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BackgroundAlthough there is substantial evidence of differential hypothalamic-pituitary-adrenal (HPA) axis activity in both generalized and abdominal obesity, consistent trends in obesity-related HPA axis perturbations have yet to be identified.ObjectivesTo systematically review the existing literature on HPA activity in obesity, identify possible explanations for inconsistencies in the literature, and suggest methodological improvements for future study.Data sourcesIncluded papers used Pubmed, Google Scholar, and the University of California Library search engines with search terms body mass index (BMI), waist-to-hip ratio (WHR), waist circumference, sagittal diameter, abdominal versus peripheral body fat distribution, body fat percentage, DEXA, abdominal obesity, and cortisol with terms awakening response, slope, total daily output, reactivity, feedback sensitivity, long-term output, and 11β-HSD expression.Study eligibility criteriaEmpirical research papers were eligible provided that they included at least one type of obesity (general or abdominal), measured at least one relevant cortisol parameter, and a priori tested for a relationship between obesity and cortisol.ResultsA general pattern of findings emerged where greater abdominal fat is associated with greater responsivity of the HPA axis, reflected in morning awakening and acute stress reactivity, but some studies did show underresponsiveness. When examined in adipocytes, there is a clear upregulation of cortisol output (due to greater expression of 11β-HSD1), but in hepatic tissue this cortisol is downregulated. Overall obesity (BMI) appears to also be related to a hyperresponsive HPA axis in many but not all studies, such as when acute reactivity is examined.LimitationsThe reviewed literature contains numerous inconsistencies and contradictions in research methodologies, sample characteristics, and results, which partially precluded the development of clear and reliable patterns of dysregulation in each investigated cortisol parameter.Conclusions and implicationsThe literature to date is inconclusive, which may well arise from differential effects of generalized obesity vs. abdominal obesity or from modulators such as sex, sex hormones, and chronic stress. While the relationship between obesity and adipocyte cortisol seems to be clear, further research is warranted to understand how adipocyte cortisol metabolism influences circulating cortisol levels and to establish consistent patterns of perturbations in adrenal cortisol activity in both generalized and abdominal obesity.

BackgroundAlthough there is substantial evidence of differential hypothalamic-pituitary-adrenal (HPA) axis activity in both generalized and abdominal obesity, consistent trends in obesity-related HPA axis perturbations have yet to be identified.ObjectivesTo systematically review the existing literature on HPA activity in obesity, identify possible explanations for inconsistencies in the literature, and suggest methodological improvements for future study.Data sourcesIncluded papers used Pubmed, Google Scholar, and the University of California Library search engines with search terms body mass index (BMI), waist-to-hip ratio (WHR), waist circumference, sagittal diameter, abdominal versus peripheral body fat distribution, body fat percentage, DEXA, abdominal obesity, and cortisol with terms awakening response, slope, total daily output, reactivity, feedback sensitivity, long-term output, and 11β-HSD expression.Study eligibility criteriaEmpirical research papers were eligible provided that they included at least one type of obesity (general or abdominal), measured at least one relevant cortisol parameter, and a priori tested for a relationship between obesity and cortisol.ResultsA general pattern of findings emerged where greater abdominal fat is associated with greater responsivity of the HPA axis, reflected in morning awakening and acute stress reactivity, but some studies did show underresponsiveness. When examined in adipocytes, there is a clear upregulation of cortisol output (due to greater expression of 11β-HSD1), but in hepatic tissue this cortisol is downregulated. Overall obesity (BMI) appears to also be related to a hyperresponsive HPA axis in many but not all studies, such as when acute reactivity is examined.LimitationsThe reviewed literature contains numerous inconsistencies and contradictions in research methodologies, sample characteristics, and results, which partially precluded the development of clear and reliable patterns of dysregulation in each investigated cortisol parameter.Conclusions and implicationsThe literature to date is inconclusive, which may well arise from differential effects of generalized obesity vs. abdominal obesity or from modulators such as sex, sex hormones, and chronic stress. While the relationship between obesity and adipocyte cortisol seems to be clear, further research is warranted to understand how adipocyte cortisol metabolism influences circulating cortisol levels and to establish consistent patterns of perturbations in adrenal cortisol activity in both generalized and abdominal obesity.

The discovery of genetic mechanisms for resistance to obesity and diabetes may illuminate new therapeutic strategies for the treatment of this global health challenge. We used the polygenic 'lean' mouse model, which has been selected for low adiposity over 60 generations, to identify mitochondrial thiosulfate sulfurtransferase (Tst; also known as rhodanese) as a candidate obesity-resistance gene with selectively increased expression in adipocytes. Elevated adipose Tst expression correlated with indices of metabolic health across diverse mouse strains. Transgenic overexpression of Tst in adipocytes protected mice from diet-induced obesity and insulin-resistant diabetes. Tst-deficient mice showed markedly exacerbated diabetes, whereas pharmacological activation of TST ameliorated diabetes in mice. Mechanistically, TST selectively augmented mitochondrial function combined with degradation of reactive oxygen species and sulfide. In humans, TST mRNA expression in adipose tissue correlated positively with insulin sensitivity in adipose tissue and negatively with fat mass. Thus, the genetic identification of Tst as a beneficial regulator of adipocyte mitochondrial function may have therapeutic significance for individuals with type 2 diabetes., Obesity prevalence seems to have plateaued at ~40% (refs. 1,2), suggesting that environmental penetrance (such as a hypercaloric diet or a sedentary lifestyle) is limited to a subpopulation of individuals [...]

An estimate of someone's IQ is a potentially informative personal datum. This study examines the association between external skull measurements and IQ scores, and uses the resulting regression equation to provide an estimate of the IQ of King Robert I of Scotland (Robert Bruce, 1274-1329). Participants were 48 relatively healthy Caucasian men (age 71-76 years) resident in Scotland. Using magnetic resonance imaging data, intracranial volume estimated from external skull length and width correlated greater than 0.5 (p less than 0.001) with measured intracranial area, which correlates very highly with brain volume. IQ scores estimated from the National Adult Reading Test (NART) correlated 0.56 (p less than 0.001) with measured intracranial area, and 0.49 (p less than 0.01) with estimated intracranial volume based on external skull width and length. The partial correlation coefficient of this latter association was 0.25 (p = 0.09) after adjustment for measured intracranial area. Thus, actual intracranial area accounts for about 74% of the variance shared by NART and estimated intracranial volume. A cast of the skull of Robert Bruce was measured and its intracranial volume estimated. A regression equation between IQ and estimated intracranial volume, based on data from the 48 subjects, estimated the IQ of Robert Bruce at about 128 (95% confidence interval 106 to much greater than 130), i.e. almost two standard deviations above the mean. NART scores show a ceiling effect, so this estimated IQ might be an underestimate. Robert Bruce's estimated high IQ is congruent with his military, political and other intellectual achievements.

External skull measurements and IQ scores from 48 Caucasian men from Scotland were used to estimate the IQ of King Robert I of Scotland. The high IQ score was attributed to his military, political and intellectual achievements.