How dieting makes some fatter: from a perspective of human body composition autoregulation

Abstract

Dieting makes you fat -the title of a book published in 1983 -embodies the notion that dieting to control body weight predisposes the individual to acquire even more body fat. While this notion is controversial, its debate underscores the large gap that exists in our understanding of basic physiological laws that govern the regulation of human body composition. A striking example is the key role attributed to adipokines as feedback signals between adipose tissue depletion and compensatory increases in food intake. Yet, the relative importance of fat depletion per se as a determinant of post-dieting hyperphagia is unknown. On the other hand, the question of whether the depletion of lean tissues can provide feedback signals on the hunger-appetite drive is rarely invoked, despite evidence that food intake during growth is dominated by the impetus for lean tissue deposition, amidst proposals for the existence of protein-static mechanisms for the regulation of growth and maintenance of lean body mass. In fact, a feedback loop between fat depletion and food intake cannot explain why human subjects recovering from starvation continue to overeat well after body fat has been restored to prestarvation values, thereby contributing to 'fat overshooting'. In addressing the plausibility and mechanistic basis by which dieting may predispose to increased fatness, this paper integrates the results derived from re-analysis of classic longitudinal studies of human starvation and refeeding. These suggest that feedback signals from both fat and lean tissues contribute to recovering body weight through effects on energy intake and thermogenesis, and that a faster rate of fat recovery relative to lean tissue recovery is a central outcome of body composition autoregulation that drives fat overshooting. A main implication of these findings is that the risk of becoming fatter in response to dieting is greater in lean than in obese individuals.

Eating Behaviors, Body Composition and Risk of Relapse among Persons withdrawing from Substance Abuse: A 3-months Follow-up Study

“…Recent research has pointed out that during cycles of weight loss/weight regain, overfeeding persists even after recovering of fat mass losses, and disappears only when fat free mass is back to normal [34]. Therefore, this population is at risk of the so-called "fat-overshooting" [34] i.e.…”

“…The interplay of eating behavior, drug abuse and body composition has potential clinical repercussions, as there is some evidence of interference with substance withdrawal outcome [13,14,33]. Also, food intake, and more specifically hyperphagia, is related with body composition: after weight loss, the increase in appetite persists after restoration of fat mass, until muscle mass is back to initial level [34]. Data on these factors are scarce and follow-up studies in "naturalistic and clinical cohorts", as pointed out by Calero et al [12], are lacking.…”

Physical Activity, Energy Intake, and Obesity: The Links Between Exercise and Appetite

“…Adipose tissue was described as a major factor in influencing energy balance through the proportional release of leptin as a marker of the body's energy stores [50]. In addition to the adipostatic control over food intake, there is growing evidence to suggest a proteinostatic mechanism in the control of food intake [51]. This theory has been strengthened by the new link between fat free mass, appetite and energy intake.…”

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

“…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.…”

“…In addition to the passive metabolic compensation resulting from diminished energy intake and changes in body weight and composition, there are clearly individuals capable of showing a large capacity for adaptive thermogenesis amounting to 300-400 kcal per day, [6][7][8][9][10] that is, an active metabolic compensation that in some individuals could be quantitatively as important as the passive metabolic compensation of 300-500 kcal that, as discussed above, 7 would occur after losing 20 kg. Such compensatory energy-conservation mechanisms, which impede weight loss and subsequently facilitate weight regain, 3 would most likely have conferred survival advantage in an ancestral lifestyle of famine and intermittent food scarcity that have characterized much of human evolution. Indeed, a role for genes in determining the capacity for such metabolic compensation and the large inter-individual variability in weight loss has been demonstrated by Hainer et al 12 in studies on identical obese twins treated with a very low energy diet.…”