Population-based actuarial studies place the upper limit of normal BMI in adults at 25 kg/m 2, define obesity as a BMI > 30 kg/m 2, and designate a BMI between these values to be “overweight.” The degree of obesity can be further subcategorized into class 1 (BMI of 30 to 40) ( 1). Consequently, an elevated body mass index (BMI), which expresses body weight (in kilograms) as a function of body height (in meters 2) as a surrogate measure of body fatness, is the most widely accepted definition of obesity. Reliable fat-mass quantitation requires sophisticated tools that are not widely available ( e.g., magnetic resonance imaging or dual energy X-ray absorptiometry), and this has hampered efforts to arrive at a more specific definition. Obesity is broadly defined as an excess of body-fat mass. In this statement, we focus on factors for which compelling evidence exists that implicates them in the pathogenesis of either the accumulation or maintenance of excess body fat mass.
When processing this information, one must also be mindful that although there are many interventions that can cause obesity in an experimental setting, the key question is whether they do cause obesity in a naturalistic environment. Mechanistic formulations must draw from disciplines that include: the neuroscience of feeding behavior the psychology of food reward the metabolic impact of specific nutrients and changes of physical activity as well as genetics, epigenetics, and developmental biology relevant to energy balance control, and the influence of exposure to environmental variables ranging from endocrine-disrupting chemicals (EDCs) to socioeconomic factors. The need to integrate molecular, genetic, developmental, behavioral, and environmental factors highlights the substantial challenge inherent in achieving a comprehensive understanding of obesity pathogenesis. How these inputs interact with genetic, epigenetic and developmental factors that predispose to obesity is a key question for future research. Stated differently, "a calorie is a calorie.” Thus, habitual consumption of highly palatable and energy-dense diets predispose to excess weight gain irrespective of macronutrient content.īeyond diet, environmental factors ranging from socioeconomic status to chemical exposures to sedentary lifestyle can confer obesity risk. The impact of diet on obesity risk is explained largely by its effect on calorie intake, rather than by changes of either energy expenditure or the internal metabolic environment. Therapeutic strategies that target these mechanisms have the potential to reset the defended level of body weight at a lower, more normal value. How the increased body weight comes to be biologically defended remains uncertain, although ongoing research is beginning to shed some light on underlying mechanisms. The latter process explains why weight lost through changes of diet and/or lifestyle tends to be regained over time, a major obstacle to effective obesity treatment. Obesity pathogenesis involves two related but distinct processes: (1) sustained positive energy balance (energy intake > energy expenditure) and (2) resetting of the body weight “set point” at an increased value.
The scientific goal is to elucidate obesity pathogenesis so as to better inform treatment, public policy, advocacy, and awareness of obesity in ways that ultimately diminish its public health and economic consequences. The ongoing study of how genetic, developmental, and environmental forces affect the energy homeostasis system will help us better understand these mechanisms and are therefore a major focus of this statement. We need to elucidate the mechanisms underlying this “upward setting” or “resetting” of the defended level of body-fat mass, whether inherited or acquired. Growing evidence suggests that obesity is a disorder of the energy homeostasis system, rather than simply arising from the passive accumulation of excess weight. A major area of emphasis is the science of energy homeostasis, the biological process that maintains weight stability by actively matching energy intake to energy expenditure over time.
We included evidence from basic science, clinical, and epidemiological literature to assess current knowledge regarding mechanisms underlying excess body-fat accumulation, the biological defense of excess fat mass, and the tendency for lost weight to be regained.
A lack of effective options for long-term weight reduction magnifies the enormity of this problem individuals who successfully complete behavioral and dietary weight-loss programs eventually regain most of the lost weight. Estimates suggest that in the United States obesity affects one-third of adults, accounts for up to one-third of total mortality, is concentrated among lower income groups, and increasingly affects children as well as adults. Obesity is among the most common and costly chronic disorders worldwide.
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