Exposure to secondhand smoke can lead to symptoms of major depressive disorder, generalized anxiety disorder, attention-deficit/hyperactivity
disorder, and conduct disorder in children and adolescents, according to a report in the April Archives of Pediatric and Adolescent Medicine. The results were gleaned from the National Health and Nutrition Examination Survey (NHANES), a program of studies designed
to assess the health and nutritional status of adults and children in the United States. The survey is unique in that it combines
interviews and physical examinations. NHANES is a major program of the National Center for Health Statistics, part of the
Centers for Disease Control and Prevention.
Frank Bandiera, M.P.H., of the Department of Epidemiology and Public Health at the University of Miami Miller School of Medicine,
and his colleagues looked at children and adolescents aged 8 to 15 who participated in the NHANES from 2001 to 2004. Serum
levels of cotinine, a metabolite of nicotine that serves as a biomarker for exposure to tobacco smoke, were determined to
confirm secondhand smoke exposure among nonsmokers. Information on mental disorders in the study participants was derived
from the National Institute of Mental Health's Diagnostic Interview Schedule for Children Version IV.
The association of serum cotinine levels with symptoms of mental health disorders remained even after adjusting for survey
design, age, sex, race/ethnicity, poverty, migraine, asthma, hay fever, maternal smoking during pregnancy, and allostatic
load. These associations were more apparent for boys and for subjects of non-Hispanic white race/ethnicity.
"Future research is warranted to establish the biological or psychological mechanisms of association," said Bandiera and colleagues.
Bandiera FC, Kalaydjian Richardson A, Lee DJ, et al.: Secondhand Smoke Exposure and Mental Health Among Children and Adolescents.
Arch Pediatr Adolesc Med. 2011; 165 (4): 332-338. An abstract is posted at <http://archpedi.ama-assn.org/cgi/content/abstract/165/4/332>.
For many patients, weight gain poses a serious threat to successful treatment for psychosis. Especially in women, it can lead
to other morbidities, including type II diabetes mellitus, hypertension, and other cardiovascular diseases. It may also contribute
to reduced treatment compliance. While the atypical antipsychotics olanzapine and clozapine are the more well-known culprits
in weight gain, almost none of the atypical and typical antipsychotics are free of this side effect. The idea that certain
genetic risk factors may be important to produce weight gain and therefore enable individualized treatment in patients receiving
antipsychotics is supported by the substantial interindividual and interracial differences in antipsychotic-induced weight
One gene possibly involved in the multifaceted development of antipsychotic-induced obesity is the roundabout axon guidance
receptor, homolog 1 (ROBO1) gene. In a recently published cross-sectional study of a pooled sample of Dutch Caucasian psychiatric
patients, 435 patients—335 of whom had a diagnosis in the schizophrenia spectrum, 77 of whom had schizoaffective disorder,
two of whom had schizophreniform disorder, and 21 of whom had a psychotic disorder not otherwise specified—were evaluated
for a single nucleotide polymorphism (rs1455832) of ROBO1. Investigators then investigated the association between body mass
index (BMI) of the subjects and the presence of rs1455832.
The results were gender specific: The rs1455832 polymorphism studied was significantly associated with BMI and obesity in
female patients and therefore may play a role in inducing obesity in female patients using antipsychotics. This association
was not exhibited in male patients.
The study was conducted by Jelle Vehof, M.D., of the departments of Psychiatry and Epidemiology of the University Medical
Center Groningen, Groningen, the Netherlands, and colleagues.
Vehof J, Al Hadithy, AFY, Burger H, et al.: Association Between the ROBO1 Gene and Body Mass Index in Patients Using Antipsychotics.
Psych Gen. 2011; [Epub ahead of print March 15]. An abstract is posted at <http://journals.lww.com/psychgenetics/Abstract/publishahead/Association_between_the_ROBO1_gene_and_body_mass.99862.aspx>.
A new study has determined that migrants from Mexico to the United States are more prone to depressive or anxiety disorders
than are the nonmigrant family members they left behind. Researchers in California and Mexico performed a population survey
of 554 Mexican migrants to the United States and 2,519 nonmigrant family members in Mexico, looking for the first onset of
any depressive or anxiety disorder.
Results indicated that, after arrival in the United States, migrants had a significantly higher risk for first onset of any
depressive or anxiety disorder than did nonmigrant family members of migrants in Mexico. The associations between migration
and disorder varied with age, but the elevated risk was restricted to those aged 18 to 35, with particularly strong association
in the youngest migrants, aged 18 to 25.
"The findings are consistent with the hypothesized adverse effect of migration from Mexico to the United States on the mental
health of migrants, but only among migrants in recent birth cohorts," said Joshua Breslau, Ph.D., of the Department of Internal
Medicine at the University of California, Davis, School of Medicine and colleagues.
Breslau J, Borges G, Tancredi D, et al.: Migration from Mexico to the United States and Subsequent Risk for Depressive and
Anxiety Disorders. Arch Gen Psych. 2011; 68(4):428-433. An abstract is posted at <http://archpsyc.ama-assn.org/cgi/content/abstract/68/4/428>.
A study published in the March 8 Neurology examined the use of ibuprofen in relation to the risk for Parkinson's disease (PD). The study, conducted in Boston, sought
to determine whether the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in general, and ibuprofen in particular, might
mediate the neuroinflammation that contributes to the pathogenesis of PD. Researchers prospectively examined whether use of
ibuprofen or other NSAIDs was associated with lower risk for PD among 136,197 participants in the Nurses' Health Study (NHS)
and the Health Professionals Follow-Up Study (HPFS) free of PD at baseline (1998 for NHS, and 2000 for HPFS). During six years
of follow-up, 291 incident PD cases were identified. Users of ibuprofen had a significantly lower risk than nonusers after
adjustment for age, smoking, caffeine intake, and other covariates. Use of other types of analgesics was not associated with
lower risk. "The association between use of ibuprofen and lower PD risks, not shared by other NSAIDS or acetaminophen, suggests
ibuprofen should be further investigated as a potential neuroprotective agent against PD," concluded the researchers.
Gao X, Chen H, Schwarzschild MA J, et al.: Use of Ibuprofen and Risk of Parkinson Disease. Neurology. 2011; 76(10):863-869.
An abstract is posted at <www.neurology.org/content/early/2011/03/01/WNL.0b013e31820f2d79>.