Highlightsd 20 inpatient adults received ultra-processed and unprocessed diets for 14 days each d Diets were matched for presented calories, sugar, fat, fiber, and macronutrients d Ad libitum intake was 500 kcal/day more on the ultraprocessed versus unprocessed diet d Body weight changes were highly correlated with diet differences in energy intake

Objective To measure long-term changes in resting metabolic rate (RMR) and body composition in participants of The Biggest Loser competition. Methods Body composition was measured by dual energy X-ray absorptiometry and RMR was determined by indirect calorimetry at baseline, at the end of the 30 week competition, and 6 years later. Metabolic adaptation was defined as the residual RMR after adjusting for changes in body composition and age. Results Of the 16 Biggest Loser competitors originally investigated, 14 participated in this follow-up study. Weight loss at the end of the competition was (mean±SD) 58.3±24.9 kg (p<0.0001) and RMR decreased by 610±483 kcal/d (p=0.0004). After 6 years, 41.0±31.3 kg of the lost weight was regained (p=0.0002) while RMR was 704±427 kcal/d below baseline (p<0.0001) and metabolic adaptation was −499±207 kcal/d (p<0.0001). Weight regain was not significantly correlated with metabolic adaptation at the competition’s end (r=−0.1, p=0.75) but those subjects maintaining greater weight loss at 6 years also experienced greater concurrent metabolic slowing (r=0.59, p=0.025). Conclusions Metabolic adaptation persists over time and is likely a proportional, but incomplete, response to contemporaneous efforts to reduce body weight.

Food waste contributes to excess consumption of freshwater and fossil fuels which, along with methane and CO2 emissions from decomposing food, impacts global climate change. Here, we calculate the energy content of nationwide food waste from the difference between the US food supply and the food consumed by the population. The latter was estimated using a validated mathematical model of metabolism relating body weight to the amount of food eaten. We found that US per capita food waste has progressively increased by ∼50% since 1974 reaching more than 1400 kcal per person per day or 150 trillion kcal per year. Food waste now accounts for more than one quarter of the total freshwater consumption and ∼300 million barrels of oil per year.

The isocaloric KD was not accompanied by increased body fat loss but was associated with relatively small increases in EE that were near the limits of detection with the use of state-of-the-art technology. This trial was registered at clinicaltrials.gov as NCT01967563.

Weight changes are accompanied by imbalances between calorie intake and expenditure. This fact is often misinterpreted to suggest that obesity is caused by gluttony and sloth and can be treated by simply advising people to eat less and move more. However, various components of energy balance are dynamically interrelated and weight loss is resisted by counterbalancing physiological processes. While low-carbohydrate diets have been suggested to partially subvert these processes by increasing energy expenditure and promoting fat loss, our meta-analysis of 32 controlled feeding studies with isocaloric substitution of carbohydrate for fat found that both energy expenditure (26 kcal/d; P <.0001) and fat loss (16 g/d; P <.0001) were greater with lower fat diets. We review the components of energy balance and the mechanisms acting to resist weight loss in the context of static, settling point, and set-point models of body weight regulation, with the set-point model being most commensurate with current data.

We used a bivariate (multivariate) linear mixed-effects model to estimate the narrow-sense heritability (h2) and heritability explained by the common SNPs (hg2) for several metabolic syndrome (MetS) traits and the genetic correlation between pairs of traits for the Atherosclerosis Risk in Communities (ARIC) genome-wide association study (GWAS) population. MetS traits included body-mass index (BMI), waist-to-hip ratio (WHR), systolic blood pressure (SBP), fasting glucose (GLU), fasting insulin (INS), fasting trigylcerides (TG), and fasting high-density lipoprotein (HDL). We found the percentage of h2 accounted for by common SNPs to be 58% of h2 for height, 41% for BMI, 46% for WHR, 30% for GLU, 39% for INS, 34% for TG, 25% for HDL, and 80% for SBP. We confirmed prior reports for height and BMI using the ARIC population and independently in the Framingham Heart Study (FHS) population. We demonstrated that the multivariate model supported large genetic correlations between BMI and WHR and between TG and HDL. We also showed that the genetic correlations between the MetS traits are directly proportional to the phenotypic correlations.

The obesity epidemic is believed to be driven by a food environment that promotes consumption of inexpensive, convenient, high-calorie, palatable foods. Individual differences in obesity susceptibility or resistance to weight loss may arise due to alterations in the neurocircuitry supporting food reward and eating habits. In particular, dopamine signaling in the ventromedial striatum is thought to encode food reward and motivation, whereas dopamine in the dorsal and lateral striatum orchestrates the development of eating habits. We measured striatal dopamine D2-like receptor binding potential (D2BP) using positron emission tomography (PET) with [18F]fallypride in 43 human subjects with body mass indices (BMI) ranging from 18–45 kg/m2. Opportunistic eating behavior and BMI were both positively associated with D2BP in the dorsal and lateral striatum, whereas BMI was negatively associated with D2BP in the ventromedial striatum. These results suggest that obese people have alterations in dopamine neurocircuitry that may increase their susceptibility to opportunistic overeating while at the same time making food intake less rewarding, less goal-directed, and more habitual. Whether or not the observed neurocircuitry alterations pre-existed or occurred as a result of obesity development, they may perpetuate obesity given the omnipresence of palatable foods and their associated cues.

Summary Dietary carbohydrate restriction has been purported to cause endocrine adaptations that promote body fat loss more than dietary fat restriction. We selectively restricted dietary carbohydrate versus fat for 6 days following a 5 day baseline diet in 19 adults with obesity confined to a metabolic ward where they exercised daily. Subjects received both isocaloric diets in random order during each of two inpatient stays. Body fat loss was calculated as the difference between daily fat intake and net fat oxidation measured while residing in a metabolic chamber. Whereas carbohydrate restriction led to sustained increases in fat oxidation and loss of 53±6 g/d of body fat, fat oxidation was unchanged by fat restriction leading to 89±6 g/d of fat loss and was significantly greater than carbohydrate restriction (p=0.002). Mathematical model simulations agreed with these data, but predicted that the body acts to minimize body fat differences with isocaloric diets varying in carbohydrate and fat.