We argue that despite inconsistencies in the definition , patterns across studies clearly show that healthy obesity is a state of intermediate disease risk .
Expert commentary : Given the current state of population -level evidence , we conclude that obesity and metabolic dysfunction are inseparable and that healthy obesity is best viewed only as a state of relative health but not of absolute health .
INTRODUCTION Obesity is a top public health priority but interventions to reverse the condition have had limited success .
About one-in-three obese adults are free of metabolic risk factor clustering and are considered ' healthy ' , and much attention has focused on the implication s of this state for obesity management .
'Mendelian randomization': can genetic epidemiology contribute to understanding environmental determinants of disease?
Associations between modifiable exposures and disease seen in observational epidemiology are sometimes confounded and thus misleading , despite our best efforts to improve the design and analysis of studies . Mendelian r and omization-the r and om assortment of genes from parents to offspring that occurs during gamete formation and conception-provides one method for assessing the causal nature of some environmental exposures . The association between a disease and a polymorphism that mimics the biological link between a proposed exposure and disease is not generally susceptible to the reverse causation or confounding that may distort interpretations of conventional observational studies . Several examples where the phenotypic effects of polymorphisms are well documented provide encouraging evidence of the explanatory power of Mendelian r and omization and are described . The limitations of the approach include confounding by polymorphisms in linkage disequilibrium with the polymorphism under study , that polymorphisms may have several phenotypic effects associated with disease , the lack of suitable polymorphisms for study ing modifiable exposures of interest , and canalization-the buffering of the effects of genetic variation during development . Nevertheless , Mendelian r and omization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to underst and ing and preventing the adverse effects on human health of modifiable exposures
We argue that despite inconsistencies in the definition , patterns across studies clearly show that healthy obesity is a state of intermediate disease risk .
Expert commentary : Given the current state of population -level evidence , we conclude that obesity and metabolic dysfunction are inseparable and that healthy obesity is best viewed only as a state of relative health but not of absolute health .
INTRODUCTION Obesity is a top public health priority but interventions to reverse the condition have had limited success .
About one-in-three obese adults are free of metabolic risk factor clustering and are considered ' healthy ' , and much attention has focused on the implication s of this state for obesity management .