Margriet S. Westerterp-Plantenga

The influence of single nucleotide polymorphisms (SNP) of the FTO gene has been shown to change over time. The aim was to investigate the relationship between a SNP of the FTO gene (rs9939609) and obesity-related characteristics longitudinally during childhood and puberty. From 101 children (58 boys and 43 girls), the FTO (rs9939609) genotype and yearly anthropometric data from birth to age 7 yr were determined. From ages 12 to 17 yr, we measured anthropometry, body composition, leptin concentrations, physical activity, hours watching television, and attitude toward eating yearly; parental characteristics were determined as well. At age 17 yr, 20% of the children were overweight/obese, and 88% of the overweight/obese children had the A allele in contrast to 45% of the lean children (P < 0.001). The A allele carriers had a higher fat mass index (kilograms per square meter) and higher leptin concentrations (micrograms per liter) during puberty, except at age 14 yr. Multiple regression analyses with body mass index (BMI; kilograms per square meter) as the dependent variable showed that at ages 12 and 17 yr, dietary restraint score, disinhibition score, BMI of the mother, and the FTO A allele significantly contributed to the model (R(2) = 0.29, P < 0.002; and R(2) = 0.39, P < 0.001). At age 14 yr, dietary restraint score, disinhibition score, and leptin concentrations per kilogram of fat mass significantly contributed to the model (R(2) = 0.25; P < 0.02). The FTO A allele (rs9939609) is associated with higher BMI, fat mass index, and leptin concentrations from the age of 12 yr, whereas the associations show a dip at ages 13-14 yr and become stronger at age 17 yr. The dip is presumably caused by the dominating endocrinological changes at midpuberty.

Human eating behavior may be influenced non-homeostatically by the rewarding value of foods, i.e. ‘liking’ (pleasure/palatability) and ‘wanting’ (incentive motivation). Stress appeared to diminish the rewarding value of food, i.e. ‘liking’ and ‘wanting’, leading to eating in the absence of hunger in the visceral overweight subjects. Postprandial energy intake was relatively higher during stress vs rest, resulting from more choice for crispiness and fullness of taste(p<.05). Then brain activation was reduced in reward-areas: Amygdala, hippocampus and cingulate cortex (AUC=-4.7,-2.5, -1.4 %BOLDØsec, p<.05). Putamen activation was decreased postprandially (AUC=-1.2 %BOLDØsec, p<.05). Conclusion: Reward signaling and reward sensitivity was significantly lower under stress, coinciding with increased energy intake from food choice for more crispiness and fullness of taste. The changes in putamen activation may reflect specifically decreased reward prediction sensitivity.

The role of dietary protein in weight loss and weight maintenance encompasses influences on crucial targets for body weight regulation, namely satiety, thermogenesis, energy efficiency, and body composition. Protein-induced satiety may be mainly due to oxidation of amino acids fed in excess, especially in diets with “incomplete” proteins. Protein-induced energy expenditure may be due to protein and urea synthesis and to gluconeogenesis; “complete” proteins having all essential amino acids show larger increases in energy expenditure than do lower-quality proteins. With respect to adverse effects, no protein-induced effects are observed on net bone balance or on calcium balance in young adults and elderly persons. Dietary protein even increases bone mineral mass and reduces incidence of osteoporotic fracture. During weight loss, nitrogen intake positively affects calcium balance and consequent preservation of bone mineral content. Sulphur-containing amino acids cause a blood pressure–raising effect by loss of nephron mass. Subjects with obesity, metabolic syndrome, and type 2 diabetes are particularly susceptible groups. This review provides an overview of how sustaining absolute protein intake affects metabolic targets for weight loss and weight maintenance during negative energy balance, i.e., sustaining satiety and energy expenditure and sparing fat-free mass, resulting in energy inefficiency. However, the long-term relationship between net protein synthesis and sparing fat-free mass remains to be elucidated.

Objective: To find factors associated with successful weight maintenance (WM) in overweight and obese subjects after a very low‐calorie diet (VLCD).Research Methods and Procedures: Subjects (133) followed a VLCD (2.1 MJ/d) for 6 weeks in a free‐living situation. Of these, 103 subjects (age, 49.6 ± 9.7 years; BMI, 30.9 ± 3.8 kg/m²) completed the following 2‐year WM period. Body weight (BW), body composition, leptin concentration, attitude toward eating, and physical activity were determined right before (t0) and after (t1) the VLCD, after 3 months (t2), after 1 year (t3), after 1.5 years (t4), and after 2 years (t5).Results: BW loss during VLCD was 7.2 ± 3.1 kg. After 2 years, follow‐up BW regain was 69.0 ± 98.4%. After 2 years of WM, 13 subjects were successful (10% BW regain). At baseline, these groups were significantly different in BMI (33.7 ± 4.7 vs. 30.5 ± 3.5 kg/m², respectively; p < 0.05) and fat mass (38.3 ± 9.8 vs. 32.1 ± 8.3 kg, p < 0.05). Successful subjects increased their dietary restraint significantly more during the whole study period (dietary restraint score, −4.9 ± 4.4 vs. −2.1 ± 3.8). Furthermore, %BW regain was associated with the amount of percentage body fat lost during VLCD, which indicates that the more fat lost, the better the WM, suggesting a fat free mass‐sparing effect.Discussion: Characteristics such as the ability to increase dietary restraint and maintain this high level of restraint, fat free mass sparing, and a relatively high baseline BMI and fat mass were associated with successful long‐term WM (<10% regain after 2 years).