We examined how BMI, BMI trajectories, and BMI fluctuation around these trajectories in adolescence were correlated with BMI trajectories and BMI fluctuation in early adulthood, as well as the genetic basis of these associations. BMI data from Finnish twins (N = 1379, 48% males) were collected at ages 11.5, 14, 17.5, 24, and 37 years. BMI trajectories in adolescence (11.5–17.5 years) and early adulthood (17.5–37 years) were estimated using linear mixed-effect models. BMI fluctuation was calculated as the average squared differences between observed and expected BMI around these trajectories. Genetic twin models and a polygenic risk score for BMI (PRSBMI) were used to assess genetic contributions to BMI fluctuation and its associations with BMI and BMI trajectories. Adolescent BMI fluctuation was positively correlated with early adulthood BMI trajectories in females, while in males, adolescent BMI trajectories were positively associated with BMI fluctuation in early adulthood. Genetic factors affected BMI fluctuation in both adolescence and early adulthood when estimated using twin modelling and PRSBMI. Adolescent BMI was positively associated with early adulthood fluctuation in both sexes, with genetic factors playing a role (genetic correlations .08–.29). It was concluded that genetic factors play a significant role in BMI fluctuations in adolescence and early adulthood, with some overlap with the genetics of BMI.

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 pre-starvation 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.