The data is against proana. The data is against fat acceptance.

When I last talked about eating disorders one of the registrars asked if obesity counted. I replied it should, but it was not as yet classified in DSM. There are a bunch of people who hate the idea that obesity is a metabolic disorder, and would descent with elephantine tread and placards if us psychiatrists put it in our classification system. But we may be wrong.

This week’s reading includes an intriguing Genome wide association study (GWAS) on anorexia nervosa (plus the restricting subtype of eating disorders NOS — DSM IV and 5 have limited utility here). They foun a series of genes that are associated with genetic risk factors. And these associated with not merely neuroticism, obsessionality and high academic achievement but with obesity.

To our knowledge, this is the first report of a genome-wide significant association for anorexia nervosa. As is typical of many GWAS loci for complex disorders, the region has a common top variant (MAFcontrols=0.44) that shows a modest odds ratio of 1.2 and implicates a broad region encompassing multiple genes . Consistent with other GWAS , our genome-wide h2SNP estimate of 20% for anorexia nervosa supports a substantial role for common genetic variation, which accounts for a sizable portion of twin-based heritability (h2Twin=48%–74%). Furthermore, these results fit with the expectation that h2Twin should exceed h2SNP, because the former captures the effects of all types of genetic variation (common and rare, as well as variation not captured with current methods).

The observed pattern of genetic correlations with psychiatric, personality, educational, and metabolic phenotypes provides grounds for broadening our conceptualization of the disorder. First, the strong positive genetic correlations of anorexia nervosa with OCD and neuroticism reinforce clinical and epidemiological observations. Anorexia nervosa is commonly comorbid with OCD, and twin studies have reported high twin-based genetic correlations. High neuroticism in adolescence predicts subsequent onset of anorexia nervosa (1). In addition, anorexia nervosa is commonly comorbid with multiple anxiety phenotypes, which often predate the onset of anorexia nervosa.

Second, the positive genetic correlations seen with schizophrenia and the cross–psychiatric disorder phenotype firmly anchor anorexia nervosa with other psychiatric disorders and reflect the substantial evidence for partially shared genetic risk across many psychiatric disorders. Third, congruent with our results, positive associations between anorexia nervosa and educational attainment have been reported (30) and have been conjectured to reflect greater internal and external demands for academic success in highly educated families. Our results, in contrast, suggest that genetic factors may partially account for these reported associations.

Fourth, the identification of significant negative correlations between anorexia nervosa and BMI-related and anthropometric measures could potentially serve as an important first step toward gaining a better understanding of the shared biology underlying extremes of weight dysregulation (i.e., obesity versus anorexia nervosa). This is of critical importance because adequate explanations for how individuals with anorexia nervosa reach, sustain, and revert to exceedingly low BMIs have been elusive. Clinically, one of the most perplexing features of anorexia nervosa is how patients’ bodies seem to revert rapidly to a “low set point” after renourishment, which may represent the biological inverse of the reversion to high set points commonly seen in the unsuccessful treatment of obesity

From a clinical point of view, refeeding the extremely thin is a challenge, and repeating it becomes tiring. Anorexia has a high mortality, which is higher with anorexia than morbid (class III) obesity. .

After re-extracting all data and using statistical modeling techniques that allowed for inclusion of studies with zero deaths without the need for continuity corrections that artificially inflate estimates, we estimated that participants with AN are 5.2 times more likely to die prematurely from any cause, and 18.1 times more likely to die by suicide, when compared with 15–34 year old females in the population studied.

In minimally adjusted models, we observed a sharp gradient in relative risk with higher values of BMI across the class III obesity levels that was consistent with a linear increase. The HRs from models of BMI categories were slightly, but not fully, attenuated with additional adjustment for race/ethnicity, education, alcohol intake, and physical activity level. Compared with adults with BMI in the 18.5–24.9 kg/m2 range, multivariable-adjusted HRs (95% CIs) for those with BMI of 40.0–44.9, 45.0–49.9, 50.0–54.9, and 55.0–59.9 kg/m2 were 2.25 (2.07–2.43), 3.32 (2.92–3.77), 3.48 (2.82–4.31), and 5.91 (4.24–8.24), respectively. This trend of increasing risk of death with increasing level of BMI was apparent in categorical and continuous models (HR per 5 kg/m2?=?1.40, 95% CI: 1.31–1.51) after restricting to the BMI 40.0–59.9 kg/m2 range.

We should avoid being overly fat: it is a significant risk. But we should avoid the temptation to starve ourselves to perfection more. It does more damage. And neither are normal. Those who say we should accept all body shapes are damaging many women and men.

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