The saimie paper suggests how susceptible individuals could reduce their total intake of aluminium. In presenting the cpidemiological evidence for a link betveen aluminium and Alzheimcr's, Nart'n suggests that although definite proof is still lacking, there is more than enough positixe evidence to fuel further epidemiological investigation. It states that such investigations might specificallx address the issue of the confounding cffect of silicon and an assessment of exposure to spccific

https://jech.bmj.com/content/jech/47/6/511.4.full.pdf

Methodology for Genetic Studies of Twins and Families

The authors review research on risk factors for eating disorders, restricting their focus to studies in which clear precedence of the hypothesized risk factor over onset of the disorder is established. They illustrate how studies of sociocultural risk factors and biological factors have progressed on parallel tracks and propose that major advances in understanding the etiology of eating disorders require a new generation of studies that integrate these domains. They discuss how more sophisticated and novel conceptualizations of risk and causal processes may inform both nosology and intervention efforts.

Risk factors for eating disorders.

Context Anorexia nervosa (AN) is a serious mental illness with marked morbidity and mortality. Objective To explore the prevalence, heritability, and prospectively assessed risk factors for AN in a large population-based cohort of Swedish twins. Design During a 4-year period ending in 2002, all living, contactable, interviewable, and consenting twins in the Swedish Twin Registry (N = 31 406) born between January 1, 1935, and December 31, 1958, underwent screening for a range of disorders, including AN. Information collected systematically in 1972 to 1973, before the onset of AN, was used to examine prospective risk factors for AN. Setting Population-based sample of twins in Sweden. Participants Cases of AN were identified as those individuals who met full DSM-IV criteria by means of clinical interview of the Swedish Twin Registry, who had a hospital discharge diagnosis of AN, or who had a cause-of-death certificate including an AN diagnosis. Results The overall prevalence of AN was 1.20% and 0.29% for female and male participants, respectively. The prevalence of AN in both sexes was greater among those born after 1945. Individuals with lifetime AN reported lower body mass index, greater physical activity, and better health satisfaction than those without lifetime AN. Anorexia nervosa was inversely associated with the development of overweight (odds ratio, 0.29; 95% confidence interval [CI], 0.16-0.54 [ P DSM-IV AN (additive genetic effects) was estimated to be a 2  = 0.56 (95% CI, 0.00-0.87), with the remaining variance attributable to shared environment (c 2  = 0.05; 95% CI, 0.00-0.64) and unique environment (e 2  = 0.38; 95% CI, 0.13-0.84). Neuroticism measured about 3 decades before the diagnostic assessment was significantly associated with the development of later AN (odds ratio, 1.62; 95% CI, 1.27-2.05 [ P Conclusions The prevalence of AN was higher in both male and female participants born after 1945. Individuals who survive AN and who no longer have body mass indexes in the AN range appear to be at lower risk for the development of overweight. Prospectively assessed neuroticism was associated with the subsequent development of AN, the liability to which is under considerable genetic influence.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/209373/YOA50049.pdf

Prevalence, Heritability, and Prospective Risk Factors for Anorexia Nervosa

The authors explore the extent to which eating disorders, specifically anorexia nervosa (AN) and bulimia nervosa (BN), represent culture-bound syndromes and discuss implications for conceptualizing the role genes play in their etiology. The examination is divided into 3 sections: a quantitative meta-analysis of changes in incidence rates since the formal recognition of AN and BN, a qualitative summary of historical evidence of eating disorders before their formal recognition, and an evaluation of the presence of these disorders in non-Western cultures. Findings suggest that BN is a culture-bound syndrome and AN is not. Thus, heritability estimates for BN may show greater variability cross-culturally than heritability estimates for AN, and the genetic bases of these disorders may be associated with differential pathoplasticity.

https://my.ilstu.edu/%7Edfgrayb/Personal/EatingDisordersCultural.pdf

Are Eating Disorders Culture-Bound Syndromes? Implications for Conceptualizing Their Etiology

Large-scale genomic investigations have just begun to illuminate the molecular genetic contributions to major psychiatric illnesses, ranging from small-effect-size common variants to larger-effect-size rare mutations. The findings provide causal anchors from which to understand their neurobiological basis. Although these studies represent enormous success, they highlight major challenges reflected in the heterogeneity and polygenicity of all of these conditions and the difficulty of connecting multiple levels of molecular, cellular, and circuit functions to complex human behavior. Nevertheless, these advances place us on the threshold of a new frontier in the pathophysiological understanding, diagnosis, and treatment of psychiatric disease.

/pdf/genetics-and-genomics-of-psychiatric-disease-27xoap3bj7.pdf

Genetics and genomics of psychiatric disease.

Background. Twin studies have concluded that there is a substantial genetic contribution to the aetiology of eating disorders. The aim of the present study was to estimate the genetic contribution to the aetiology of self-reported eating disorders in a sample of representative twins.Method. A population cohort of 34142 young Danish twins was screened for eating disorders by a mailed questionnaire.Results. Concordance rates differed significantly across monozygotic and dizygotic twin pairs for broadly defined self-reported anorexia nervosa and bulimia nervosa. Heritability estimates of 0·48, 0·52 and 0·61 respectively were estimated for narrow and broad definitions of self-reported anorexia nervosa and for self-reported bulimia nervosa.Conclusions. There is a genetic contribution to the aetiology of self-reported eating disorders in the general population. The relationship between self-reported and clinical eating disorder remains to be examined.

A preliminary population-based twin study of self-reported eating disorder

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A preliminary population-based twin study of self-reported eating disorder