“Growing evidence suggests that obesity is a disorder of the energy homeostasis system [and scientists] need to elucidate the mechanisms underlying this ‘upward setting’ or ‘resetting’ of the defended level of body-fat mass,” according to a new scientific statement published by the Endocrine Society published June 26 in Endocrine Reviews.
Moreover, given that “recovery of lost weight . . . is the largest single obstacle to effective long-term weight loss, we cannot overstate the importance of a coherent understanding of obesity-associated alterations of the energy homeostasis system,” Michael W Schwartz, MD, from the University of Washington, Seattle and colleagues stress in the statement.
It summarizes what is known about how the body always tries to “defend” the level of body fat stores and then readjusts this “stable weight” at a higher level when a person gains excess weight.
Dr Schwartz and colleagues say that they have published their report now because scientists have figured out the underlying disease mechanisms for many other endocrine disorders and have developed therapies to target these mechanisms, “in contrast, [for obesity] we have a very limited understanding of its pathogenesis, despite decades of research and billions of dollars spent each year on its treatment.”
More research is desperately needed to unravel the pathogenesis of obesity “to better inform [obesity] treatment, public policy, advocacy, and awareness . . . in ways that ultimately diminish its public health and economic consequences,” they urge.
Unclear How Excess Weight Is “Biologically Defended”
Currently, an estimated one in three US adults is considered obese (body mass index > 30 kg/m2), and so there is an enormous demand for weight-loss products and services, the authors write.
However, because of a lack of consensus about the biological mechanisms that cause obesity, “nonscientific ideologies and products . . . continue to flourish despite being largely ineffective, sometimes dangerous, and almost entirely unregulated.”
“Fundamentally, humans have an ‘evolutionary physiology’ that is predisposed to conserve body fat as a factor of survival,” they explain.
For example, individuals who are not obese have “remarkable” body-weight stability over long periods of time, as shown in a 10-year study of more than 15,000 healthy Swedish women.
Moreover, “it is clear that obesity is generally the consequence of small, cumulative imbalances of energy intake and expenditure . . . and once individuals who are obese and individuals who never were obese achieve their ‘customary’ body weights and composition, they tend to maintain and defend those weights by identical mechanisms.”
Dr Schwartz and colleagues list four “essential points” to take away from their statement:
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“Obesity pathogenesis involves . . . sustained positive energy balance (energy intake > energy expenditure) and . . . resetting of the body weight ‘set point’ at an increased value.” This ‘reset’ may partly explain why it is so hard to lose excess weight and maintain this weight loss.
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It is still not clear “how excess body-fat mass comes to be biologically defended.”
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“The impact of diet on obesity risk is explained largely by its effect on calorie intake.” That is, it is fewer calories that count, not necessarily the type of calories (eg, carbohydrates or fats).
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Last, “beyond diet, environmental factors ranging from socioeconomic status to chemical exposures to sedentary lifestyle can confer obesity risk.”
Weight Regain Is an Expected Physiological Response to Weight Loss
“Rather than viewing recovery of lost weight as a therapeutic failure or as evidence of noncompliance with a prescribed treatment regimen, patients and practitioners alike should view this phenomenon as an expected physiological response to weight loss,” the statement advises.
The statement calls for wide-ranging research to better understand “how genetic, developmental, and environmental forces affect the energy homeostasis system.”
Work is needed to examine how obesity is affected by genetics, endocrine-disrupting chemicals, gut microbiome, diet composition, and brain signals, and why bariatric surgery is successful, they conclude.
The work was supported by the National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Disease–funded Nutrition Obesity Research Center at the University of Washington, and Russell Berrie Foundation. Dr Schwartz receives research funding from and serves as a consultant to Novo Nordisk. Disclosures of the other authors are listed in the paper.
Endocr Rev . Published online June 26, 2017. Full text
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