Obesity

Objective: Recent studies conclude childhood intelligence has no direct effect on adult obesity net of education, but evolutionary psychological theories suggest otherwise.

Design and Methods: A population (n = 17,419) of British babies has been followed since birth in 1958 in a prospectively longitudinal study. Childhood general intelligence is measured at 7, 11, and 16, and adult BMI and obesity are measured at 51.

Results: Childhood general intelligence has a direct effect on adult BMI, obesity, and weight gain, net of education, earnings, mother's BMI, father's BMI, childhood social class, and sex. More intelligent children grow up to eat more healthy foods and exercise more frequently as adults.

Conclusion: Childhood intelligence has a direct effect on adult obesity unmediated by education or earnings. General intelligence decreases BMI only in adulthood when individuals have complete control over what they eat.

Obesity is associated with increased cardiovascular risk. Although short‐term weight loss improves vascular endothelial function, longer term outcomes have not been widely investigated. We examined brachial artery endothelium‐dependent vasodilation and metabolic parameters in 29 severely obese subjects who lost ≥10% body weight (age 45 ± 13 years; BMI 48 ± 9 kg/m²) at baseline and after 12 months of dietary and/or surgical intervention. We compared these parameters to 14 obese individuals (age 49 ± 11 years; BMI 39 ± 7 kg/m²) who failed to lose weight. For the entire group, mean brachial artery flow‐mediated dilation (FMD) was impaired at 6.7 ± 4.1%. Following sustained weight loss, FMD increased significantly from 6.8 ± 4.2 to 10.0 ± 4.7%, but remained blunted in patients without weight decline from 6.5 ± 4.0 to 5.7 ± 4.1%, P = 0.013 by ANOVA. Endothelium‐independent, nitroglycerin‐mediated dilation (NMD) was unaltered. BMI fell by 13 ± 7 kg/m² following successful weight intervention and was associated with reduced total and low‐density lipoprotein cholesterol, glucose, hemoglobin A_1c, and high‐sensitivity C‐reactive protein (CRP). Vascular improvement correlated most strongly with glucose levels (r = −0.51, P = 0.002) and was independent of weight change. In this cohort of severely obese subjects, sustained weight loss at 1 year improved vascular function and metabolic parameters. The findings suggest that reversal of endothelial dysfunction and restoration of arterial homeostasis could potentially reduce cardiovascular risk. The results also demonstrate that metabolic changes in association with weight loss are stronger determinants of vascular phenotype than degree of weight reduction.

Objective: Obesity is linked with large vessel atherosclerosis and diabetes. Its association with microvascular changes is less clear. We investigated the associations among retinal vessel diameters, vessel wall signs, and BMI in an older population.

Research Methods and Procedures: Retinal photographs were taken on 3654 persons aged 49+ years at baseline of the Blue Mountains Eye Study in Australia. Arteriolar and venular diameters were measured from digitized retinal photographs of the right eyes. BMI was calculated as weight (kilograms)/height (meters²). Incident obesity was defined in persons with BMI ≤ 30 at baseline but >30 after 5 years. A significant weight gain was defined as an increase in BMI of 2+ SDs (4 or more units) over the 5‐year period.

Results: At baseline, mean BMI was 26.1 (±4.6) in this population. At 5‐year examinations, 177 (10.0% of 1773 at risk) developed incident obesity, and 136 (6.4% of 2143 at risk) had significant weight gain. After adjusting for age, sex, smoking, triglyceride levels, and mean arterial blood pressure, persons with wider retinal venular diameters had a higher risk of incident obesity (odds ratio, 1.8; 95% confidence interval, 1.0 to 3.1, comparing the highest with lowest venular diameter quintiles) and significant weight gain (odds ratio, 1.7; 95% confidence interval, 0.9 to 3.2). These associations were attenuated with further adjustment for baseline BMI. Arteriolar diameter was unrelated with baseline or change in BMI.

Discussion: Wider retinal venular diameter is associated with risk of obesity, independent of hypertension, diabetes, lipids, and cigarette smoking. These data may support a role for impaired microvascular function in the course of weight gain.

We examined dietary supplement use for weight loss and perceptions about safety, efficacy, and regulatory oversight of these products. A random digit‐dialed telephone survey was conducted in 2005–2006, with a representative sample of 3,500 US adults. The survey assessed the beliefs and practices related to weight control. Outcome measures included the prevalence of dietary supplement use for weight reduction, demographic profile of supplement users, and knowledge about safety, efficacy, and regulation of dietary supplements. Of the adults who made a serious weight‐loss attempt (n = 1,444), 33.9% reported ever using a dietary supplement for weight loss. Supplement use was more common among women (44.9%) vs. men (19.8%); those aged 25–34; African Americans (48.7%) or Hispanics (41.6%) vs. whites (31.2%); less educated (38.4% high school degree or less vs. 31.1% some college or more); lower income households (41.8% made <$40K vs. 30.3% made ≥$40K); obese (40.7%) vs. overweight (29.1%); those who made more lifetime weight‐loss attempts (42.0% made ≥3 vs. 22.1% made <3); and those who used more weight‐loss methods (48.2% used ≥4 vs. 25.2% used <4). Many users and non‐users of dietary supplements had misperceptions about these products—many believed they are evaluated for safety and efficacy by the Food and Drug Administration (FDA) before marketing, and that dietary supplements are safer than over‐the‐counter (OTC) or prescription medications. Use of dietary supplements for weight loss is common. More information about dietary supplements is necessary to correct misperceptions and encourage the use of safe and effective weight‐loss methods.

The glucocorticoid receptor (GR) may be a common link between human obesity/metabolic syndrome and Cushing's syndrome. The effects of glucocorticoids are mediated through the functional isoform, GRα. An alternative isoform, GRβ, behaves as a dominant negative inhibitor of GRα and has been implicated as a contributing factor to glucocorticoid resistance. A naturally occurring ATTTA to GTTTA single nucleotide polymorphism (A3669G) located in the 3′ end of exon 9β results in increased stability of GRβ mRNA and increased GRβ protein expression. Enhanced GRβ expression may result in greater inhibition of GRα transcriptional activity, resulting in glucocorticoid insensitivity. To test the hypothesis that the 3669G allele would result in a phenotype less likely to express features of glucocorticoid excess, we studied the prevalence of this polymorphism and its relationship with obesity and features of the metabolic syndrome in 322 Europid and 262 South‐Asian subjects in northeast England. We report evidence that 3669G allele is associated with reduced central obesity in Europid women and a more favorable lipid profile in Europid men. These data suggest that the 3669G allele may attenuate the undesirable effects of glucocorticoids on fat distribution and lipid metabolism, although its penetrance may vary in different ethnic groups.

Objective: Pre‐receptor amplification of glucocorticoids is, in part, determined by the isoenzymes 11β‐hydroxysteroid dehydrogenase (11β‐HSD) type 1 and type 2, interconverting inert cortisone and active cortisol. Increased tissue activity of cortisol may play a part in features of the metabolic syndrome. Our objective was to compare 11β‐HSD1 gene expression in different fat depots (visceral, subcutaneous abdominal, and subcutaneous gluteal) in lean and obese men and women.

Research Methods and Procedures: A cross‐sectional study design was used for healthy patients undergoing minor abdominal surgery (lean men, 10), minor gynecological surgery (lean woman, 10), or gastric banding operations (obese men, 10; and obese women, 10). Gene expressions of 11β‐HSD1 in adipose tissue samples were determined by real‐time reverse transcriptase polymerase chain reaction (RT‐PCR).

Results: Lean women had lower 11β‐HSD1 gene expression in subcutaneous adipose tissue compared with men (62% lower, p < 0.01), whereas no significant difference was found between obese men and women. 11β‐HSD1 mRNA in human adipose tissue was higher in obese subjects compared with lean subjects in both women and men and in both subcutaneous and visceral adipose tissue. No difference in mRNA expression of 11β‐HSD1 between visceral and subcutaneous adipose tissue or between subcutaneous adipose tissue from different depots was found.

Conclusions: 11β‐HSD1 in adipose tissue is increased in obesity in both women and men, and may contribute to the associated metabolic syndrome. As 11β‐HSD1 expression in lean women was found to be significantly lower than in lean males, the up‐regulation associated with obesity may be relatively more devastating in women than in men, and may help explain the higher relative risk of cardiovascular disease in women suffering from the metabolic syndrome.