Reducing Racial/Ethnic Disparities in Childhood Obesity: The Role of Early Life Risk Factors.

Reducing Racial/Ethnic Disparities in Childhood Obesity: The Role of Early Life Risk Factors.

JAMA Pediatr. 2013 Jun 3; 1-7
Taveras EM, Gillman MW, Kleinman KP, Rich-Edwards JW, Rifas-Shiman SL

IMPORTANCE Many early life risk factors for childhood obesity are more prevalent among blacks and Hispanics than among whites and may explain the higher prevalence of obesity among racial/ethnic minority children. OBJECTIVE To examine the extent to which racial/ethnic disparities in adiposity and overweight are explained by differences in risk factors during pregnancy (gestational diabetes and depression), infancy (rapid infant weight gain, feeding other than exclusive breastfeeding, and early introduction of solid foods), and early childhood (sleeping <12 h/d, presence of a television set in the room where the child sleeps, and any intake of sugar-sweetened beverages or fast food). DESIGN Prospective prebirth cohort study. SETTING Multisite group practice in Massachusetts. PARTICIPANTS Participants included 1116 mother-child pairs (63% white, 17% black, and 4% Hispanic) EXPOSURE Mother’s report of child’s race/ethnicity. MAIN OUTCOMES AND MEASURES Age- and sex-specific body mass index (BMI) z score, total fat mass index from dual-energy x-ray absorptiometry, and overweight or obesity, defined as a BMI in the 85th percentile or higher at age 7 years. RESULTS Black (0.48 U [95% CI, 0.31 to 0.64]) and Hispanic (0.43 [0.12 to 0.74]) children had higher BMI z scores, as well as higher total fat mass index and overweight/obesity prevalence, than white children. After adjustment for socioeconomic confounders and parental BMI, differences in BMI z score were attenuated for black and Hispanic children (0.22 U [0.05 to 0.40] and 0.22 U [-0.08 to 0.52], respectively). Adjustment for pregnancy risk factors did not substantially change these estimates. However, after further adjustment for infancy and childhood risk factors, we observed only minimal differences in BMI z scores between whites, blacks (0.07 U [-0.11 to 0.26]), and Hispanics (0.04 U [-0.27 to 0.35]). We observed similar attenuation of racial/ethnic differences in adiposity and prevalence of overweight or obesity. CONCLUSIONS AND RELEVANCE Racial/ethnic disparities in childhood adiposity and obesity are determined by factors operating in infancy and early childhood. Efforts to reduce obesity disparities should focus on preventing early life risk factors. HubMed – depression


EEG Alpha Power as an Intermediate Measure Between Brain-Derived Neurotrophic Factor Val66Met and Depression Severity in Patients With Major Depressive Disorder.

J Clin Neurophysiol. 2013 Jun; 30(3): 261-7
Zoon HF, Veth CP, Arns M, Drinkenburg WH, Talloen W, Peeters PJ, Kenemans JL

: Major depressive disorder has a large impact on patients and society and is projected to be the second greatest global burden of disease by 2020. The brain-derived neurotrophic factor (BDNF) gene is considered to be one of the important factors in the etiology of major depressive disorder. In a recent study, alpha power was found to mediate between BDNF Met and subclinical depressed mood. The current study looked at a population of patients with major depressive disorder (N = 107) to examine the association between the BDNF Val66Met polymorphism, resting state EEG alpha power, and depression severity. For this purpose, repeated-measures analysis of variance, partial correlation, and multiple linear models were used. Results indicated a negative association between parietal-occipital alpha power in the eyes open resting state and depression severity. In addition, Met/Met patients showed lower global absolute alpha power in the eyes closed condition compared with Val-carriers. These findings are in accordance with the previously uncovered pathway between BDNF Val66Met, resting state EEG alpha power, and depression severity. Additional research is needed for the clarification of this tentative pathway and its implication in personalized treatment of major depressive disorder. HubMed – depression


Poor sleep maintenance and subjective sleep quality are associated with postpartum maternal depression symptom severity.

Arch Womens Ment Health. 2013 Jun 4;
Park EM, Meltzer-Brody S, Stickgold R

Women are at increased risk of developing mood disorders during the postpartum period, and poor postpartum sleep may be a modifiable risk factor for the development of depression. This longitudinal study investigated the relationship between sleep variables and postpartum depression symptoms using wrist actigraphy and self-report surveys. Twenty-five healthy primiparous women were recruited from their outpatient obstetricians’ offices from July 2009 through March 2010. Subjects wore wrist actigraphs for 1 week during the third trimester of pregnancy and again during the 2nd, 6th, 10th, and 14th weeks postpartum while completing sleep logs and sleep surveys. Subjective assessments of mood were collected at the end of each actigraph week. Subjective sleep assessments were strongly predictive of depression severity scores as measured by the Edinburgh Postnatal Depression Scale (EPDS) across all weeks (p?HubMed – depression


Pharmacogenetics in major depression: a comprehensive meta-analysis.

Prog Neuropsychopharmacol Biol Psychiatry. 2013 May 31;
Niitsu T, Fabbri C, Bentini F, Serretti A

A number of candidate gene studies focused on major depression (MD) and antidepressant (AD) efficacy have been carried out, but results mainly remain inconclusive. We performed a comprehensive meta-analysis of published candidate gene studies focused on AD efficacy in MD to evaluate the cumulative evidence. A random-effect model was applied to study the polymorphisms with genotypic counts available from at least three independent studies. On the base of previous evidence, the analysis was stratified by ethnicity (Caucasian, Asian, and other/mixed), and AD class (SSRIs and mixed/other ADs). Genotypic data were available for 16 polymorphisms in 11 genes. After the exclusion of 5-HTTLPR in SLC6A4 included in another recent meta-analysis, 15 polymorphisms in 11 genes were included in the present meta-analysis (BDNF rs6265, SLC6A4 STin2, HTR1A rs6295, HTR2A rs6311, rs6313 and rs7997012, HTR6 rs1805054, TPH1 rs1800532, SLC6A2 rs5569, COMT rs4680, GNB3 rs5443, FKBP5 rs1360780 and rs3800373, and ABCB1 rs1045642 and rs2032582). Our results suggested that BDNF rs6265 (Val66Met) heterozygous genotype was associated with better SSRIs response compared to the homozygous genotypes, particularly in Asians (OR=1.53, 95%CI 1.12-2.07, p=0.007). SLC6A4 STin2, HTR2A rs6311 and rs7997012, GNB3 rs5443, FKBP5 rs1360780 and rs3800373, and ABCB1 rs2032582 showed associations with AD efficacy, but these results were highly dependent on one or two single studies. In conclusion, our findings suggested the BDNF Val66Met as the best single candidate involved in AD response, with a selective effect in SSRI treatment. Our overall results supported no major effect of any single gene variant on AD efficacy. HubMed – depression