD, Brownell KD, Rawlins M, Jeyaram S. Demonstrations of implicit anti-fat bias: the impact of providing causal information and evoking empathy. Health Psychol. 2003;22(1):68-78.
31.    Chambliss HO, Finley CE, Blair SN. Attitudes toward obese individuals among exercise science students. Med Sci Sports Exerc. 2004;36(3):468-474.
32.    Falkner NH, French SA, Jeffery RW, Neumark-Sztainer D, Sherwood NE, Morton N. Mistreatment due to weight: prevalence and sources of perceived mistreatment in women and men. Obes Res. 1999;7(6):572-576.
33.    Foster GD, Wadden TA, Makris AP, et al. Primary care physicians’ attitudes about obesity and its treatment. Obes Res. 2003;11(10):1168-1177.
34.    Hebl MR, Mannix LM. The weight of obesity in evaluating others: a mere proximity effect. Pers Soc Psychol Bull. 2003;29(1):28-38.
35.    Puhl RM, Schwartz MB, Brownell KD. Impact of perceived consensus on stereotypes about obese people: a new approach for reducing bias. Health Psychol. 2005;24(5):517-525.
36.    Schwartz MB, Chambliss HO, Brownell KD, Blair SN, Billington C. Weight bias among health professionals specializing in obesity. Obes Res. 2003;11(9):1033-1039.
37.    Stunkard AJ, Sorensen TI. Obesity and socioeconomic status–a complex relation. N Engl J Med. 1993;329(14):1036-1037.
38.    Puhl RM, Moss-Racusin CA, Schwartz MB. Internalization of weight bias: Implications for binge eating and emotional well-being. Obesity (Silver Spring). 2007;15(1):19-23.
39.    Wang SS, Brownell KD, Wadden TA. The influence of the stigma of obesity on overweight individuals. Int J Obes Relat Metab Disord. 2004;28(10):1333-1337.
40.    Chen E, Bocchieri-Ricciardi L, Munoz D, et al. Depressed mood in class III obesity predicted by weight-related stigma. Obes Surg. 2007;17(5):673-675.
41.    Kalarchian MA, Marcus MD, Levine MD, et al. Psychiatric disorders among bariatric surgery candidates: Relationship to obesity and functional health status. Am J Psychiatry. 2007;164(2):328-334.
42.    Kasen S, Cohen P, Chen H, Must A. Obesity and psychopathology in women: a three decade prospective study. Int J Obes (Lond). 2007;32(3):558-566.
43.    Stout AL, Applegate KL, Friedman KE, Grant JP, Musante GJ. Psychological correlates of obese patients seeking surgical or residential behavioral weight loss treatment. Surg Obes Relat Dis. 2007;3(3):369-375.
44.    van der Merwe MT. Psychological correlates of obesity in women. Int J Obes (Lond). 2007;31(suppl 2):14-18.
45.    Wadden TA, Butryn ML, Sarwer DB, et al. Comparison of psychosocial status in treatment-seeking women with class III vs. class I-II obesity. Obesity (Silver Spring). 2006;14(suppl 2):90-98.
46.    Wadden TA, Sarwer DB, Fabricatore AN, Jones L, Stack R, Williams NS. Psychosocial and behavioral status of patients undergoing bariatric surgery: what to expect before and after surgery. Med Clin N Am. 2007;91(3):451-469.
47.    Bouchard C. The biological predisposition to obesity: beyond the thrifty genotype scenario. Int J Obes (Lond). 2007;31(9):1337-1339.
48.    Farooqi IS, O’Rahilly S. Genetic factors in human obesity. Obes Rev. 2007;8(suppl 1):37-40.
49.    Wardle J, Carnell S, Haworth CM, Plomin R. Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment. Am J Clin Nutr. 2008;87(2):398-404.
50.    Bray GA, Ryan DH. Drug treatment of the overweight patient. Gastroenterology. 2007;132(6):2239-2252.
51.    Dansinger ML, Tatsioni A, Wong JB, Chung M, Balk EM. Meta-analysis: the effect of dietary counseling for weight loss. Ann Intern Med. 2007;147(1):41-50.
52.    Elfhag K, Rossner S. Who succeeds in maintaining weight loss? A conceptual review of factors associated with weight loss maintenance and weight regain. Obes Rev. 2005;6(1):67-85.
53.    Foster GD, Makris AP, Bailer BA. Behavioral treatment of obesity. Am J Clin Nutr. 2005;82(1 suppl):230-235.
54.    Mun EC, Blackburn GL, Matthews JB. Current status of medical and surgical therapy for obesity. Gastroenterology. 2001;120(3):669-681.
55.    Wadden TA, Butryn ML, Byrne KJ. Efficacy of lifestyle modification for long-term weight control. Obes Res. 2004;12(suppl):151-162.
56.    Wadden TA, Butryn ML, Wilson C. Lifestyle modification for the management of obesity. Gastroenterology. 2007;132(6):2226-2238.
57.    Adams TD, Gress RE, Smith SC, et al. Long-term mortality after gastric bypass surgery. N Engl J Med. 2007;357(8):753-761.
58.    Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292(14):1724-1737.
59.    Buchwald H. Bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payers. J Am Coll Surg. 2005;200(4):593-604.
60.    Fabricatore AN, Wadden TA, Sarwer DB, Faith MS. Health-related quality of life and symptoms of depression in extremely obese persons seeking bariatric surgery. Obes Surg. 2005;15(3):304-309.
61.    Wadden TA, Sarwer DB. Behavioral assessment of candidates for bariatric surgery: a patient-oriented approach. Obesity (Silver Spring). 2006;14(suppl 2):53-62.
62.    Rand CS, Kowalske K, Kuldau JM. Characteristics of marital improvement following obesity surgery. Psychosomatics. 1984;25(3):221-223,226.
63.    Hafner RJ. Morbid obesity: effects on the marital system of weight loss after gastric restriction. Psychother Psychosom. 1991;56(3):162-166.
64.    Applegate KL, Friedman KE, Grant JP. Assessments of relationship satisfaction and stability one year after weight loss surgery: a prospective study [abstract]. Surg Obes Relat Dis. 2006;2(3):310.
65.    Cooper KM, Wells M. Effects of bariatric surgery on marital satisfaction [abstract]. Surg Obes Relat Dis. 2006;2(3):334.
66.    Kinzl JF, Trefalt E, Fiala M, Hotter A, Biebl W, Aigner F. Partnership, sexuality, and sexual disorders in morbidly obese women: Consequences of weight loss after gastric banding. Obes Surg. 2001;11(4):455-458.
67.    Kinzl JF, Traweger C, Trefalt E, Biebl W. Psychosocial consequences of weight loss following gastric banding for morbid obesity. Obes Surg. 2003;13(1):105-110.
68.    Rand CS, Kuldau JM, Robbins L. Surgery for obesity and marriage quality. JAMA. 1982;247(10):1419-1422.
69.    Sarwer DB, Wadden TA, Fabricatore AN. Psychosocial and behavioral aspects of bariatric surgery. Obes Res. 2005;13(4):639-648.
70.    Camps MA, Zervos E, Goode S, Rosemurgy AS. Impact of bariatric surgery on body image perception and sexuality in morbidly obese patients and their partners. Obes Surg. 1996;6(4):356-360.
71.    Ray EC, Nickels MW, Sayeed S, Sax HC. Predicting success after gastric bypass: the role of psychosocial and behavioral factors. Surgery. 2003;134(4):555-563.
72.    Andrews G. Intimate saboteurs. Obes Surg. 1997;7(5):445-448.
73.    Klein D, White J. Family Theories: An Introduction (Understanding Families). 2nd ed. Thousand Oaks, CA: Sage Publicatons; 2002.
74.    Hsu LK, Benotti PN, Dwyer J, et al. Nonsurgical factors that influence the outcome of bariatric surgery: a review. Psychosom Med. 1998;60(3):338-346.
75.    Felitti VJ. Childhood sexual abuse, depression, and family dysfunction in adult obese patients: a case control study. South Med J. 1993;86(7):732-736.
76.    Wiederman MW, Sansone RA, Sansone LA. Obesity among sexually abused women: an adaptive function for some? Women Health. 1999;29(1):89-100.
77.    Clark M, Hanna B, Mai J, et al. Sexual abuse survivors and psychiatric hospitalization after bariatric surgery. Obes Surg. 2007;17(4):465-469.
78.    Buser A, Dymek-Valentine M, Hilburger J, Alverdy J. Outcome following gastric bypass surgery: impact of past sexual abuse. Obes Surg. 2004;14(2):170-174.
79.    Fujioka K, Yan E, Wang HJ, Li Z. Evaluating preoperative weight loss, binge eating disorder, and sexual abuse history on Roux-en-Y gastric bypass outcome. Surg Obes Relat Dis. 2008;4(2):137-143.
80.    Larsen JK, Geenen R. Childhood sexual abuse is not associated with a poor outcome after gastric banding for severe obesity. Obes Surg. 2005;15(4):534-537.
81.    Oppong BA, Nickels MW, Sax HC. The impact of a history of sexual abuse on weight loss in gastric bypass patients. Psychosomatics. 2006;47(2):108-111.
82.    Wax JR, Pinette MG, Cartin A, Blackstone J. Female reproductive issues following bariatric surgery. Obstet Gynecol Surv. 2007;62(9):595-604.
83.    Woodard CB. Pregnancy following bariatric surgery. J Perinat Neonatal Nurs. 2004;18(4):329-340.
84.    Sogg S, Mori DL. Revising the Boston Interview: incorporating new knowledge and experience. Surg Obes Relat Dis. 2008;4(3):455-463.
85.    Bauchowitz A, Azarbad L, Day K, Gonder-Frederick L. Evaluation of expectations and knowledge in bariatric surgery patients. Surg Obes Relat Dis. 2007;3(5):554-558.
86.    Lanyon R, Maxwell B. Predictors of outcome after gastric bypass surgery. Obes Surg. 2007;17(3):321-328.
87.    Sogg S, Mori DL. The boston interview for gastric bypass: determining the psychological suitability of surgical candidates. Obes Surg. 2004;14(3):370-380.
88.    Greenberg I, Sogg S, Perna F. Behavioral and psychological care in weight loss surgery–best practice update. Obesity. In press.

 

Dr. Robinson is a consultant with Worldwide Drug Development in Burlington, Vermont.

Disclosure: Dr. Robinson has served as a consultant to Bristol-Myers Squibb, Epix, Johnson and Johnson, PGxHealth, Pfizer, and Schering.

 


 

The profound influence of the pharmaceutical and drug devices industry on clinical medicine, medical education, and research is a source of growing concern raised in the medical literature and media.1,2 The potential for bias due to commercial interests prompted editors of leading international medical journals to endorse greater transparency in reporting of clinical trials regarding authorship, financial support, and potential conflict of interest as a prerequisite for reviewing submitted manuscripts.3,4 This editorial posture taken by prestigious medical journals worldwide helped foster legislation that requires advance registration of phase II and III clinical trials prior to study inception.5

Evidence-based medicine has become the accepted standard for the teaching and practice of medicine.6 A basic premise underlying informed decision-making is accurate and complete reporting of clinical trial outcomes. Applying principles of evidence-based medicine to psychiatric practice is essential.7,8 Three recent articles9-11 explore issues of selective reporting of clinical trial data, guest authorship, and ghostwriting in reports of drugs with psychotropic effects.

 

Selective Publication of Antidepressant Efficacy Trials

Academic investigators lacking ties to the pharmaceutical industry conducted a comprehensive review9 of Food and Drug Administration documents pertaining to pre-approval phase 2 and phase 3 efficacy trials of 12 antidepressants. These antidepressants, approved for marketing between 1987 and 2004, involved enrollment of >12,500 adult patients in efficacy trials. FDA medical and statistical review documents for each of the antidepressants were procured through the Freedom of Information Act12 and the FDA Web site.13 Turner and colleagues9 examined efficacy data from randomized, double-blind, placebo-controlled trials reported to the FDA and compared these data with that contained in published reports of efficacy trials for each of these drugs. Only data for approved dosages were included in the analyses. Each efficacy trial is categorized in the FDA Summary Basis of Approval (SBA) document as positive (ie, indicative of efficacy) or negative (ie, inconclusive or no efficacy).

Turner and colleagues9 conducted an exhaustive literature search to identify all placebo-controlled clinical trials published for each of the antidepressants. Their search strategy involved several steps: searching for articles in PubMed; searching for references cited in review articles; searching the Cochrane Central Registry of Controlled Trials; contacting the medical information department of each pharmaceutical sponsor; and finally, contacting in writing by certified letter addressed to the medical-information department of the drug sponsor to request a written response to the query of whether the results of an efficacy trial listed in the SBA document had been published. If none of these steps yielded evidence of publication, it was concluded that the efficacy results for the trial had never been reported.

Comparison of FDA regulatory data with published data included statistical analyses that compared sample sizes as reported to the FDA and in published trial reports, and computed effect-sizes for each drug from data contained in FDA documents versus published reports. A single weighted effect size for each antidepressant was derived by pooling data from published journal articles. This value was compared with the computed effect size from the FDA medical and statistical review documents, which contain complete data sets for each antidepressant, both published and unpublished.

 

Efficacy Outcome and Publication Status

Turner and colleagues9 examined the publication status of FDA-registered antidepressant efficacy trials over the period from the mid-1980s onward. Of 74 clinical trials registered with the FDA and included in the new drug applications of the 12 antidepressants, no evidence of publication was found for 23 (31%) of the placebo-controlled efficacy trials (Table). Unavailability of published data in peer-reviewed journals for 23 of these antidepressants amounts to information on a total of 3,500 patients in therapeutic trials unavailable to public scrutiny.

 

 

In the FDA medical and statistical reviews, it was deemed that 38 of the 74 efficacy trials (51%) were positive studies, and all but one of these trials have been published. The remaining 36 studies (49%) were either negative (n=24) or were considered inconclusive for efficacy (n=12). Of these, 11 studies were published as being positive efficacy trials even though they conflicted with the FDA assessment. Only three of 24 negative efficacy trials (13%) have been published.

An important finding of this analysis is that negative efficacy trials of antidepressants (and presumably, most psychotropics) are infrequently reported in the medical literature. Furthermore, trials with mixed or inconclusive efficacy outcomes are often reported as positive studies, even though the primary outcome measure may have failed to show efficacy and may not be apparent in the report.

 

Effect Sizes of Antidepressants versus Published Data

Turner and colleagues9 computed weighted effect-size values from pooling of journal reports for each antidepressant and compared this value with effect sizes computed from the FDA summary documents. In each instance, the computed effect-size based on the published literature was higher than the effect-size value based on FDA documentation. The weighted effect sizes from the published literature ranged from 11% to 69% higher than the effect sizes computed from FDA data (mean=32%, P<.001). It is interesting that effect sizes using the FDA database ranged from 0.2–0.4 for the 12 antidepressants, where 0.2 is regarded as a small effect size and 0.5 a medium effect size. Effect sizes based on pooled published reports were consistently higher for every one of the 12 antidepressants, and effect size exceeded 0.5 for mirtazapine, paroxetine, and venlafaxine.

The findings of this study should be interpreted cautiously. It must be kept in mind that absence of statistical significance in a trial does not necessarily signify lack of efficacy. There can be valid reasons during the second and third phases of development for trials to fail unrelated to intrinsic efficacy of the agent. Failed and negative trials may result from escalating placebo response rates in efficacy studies, a changing population of depressed subjects recruited primarily by advertisement, or a relative dearth of competent investigators who carefully select and rate patients who are likely to be drug responsive.14,15 There are numerous factors influencing whether results of a study may go unpublished, including failure to submit manuscripts or decisions by journal editors not to accept negative trials. The recently established clinical trial registries and the requirement of journals and the FDA that trials be registered may foster wider dissemination of efficacy outcomes of trials.4,5

 

Guest Authorship and Ghostwriting

Apparent misrepresentation of clinical trial results and manipulation of research articles relating to rofecoxib (Vioxx) has emerged as a result of litigation.1,10,11 Court documents originally obtained during litigation against Merck and Company allowed access to company policies and decision making regarding publication of clinical trial results of rofecoxib.

A recent study10 by authors involved in the litigation and interested in company practices about guest authorship, ghostwriting, and financial disclosures examined several thousand court documents to investigate these issues. Guest authorship is defined as designation of an individual as author who does not meet accepted authorship criteria; that is, an individual who did not make a substantial contribution to the research or writing the manuscript.16 Inspection of the rofecoxib litigation yielded approximately 250 documents relating to publication of clinical trials of rofecoxib and allowed a determination to be made as to use of professional medical writing in manuscript preparation and subsequent recruitment of opinion leaders to be authors. Internal documents revealed that Merck marketing employees commonly hired medical writing companies to ghostwrite scientific review articles and recruited external experts to serve as authors. Recruited authors of ghostwritten papers often served as sole author and received an honorarium. Numerous instances were found where authors did not appear to be involved in the design or conduct of the study or to have made substantive contributions to the manuscript other than minor editing. Among 96 relevant published articles, the authors found that 92% (22 of 24) of published clinical trials disclosed Merck financial support, but only 50% (36 of 72) of therapeutic review articles about rofecoxib disclosed Merck sponsorship or financial compensation of the author.

 

Data Misrepresentation and Selective Reporting

Two biostatisticians, also involved in the rofecoxib litigation and familiar with the clinical data, examined internal documentation relating to three placebo-controlled clinical trials of rofecoxib in the treatment of Alzheimer patients. The authors also conducted their own independent statistical analysis of the safety data from these long-term multicenter trials.11 In April 2001, the drug sponsor conducted an intention-to-treat analysis that revealed increased risk of mortality associated with rofecoxib treatment of cognitive impairment among patients with Alzheimer’s disease, but this analysis was not submitted to the FDA until 2003. Instead, the data reported to the FDA in 2001 as part of a required annual safety update used a variety of counting methods, such as an on-treatment analyses. This type of statistical analysis, unlike a more conservative intention-to-treat analysis, minimized appearance of excess mortality risk with rofecoxib. The drug sponsor also failed to inform investigational review boards of the findings of the intention-to-treat analysis as required. Investigators in the ongoing multi-year study remained blind to this emerging safety data, unlike the Merck research staff, who failed to discern a safety issue. The company allowed the study to continue for 2 more years because of slower than planned enrollment.

A review article, funded by Merck and published in November 2001, based on a meta-analysis of cardiovascular thrombotic events in 23 clinical trials of this cyclo-oxygenase agent included two of the rofecoxib Alzheimer’s disease trials, yet the authors, five of whom were Merck employees, did not take the opportunity to report the mortality findings of the intention-to-treat analysis.11 It was not until July 2003, that a final safety report filed with the FDA furnished this evidence of excess mortality in Alzheimer’s disease patients (Hazard Ratio, 2.71, P<.001). Independent analysis by the authors of the present report of the Alzheimer’s safety data available in 2001 confirms that this excess mortality in elderly patients associated with rofecoxib treatment was known.11

 

Conclusion

Three studies that prompted a recent Journal of the American Medical Association editorial1 examined issues pertaining to the reporting clinical trial data.9-11 Greater than 30% of pre-approval, placebo-controlled, efficacy trials of antidepressants approved in the past 15 years were found never to have been published. Guest authorship and ghostwriting of articles was a frequent practice for a popular drug, later removed from the market for safety reasons. For the same drug, apparent misreporting of mortality data in Alzheimer’s disease patients occurred. Accurate and complete reporting of clinical trial results is essential to the teaching and practice of evidence-based medicine. Precautions taken by medical journals, such as submitting original study protocols and independent statistical analyses, may be necessary to ensure accuracy and transparency of published reports. PP

 

References

1.    DeAngelis CD, Fontanarosa PB. Impugning the integrity of medical science: the adverse effects of industry influence. JAMA. 2008;299:1833-1835.
2.    Carlat D. Dr drug rep. New York Times Magazine. November 25, 2007.
3.    Angell M. Time for a drug test registry. Washington Post.com. August 13, 2004:25.
4.    International Committee of Medical Journal Editors. Uniform requirements for manuscripts submitted to biomedical journals. Available at: http://icmje.org. Accessed July 9, 2008.
5.    Food and Drug Administration Amendments Act of 2007. HR3580, enacted by the House and Senate, Pub L No 110-85. Available at: http://frwebgate,access,gpo.gov/cgi-bin/getdoc.cgi?dbname=110_cong_bills&docid=f:h3580enr.txt.pdf. Accessed October 11, 2007.
6.    Sackett DL, Strauss SE, Richardson WS, et al. Evidence-Based Medicine: How to Practice and Teach EBM. New York, NY: Churchill-Livingston; 2000.
7.    Gray GE, Pinson LA. Evidence-based medicine and psychiatric practice. Psychiatr Q. 2003;74(4):387-399.
8.    Gupta M. Does evidence-based medicine apply to psychiatry? Theor Med Bioeth. 2007;28(2):103-120.
9.    Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R. Selective publication of antidepressant trials and its influence on apparent efficacy. N Engl J Med. 2008;358(3):252-260.
10.    Ross JS, Hill KP, Egilman DS, Krumholz HM. Guest authorship and ghostwriting in publications related to rofecoxib: a case study of industry documents from rofecoxib litigation. JAMA. 2008;299(15):1800-1812.
11.    Psaty BM, Kronmal RA. Reporting mortality findings in trials of rofecoxib for Alzheimer disease or cognitive impairment: a case study based on documents from rofecoxib litigation. JAMA. 2008:299(15):1813-1817.
12.    Committee on Governmental Reform, U.S. House of Representatives, 109th Congress, 1st session. A citizen’s guide on using the Freedom of Information Act and the Privacy Act of 1974 to request government records. Report no. 109-226. Washington, DC: Government Printing Office; 2005.
13.    Center for Drug Research. Food and Drug Administration. Rockville, Maryland. Available at: www.fda.gov/cder/foi/nda. Accessed July 9, 2008.
14.    Robinson DS, Rickels K. Concerns about clinical drug trials. J Clin Psychopharmacol. 2000;20(6):593-596.
15.    Kobak KA, Kane JM, Thase ME, Nierenberg AA. the problem of measurement error in clinical trials: time to test new paradigms? J Clin Psychopharmacol. 2007;27(1):1-5.
16.    Rennie D, Yank V, Emmanuel L. When authorship fails: a proposal to make contributors accountable. JAMA. 1997;278(7):579-585.

 

Dr. Vazzana is clinical assistant professor in the Department of Child and Adolescent Psychiatry at New York University (NYU) School of Medicine and member of the Harris Obesity Prevention Effort at NYU in New York City.

Disclosures: Dr. Vazzana receives grant support from Allergan.
Please direct all correspondence to: Andrea D. Vazzana, PhD, NYU Child Study Center, 577 1st Ave, New York, NY 10016; Tel: 212-263-8843; Fax: 212-263-8662; E-mail: vazzaa01@nyumc.org.

 


 

Focus Points

• Significant psychological changes follow adolescent bariatric surgery.
• Psychological factors and quality of life are important outcomes of surgery.
• A minority of adolescents exhibit poor psychosocial adjustment post-surgery.

 

Abstract

The adverse impact obesity can have on a person’s medical and mental health is overwhelming. As the prevalence and severity of childhood obesity and its related comorbidities continue to swell, there are inadequate effective, long-term solutions for the non-surgical management of morbidly obese youth. Although they are still controversial, refined surgical procedures have improved the safety and efficacy of bariatric surgery. It is being increasingly used with morbidly obese adolescents under the care of a multidisciplinary treatment team. Bariatric surgery typically results in marked weight loss and the resolution or reduction of comorbid conditions. At a more normalized weight, these adolescents often experience substantial life changes in areas that have the potential to positively, and sometimes negatively, alter a person’s quality of life. It is important to understand these complex changes in order to facilitate the adolescent’s positive long-term outcome. Despite their importance, there are limited empirical studies pertaining to adolescent psychosocial outcomes. Current results support the benefits of bariatric surgery in this population, but more rigorous research studies with prospective data collection and long-term follow up are necessary before pediatric bariatric surgery can be officially sanctioned for this special needs population.

 

Introduction

The United States has the worst epidemic of child obesity in the world.1 Seventeen percent of US adolescents are currently obese,2 and the prevalence is expected to progressively increase through at least 2010.1 The severity of obesity in youths has increased as well. Today’s heaviest children are markedly heavier than those from one generation ago.3 Four percent are morbidly obese (Table 1),4,5 and they are likely to remain obese as adults, particularly if at least one parent is also obese.6-8 Medical consequences of obesity are well documented9 and result in earlier mortality,10,11 curtailing the obese individual’s lifespan by 5–20 years.11 Indeed, the obesity epidemic undermines medical advances that would otherwise extend life span.12 Financial costs of the child obesity epidemic are also burdensome. At over $127 million/year, national hospital costs associated with child obesity and its comorbidities have tripled in the past 20 years.13

 

 

However, the greatest cost of obesity might be the psychological impact resulting from social stigma and discrimination.14,15 The pervasiveness of societal bias against obesity is widespread; it has been called the last “acceptable” form of discrimination.16 Obesity has particularly devastating psychosocial effects for adolescents, the impact of which can last through adulthood.6,17 There are indications that when obesity is limited to childhood, its adverse psychosocial impact might be minimized,6 but without radical intervention, the chances that adolescent morbid obesity will continue into adulthood are almost 100%.18

Surgery is the most, and perhaps only, effective means of long-term weight loss.19 Adolescent bariatric surgery (ABS) is a relatively new subspecialty, and it is not without controversy. Nonetheless, the few studies empirically examining the psychosocial outcomes of ABS have generally supported anecdotal observations of improved psychological functioning and quality of life (QOL).20,21

This article provides an overview of the psychological and psychosocial consequences experienced by morbidly obese adolescents. Anecdotal observations, retrospective surveys, and prospective studies documented in the literature delineate the changes that typically follow ABS. Indicators of poor adjustment following surgery are described. Finally, recommendations for future studies are provided.

 

The Morbidly Obese Adolescent

For the 4% of adolescents who are morbidly obese (body mass index [BMI] >40), the medical and psychosocial consequences of obesity increase in a dose-dependent fashion with the severity of obesity.4,22,23 With BMIs as high as 105,24 morbidly obese adolescents seeking ABS can suffer from multiple, severe comorbidities,25,26 including congestive heart failure and pulmonary hypertension.27 Socially, they tend to be marginalized; they are unlikely to have a best friend or reciprocal friendships, and individuals who befriend them are more likely to be unpopular.23 When weight-related teasing occurs from multiple sources, which is often the case with extreme cases of obesity, there is a high prevalence of emotional problems, including low self-esteem, body dissatisfaction, depression, and anxiety.28,29 Many morbidly obese adolescents prematurely terminate their schooling or are home-schooled in order to avoid torment from their peers.19,30-32 Reports of passive suicidal ideation are documented in the literature.30

Treatment for pediatric obesity include behavioral, pharmaceutical, and surgical options.33 However, nonsurgical treatments result in relatively negligible weight loss that is typically regained.34-36 Repeated failures at weight loss are demoralizing to the adolescent and have been related to “severe psychological problems” and social withdraw anecdotally.30 The 1991 National Institute of Health Consensus Conference on Obesity Surgery37 sanctioned bariatric surgery as the most effective strategy for long-term weight loss and maintenance for severely obese adults. However, the lack of longitudinal, prospective studies with adolescent populations prevented the panel from endorsing it for youths. Nonetheless, there is a growing national demand for ABS with the number of procedures increasing more than five-fold from 1997–2003.38

 

The Psychological Outcomes of Bariatric Surgery

Although the morbidity and mortality associated with morbid obesity are startling, psychological distress, both internally and externally imposed, is likely the most pervasive problem experienced by morbidly obese adolescents.39 Experts recommend early surgical intervention in order to minimize the emotional as well as physical consequences of morbid obesity.18,20,22,24,25,27,30-32,34,40-63

 

Comorbid Psychopathology

Psychiatric symptoms are frequently described in samples of morbidly obese adolescents20,21,54,58,64-67 and are one of the most common comorbidities in adolescents presenting for ABS.58 Detecting the presence of pre-existing psychiatric symptoms is important because of speculation in adult literature that suggests an undiagnosed, pre-existing psychiatric disorder is one reason for procedural reversals.68 At least one adolescent study described two instances of “psychologic intolerance” resulting in gastric band removals.64 Additionally, knowing the frequency, severity, and duration of psychiatric symptoms preceding ABS is critical to interpreting post-operative symptoms. Nevertheless, numerous descriptions of both pre- and post-surgical psychological functioning are anecdotal, nonspecific, or vaguely referenced. There have been few empirical examinations addressing whether the severity of symptoms experienced by morbidly obese adolescents seeking ABS actually meets clinical criteria for disorder.

Depending on the method of assessment, US data show a lifetime prevalence of Axis I psychiatric disorders in ≤88% of adolescent patients seeking surgery.21,65 Research indicates that mood, anxiety, disruptive behavior, and eating disorders are the most common psychiatric comorbidities experienced by these patients. In studies where psychiatric comorbidities are listed, mood disorders have been reported in up to 68% of patients21,65 but generally occur in approximately 33% to 150% of samples.20,21,26,67 Lifetime history of anxiety disorders occurs in approximately 16% of samples.65 Reports of disruptive behavior disorders, including attention deficit hyperactivity disorder and oppositional defiant disorder, occur in ≤36% of adolescent patients.21,43,65 Eating disorders, most commonly binge eating disorder, have been reported in ≤13% of adolescent cases.21,65

Anecdotally, ABS resolves or improves the psychiatric symptoms of obese adolescents.69,70 At 1-year follow up, patients appear “brighter, more alert and more outgoing.”70 In a restrospective survey conducted at 6-year follow up, 85% of patients reported they were in good spirits “daily” or “almost daily,” which was more often than they recalled prior to surgery.31 Prospective, empirical data comparing pre- and post-surgical rates of psychiatric symptoms corroborate anecdotal observations and retrospectively collected data. In a longitudinal, prospective study,20 30% of pre-surgical adolescent patients had clinically significant depressive symptoms in the moderately severe range, as measured by the Beck Depression Inventory, Second Edition (BDI-II). Follow-up data collected at 3-month intervals demonstrated progressive symptom resolution. At 9-months follow up, there was a statistically significant, 22-point decrease in BDI-II scores among those who had been clinically depressed. No patients at follow up had clinically significant symptoms.

To varying extents, weight-loss success might impact resolution of mood and anxiety symptoms. In a 4-year follow up study with a 20% attrition rate and a 63% failure rate among remaining participants, 88% of the follow-up sample had elevated rates of depression and 50% were socially anxious.71 Although lack of pre-surgical data makes interpretation of these results difficult, it is speculated that the poor weight- loss outcome perpetuated or even aggravated pre-existing psychiatric symptoms.

 

Body Image

Soper and colleagues72 noted that morbidly obese adolescents view themselves as “huge, grotesque creatures.” For many, their self-disparaging thoughts are reinforced by their amorphous clothing39 and by the social discrimination they endure.73 Negative body image can be resistant to treatment72 and can lead to self-imposed isolation and depression.74 Morbidly obese adolescents have reported feeling more comfortable interacting with cyber-friends, preventing the possibility of their being judged on appearance.21

Reports of enhanced body image following weight-loss surgery have been reported in the ABS literature.24,25 In a 6-year, retrospective follow-up study, 82% of patients felt attractive and 74% felt less embarrassed about their appearance when in public, whereas virtually all had felt unattractive before undergoing surgery.31 There are indications, however, that poor body image persists but changes in focus. In one retrospective survey, surgical scarring and loose skin resulting from massive, rapid weight loss were sited by 20% of patients as the worst aspects of their bariatric experience.31 Complaints of scarring have decreased in recent years given the advent of laparoscopic procedures. However, adolescent patients have continued to site severe skin redundance as a source of embarrassment both in public places (eg, wearing tank tops or bathing suits) and in romantic relationships.18 To date, there have been no prospective studies that include outcome data regarding body image of adolescent patients.

 

Quality of Life

Morbidly obese adolescents report innumerable ways in which weight impacts their lives (Table 2). Health-related QOL is a multidimensional construct that describes ways in which symptoms of a disease and its comorbidities affect emotional, physical, social, and overall well-being and life satisfaction.75,76 Studies have consistently shown that across domains, obese adolescents’ QOL is below that of healthy adolescents’20,21,67 and is about equivalent to that of a child diagnosed with cancer.77 The desire to improve their poor QOL is a primary motivation for adolescents seeking ABS.30

 

Retrospective follow-up assessments with adolescent patients reveal positive changes to QOL, including improved self-esteem, school performance, increased socialization, and greater activity level.18,24,25,27,30,32,39,40,46,56,60,66,69,72 At a 3-year telephone follow up of 11 adolescent patients, 93% reported an improvement in physical activity, and 72% reported improved social life and self-esteem.63 In another survey,46 12 adolescent patients at 5-year follow up reported excellent academic and occupational functioning. Ninety-two percent reported improvement in overall health and greater social involvement with peers. Likewise, at 6-year follow up, 41% of patients retrospectively reported that the best surgical outcome was their increased self-esteem.31 A gross measure of QOL, the 5-item Moorehead-Ardelt questionnaire, has also consistently shown positive post-surgical ratings of social contact, school functioning, and physical activity.26,60

Improvements in prospectively assessed QOL have also been demonstrated. At 1-year follow-up,49 adolescents demonstrated significant improvements in social, familial, and academic functioning, as determined via clinical ratings of Global Assessment of Functioning.21 Clinical impressions were corroborated by the 36-item short form health survey, a commonly used self-report questionnaire measuring QOL across eight domains. Compared with pre-surgical ratings, patients reported improvements in social functioning, physical functioning, role limitations due to physical health and emotional problems, bodily pain, general health perceptions, vitality, and mental health functioning.21 Benefits were seen regardless of initial BMI severity, extent of weight loss, gender, and age (ie, younger versus older adolescents).

Similar trends were seen in a longitudinal study assessing overall QOL at 3-month intervals using the PedsQL. Although 80% of adolescent patient’s scores were in the abnormal range before surgery, scores had improved enough to be equivalent to those of healthy children 6 months after surgery. Although patients’ QOL scores declined slightly after 3 months, scores were still markedly higher than those before weight loss.

 

Indicators of Poor Post-surgical Adjustment

In clinical practice, a minority of follow-up patients have reported engaging in high risk behaviors, including drug use, gang involvement, and unsafe sexual practices. It is possible that some patients who undergo ABS are more prone to impulsive, risk-taking behaviors than typical adolescents.78,79 However, there are also concerns that their unsafe practices could reflect poor adjustment to post-surgical psychosocial changes. After years of social isolation and rejection, post-surgical adolescents typically experience increased social interactions. In their rush to develop friendships, some might be particularly vulnerable to negative peer influences. There is also concern that adolescents who previously used food to quell negative emotions might turn to drugs after ABS restricts their food intake.

At least one case study illustrated new onset of stimulant abuse. Dutta and colleagues80 described a 17-year-old female with a pre-surgical history of peer rejection and depressed mood, but with no prior history of drug use. Within 7 months of surgery, she had become acquainted with a known drug user and was smoking methamphetamine twice a day. The study cautioned that the appetite suppression qualities of stimulants, including methamphetamine, might make them particularly attractive to individuals with weight concerns. A second study, reporting on the long-term follow up of jejunoileal bypass, incidentally noted that one of their mortalities was a female adolescent who died 16 months post surgery as a result of drug and alcohol abuse.32 Although onset of substance abuse was not noted, pre-existing substance use is routinely an exclusionary criteria for ABS.19 Therefore, it is likely that drug use began following weight loss.

Similarly, unplanned pregnancies following ABS have been reported in the literature.39,53,81 In the most compelling account, a retrospective chart review of 47 adolescent Roux-en-Y gastic bypass (RYGB) patients documented seven unplanned pregnancies among six single, white females.81 The pregnancy rate of 12.8% was noted to be almost double the national average of 6.5% for the same demographic. Of note, all six patients had a pre-existing history of depression and two had comorbid anxiety. Changes in socialization, psychiatric functioning, and risk-taking tendencies might have placed these teenagers at greater risk for pregnancy. Reports that conception occurred within several weeks of the point of patients’ greatest weight loss could suggest that increased sexual attention played a role in the pregnancy. If the girls experienced irregular menstrual cycles secondary to obesity, it is possible that they thought they were infertile and dismissed the need for contraception. A third possibility is that the girls used oral contraception that was poorly absorbed because of the RYGB.32 In addition to the usual concerns regarding adolescent pregnancies, there is the added risk with bariatric patients that nutritional deficiencies may result in harm to the fetus.81 It is important to underscore the use of contraception in adolescent weight-loss patients.

 

Psychological Benefits Occur with Relative Weight Loss

Though numerous adolescent patients’ BMIs remain in the obese range at follow up,27,44,46,56,60,63,64 psychological benefits still present. For example, in Holterman and colleagues’20 sample, clinically significant reduction of depressive symptoms was seen although 50% of patients remained morbidly obese. It appears that the relative improvement in weight has psychological benefits even when patients remain overweight by normative standards. Some studies have reported that when patients have regained weight, they continue to report psychological gains.39,56 However, adult literature has demonstrated that with time, there is a decay of psychological benefits.82,83 One explanation is that as the initial social reinforcement for weight loss wanes, attention is refocused on aspects of life that failed to meet pre-surgical expectations. In almost all cases, however, post-surgical functioning is still improved compared to pre-surgical status. With the exception of the slight decrease in QOL ratings seen in one study,20 no ABS studies have systematically examined this issue. Given reports that at least some degree of weight regain is common31,34,56,84 and that morbidly obese adolescents have previously been demoralized by previous failed attempts at weight loss,30 it is possible that weight regain could result in psychological distress.

 

Conclusion

Current ABS studies have demonstrated the efficacy and safety of the surgical procedures. However, the investigation of psychosocial impact has been secondary in comparison.84 Research findings to date have been limited by small sample sizes, retrospective and cross-sectional designs, and failure to use standardized measures both pre-operatively and at follow up.18,24,27,40,42,44-46,50,54,55,64,70,84 Moving forward, it will be important to conduct prospective, longitudinal studies focusing on psychosocial outcomes and using multivariate analyses to examine various interaction effects. Given the existing literature on ABS, the roles of gender, chosen surgical procedure, BMI severity, percentage of excess weight loss, social status, family background, and mental health will be particularly intriguing. PP

 

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