Psychiatric Dispatches: Noteworthy Briefs from the Field: April 2009
Primary Psychiatry. 2009;16(4):17-18
Depression Linked to Increase in Harmful Type of Body Fat
While obesity and weight gain have been known to be a common link to depression, depression is also actually proven to increase fat. Nicole Vogelzangs, doctoral student at VU University Medical Center in Amsterdam, and colleagues, studied >2,000 patients 70–79 years of age in Memphis, Tennessee and Pittsburgh, Pennsylvania. The study initially evaluated participants and then re-assessed them 5 years later to conclude any information correlating to obesity in general and abdominal obesity in particular. After 5 years, the evaluation consisted of determining whether or not there was a correlation between overall obesity and abdominal obesity while also considering other factors such as an individual’s lifestyle, history of diseases, and other information that could interfere with the outcome.
They found no substantial causation linked to baseline depression. However, there was a significant difference between abdominal obesity and depression. One possible theory why depressed people are more likely to have abdominal obesity is because their lifestyle is most likely unhealthy. However, this assumption is not very strong, as the researchers had factored in the additional affects of alcohol use, exercise patterns, smoking and other illnesses.
“Previous studies have reported clinically relevant depressive symptoms in 10% to 15% of older persons,” said Ms. Vogelzangs. “Physicians should be alert of the fact that persons with depressive symptoms are more prone to gain visceral fat, as this increases their risk for heart diseases. Therefore, it would be good to monitor the metabolic status of (older) persons with depressive symptoms.”
According to Vogelzangs and colleagues, the most important finding was that older individuals with depressed symptoms were twice as likely to gain visceral fat as were non-depressed older people. Although there was an increase in visceral fat, there was no change in overall obesity, such as body mass index. This implies a biologic explanation more so than poor diet as the cause.
One of the most challenging factors they found was that they did not analyze psychiatric diagnoses of depression. Instead, they used a questionnaire to calculate the symptoms.
“However, previous studies have shown that the questionnaire we used (The Center for Epidemiologic Studies Depression Scale) gives a good indication of the presence of clinically relevant depressive symptoms,” Ms. Vogelzangs said.
Funding for this research was provided by the National Institutes of Health and the Young Academy of the Royal Netherlands. (Arch Gen Psychiatry. 2008;65(12):1386-1393.) –AC
Genetic Marker Discovered to Be Strongly Associated with Delusions in Schizophrenia
Patients with schizophrenia may present with various symptoms, including delusions, hallucinations, and declines in motor and cognitive function. According to the National Institute of Mental Health, among the 1.1% of the United States population affected by the disorder, some may present with some but not all of the common symptoms of schizophrenia. Due to the varied network of symptoms associated with schizophrenia, the identification of particular genes that may be associated with the disorder is difficult. Currently, researchers have identified certain genes that may contribute to the development of schizophrenia, such as neuregulin (NRG) 1, but lack a more complete understanding of the genetic make-up for the disorder.
David Valle, MD, of the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins University School of Medicine in Baltimore, Maryland, and colleagues, studied the genetic make-up of 1,515 people with and without schizophrenia in the Ashkenazi Jewish population for genetic differences that may highlight particular genes involved in schizophrenia. In prior gene linkage studies, researchers have identified a schizophrenia susceptibility locus gene in Ashkenazi Jewish and Han Chinese from Taiwan populations.
Valle and colleagues studied 458 patients with schizophrenia (including 285 parent-child trios) and compared their genetic composition to 487 healthy controls. In addition, the authors identified 73 different symptoms of schizophrenia and separated symptoms into nine heritable quantitative disorder traits: delusion, prodromal, negative, affective, scholastic, adolescent sociability, disorganization, disability, and hallucination. Patients with schizophrenia were evaluated for presence of these traits. Focusing on the region previously implicated in schizophrenia—chromosome 10—researchers analyzed 1,414 single nucleotide polymorphisms (SNPs) to determine if any SNPs were more common among patients with schizophrenia than healthy controls.
Although they did not find any genetic markers directly related to the complete spectrum of schizophrenia symptoms, the authors did find three SNPs (rs10883866, rs10748842, and rs6584400) strongly associated with the “delusion” quantitative trait when comparing genetic differences from healthy controls. Each SNP was located at NRG3, which is primarily expressed in the central nervous system and is related to NRG1. In addition, researchers identified 20 additional SNPs that may play a role in schizophrenia development; 13 of those SNPs, which were associated with scholastic, disorganization, and hallucination traits, were located at or near NRG3.
They concluded that these biologic properties along with prior linkage studies and these association results strongly support NRG3 as a gene involved in the development of schizophrenia. Additional studies could begin sequencing the NRG3 gene to uncover any genetic variants that may contribute to schizophrenia development in affected patients.
Funding for this research was provided by the National Alliance for Research on Schizophrenia and Depression, the National Institute of Mental Health, the National Institutes of Health, and the Wasie Foundation. (Am J Hum Genet. 2009;84(1):21-34.) –CP
Bipolar Mania Symptoms Associated with Treatment-emergent Mania
Manic phases of bipolar disorder have been shown to respond to mood stabilizer treatment, but treating bipolar depression can be more complex. Prescribing an antidepressant for bipolar depression can sometimes lead to treatment-emergent mania (TEM), a rapid switch from depression to mania following the introduction of an antidepressant.
Mark A. Frye, MD, at the Mayo Clinic in Rochester, Minnesota, and colleagues, recently published a study focusing on the factors leading and related to the emergence of TEM in bipolar disorder. They analyzed data from a previous study, led by Robert Post, MD, of the Bipolar Collaborative Network in Chevy Chase, Maryland. This second study included 176 adult outpatients with bipolar disorder, enrolled in a 10-week trial. Participants were divided into three groups, according to the Clinical Global Impression Scale for Bipolar Disorder: those who responded to antidepressant treatment (N=85), those who did not respond to antidepressant treatment (N=45), and those who had TEM or hypomania (N=46).
Using factor analysis, researchers compared the TEM group to the favorable and the non-favorable antidepressant response groups. Some components of the Young Mania Rating Scale—which was included in patients’ baseline testing—were identified as correlates of TEM, including increased motor activity and speech and language-thought disorder. It is suggested, therefore, that minimal manic symptoms at baseline in otherwise full syndromal bipolar disorder are indicative of risk for TEM. (Am J Psychiatry. 2009;166:164-172.) –LS
Psychiatric dispatches is written by Amanda Cuomo, Carlos Perkins, Jr., and Lonnie Stoltzfoos.