Explaining the failures of obesity therapy: willpower attenuation, target miscalculation or metabolic compensation?

International Journal of Obesity volume  36, pages 1418–1420 (2012 )Cite this article

The ancient prescription of Hippocrates (400 BC) that the obese should ‘eat less and exercise more’ is still today, and for the foreseeable future, the cornerstone approach to treat obesity despite its well-documented failures. In most obese individuals, the amount of weight loss is far less than that expected from the imposed energy deficit, and in the overwhelming majority, the lost weight is regained within a few years.1 Most become weight cyclers, as they attempt again and again at losing weight, encouraged by their families and friends, health professionals, media that promote a slim image and a prosperous diet-industry that constantly innovate in generating hopes for better slimming successes. In the meantime, the reality begs the question: why is the short-term and long-term success rates of dieting/exercise so low?

The most common explanation centers on the failure of the obese to follow the dietary advice and prescribed exercise regimen; the dieters sooner or later revert back to the same lifestyle of ‘gluttony and sloth’ that made them obese in the first place. Psychologists, however, prefer an explanatory mechanism that is inferred by work on dietary restraint, and which centers upon terms like ‘disinhibition’ or ‘loss of inhibition’ to describe self-regulatory failure. Such periodic disinhibition by restrained eaters has been argued as a laboratory analog of binge eating, that is, periods of dietary restriction alternating with episodes of uncontrolled overeating. This notion is strongly supported by prospective studies indicating that moderate dieters are 2–5 times more likely than their non-dieting peers to develop an eating disorder, and that dieting, restrained eating or exercise for weight control actually predict weight gain.2 Whether these findings can be interpreted as dieting, or exercise will predispose to future weight gain—or to put it bluntly: ‘Dieting makes you fat’—is debatable.2, 3 It is clear, however, that the willpower to sustain dieting/exercise therapy that prevailed during the initial process of weight loss withers away in an obesogenic environment that encourages overeating and discourages physical activity. In more clinical terms, there is poor compliance to diet/exercise regimens. What physiologists will also emphasize is that willpower may also be counteracted by powerful internal signals (for example, changes in leptin, gut hormones and circulating nutrients) that sense the energy deficit or deviations in body weight and trigger compensatory mechanisms. These operate not only via the ‘energy balance’ control circuits in the hypothalamus and brain stem, but in addition impinge upon areas in the cortex and limbic system involved in cognitive, reward, emotion and executive brain functions important for ingestive and exercise behavior.4 The recent advances in functional imaging technologies for the mapping of brain circuitries have no doubt opened new avenues for research toward understanding the mechanisms that underlie poor compliance to diet and/or exercise. However, as underscored by Byrne et al.5 in a study published in this issue of IJO, factors other than lack of willpower and poor compliance can also be invoked to explain the poor outcome of diet/exercise antiobesity therapies. In this study, conducted in 19 obese men and women subjected to severe energy deficit for 3 months on a ketogenic diet and exercise intervention, and during which the tightly monitored adherence to both diet and exercise indicated high compliance, they could still observe a-third less weight loss than predicted from baseline energy deficit calculations. This discrepancy between actual and predicted weight loss, 10 kg on average but in the range of 1–22 kg, was shown to correlate strongly with reductions in the post-absorptive resting metabolic rate (RMR) and in the thermic effect of food or diet-induced thermogenesis (DIT). After adjusting for the monthly fall in RMR and DIT, with the energy conserved having been converted to the spared weight equivalent, the discrepancy between actual and predicted weight loss was markedly reduced from 10 to 3 kg on average. Consequently, the less-than-expected weight loss during dieting/exercise can also be attributed to quantitatively important reductions in energy needs of the obese individuals as they lose weight; that is, to metabolic compensations that impede weight loss.

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