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Adipocyte mitochondrial respiration may influence metabolic fuel partitioning into oxidation versus storage, with implications for whole-body energy expenditure. Although insulin has been shown to influence mitochondrial respiration, the effects of dietary macronutrient composition have not been well characterized. The aim of this exploratory study was to test the hypothesis that a high-carbohydrate diet lowers the oxygen flux of adipocyte mitochondria ex vivo. Among participants in a randomized-controlled weight-loss maintenance feeding trial, those consuming a high-carbohydrate diet (60% carbohydrate as a proportion of total energy, n = 10) had lower rates of maximal adipose tissue mitochondrial respiration than those consuming a moderate-carbohydrate diet (40%, n = 8, p = 0.039) or a low-carbohydrate diet (20%, n = 9, p = 0.005) after 10 to 15 weeks. This preliminary finding may provide a mechanism for postulated calorie-independent effects of dietary composition on energy expenditure and fat deposition, potentially through the actions of insulin on fuel partitioning.

Fat-free mass (FFM) often serves as a body composition outcome variable in weight loss studies. An important assumption is that the proportions of components that make up FFM remain stable following weight loss; some body composition models rely on these "constants". This exploratory study examined key FFM component proportions before and following weight loss in two studies of participants with overweight and obesity.201 men and women consumed calorie-restricted moderate- or very-low carbohydrate diets leading to 10-18% weight loss in 9-15 weeks. Measured total body fat, lean mass, bone mineral, total body water (TBW), and body weight at baseline and follow-up were used to derive FFM and its chemical proportions using a four-component model.A consistent finding in both studies was a non-significant reduction in bone mineral and a corresponding increase (p 0.001) in bone mineral/FFM; FFM density increased significantly in one group of women and in all four participant groups combined (both, p 0.05). FFM hydration (TBW/FFM) increased in all groups of men and women, one significantly (p 0.01), and in the combined sample (borderline, p 0.10). The proportion of FFM as protein decreased across all groups, two significantly (p 0.05-0.01) and in the combined sample (p 0.05).FFM relative proportions of chemical components may not be identical before and after short-term weight loss, an observation impacting some widely used body composition models and methods. Caution is thus needed when applying FFM as a safety signal or to index metabolic evaluations in clinical trials when these body composition approaches are used.

The obesity pandemic continues unabated despite a persistent public health campaign to decrease energy intake ("eat less") and increase energy expenditure ("move more"). One explanation for this failure is that the current approach, based on the notion of energy balance, has not been adequately embraced by the public. Another possibility is that this approach rests on an erroneous paradigm. A new formulation of the energy balance model (EBM), like prior versions, considers overeating (energy intakeexpenditure) the primary cause of obesity, incorporating an emphasis on "complex endocrine, metabolic, and nervous system signals" that control food intake below conscious level. This model attributes rising obesity prevalence to inexpensive, convenient, energy-dense, "ultra-processed" foods high in fat and sugar. An alternative view, the carbohydrate-insulin model (CIM), proposes that hormonal responses to highly processed carbohydrates shift energy partitioning toward deposition in adipose tissue, leaving fewer calories available for the body's metabolic needs. Thus, increasing adiposity causes overeating to compensate for the sequestered calories. Here, we highlight robust contrasts in how the EBM and CIM view obesity pathophysiology and consider deficiencies in the EBM that impede paradigm testing and refinement. Rectifying these deficiencies should assume priority, as a constructive paradigm clash is needed to resolve long-standing scientific controversies and inform the design of new models to guide prevention and treatment. Nevertheless, public health action need not await resolution of this debate, as both models target processed carbohydrates as major drivers of obesity.

A large feeding study reported that total energy expenditure (TEE) was greater on a low- versus high-carbohydrate diet, supporting the carbohydrate-insulin model of obesity. Recently, the validity of this finding was challenged in a post-hoc analysis excluding participants with putative non-adherence to the study diets. Here, we show why that analysis, based on a post-randomization variable linked to the outcome, introduced severe confounding bias. With control for confounding, the diet effect on TEE remained strong in a reanalysis. Together with sensitivity analyses demonstrating robustness to plausible levels of non-adherence, these data provide experimental support for a potentially novel metabolic effect of macronutrients that might inform the design of more effective obesity treatment.

Adipocyte mitochondrial respiration may influence metabolic fuel partitioning into oxidation versus storage, with implications for whole-body energy expenditure. Although insulin has been shown to influence mitochondrial respiration, the effects of dietary macronutrient composition have not been well characterized. The aim of this exploratory study was to test the hypothesis that a high-carbohydrate diet lowers the oxygen flux of adipocyte mitochondria ex vivo. Among participants in a randomized-controlled weight-loss maintenance feeding trial, those consuming a high-carbohydrate diet (60% carbohydrate as a proportion of total energy, n = 10) had lower rates of maximal adipose tissue mitochondrial respiration than those consuming a moderate-carbohydrate diet (40%, n = 8, p = 0.039) or a low-carbohydrate diet (20%, n = 9, p = 0.005) after 10 to 15 weeks. This preliminary finding may provide a mechanism for postulated calorie-independent effects of dietary composition on energy expenditure and fat deposition, potentially through the actions of insulin on fuel partitioning.

Objective: Limited inter-person variability in nutrient intake hampers epidemiologic studies of diet–disease relationships. Despite conjecture about non-traditional study bases providing large inter-person differences, virtually nothing is known about variations in nutrient intake outside of Europe and North America. The current study was conducted in India to determine sources of variability in the intakes of nutrients thought to be of public health importance. Design: Adult subjects in Gujarat (North India; n=60) and in Kerala (South India, n=60) were administered 24 h diet recall interviews six and eight times, respectively, over a 1 y period. To assess subject (inter-person) and residual (intra-person) contributions to variance, regression models were fit to the data. From this, the variance ratio (VR, total within or intra-person: total between or inter-person) was computed. Setting: Rural communities in North and South India. Results: In both regions, inter-person variability was larger than that observed in the West. This was most pronounced in Gujarat, for which the VR was 20% of variance for fat, iron, copper, zinc, β-carotene and riboflavin in both men and women. With the region term removed from this model, virtually all of the variability ascribed to region contributed to inter-person variability. Conclusions: The relatively large inter-person variability observed here could contribute to improved ‘resolution’ of diet–outcome relationships in epidemiologic studies. While this applies to data from each region, it was especially evident in analyses of the combined data. Sponsorship: This work was supported by the Special Foreign Currency Program of the Fogarty International Center (National Institutes of Health) grant number N-406-645, a USIA Fulbright Senior Research Fellowship to Dr James R Hebert for the 1997–1998 academic year through the US Educational Foundation in India, and a UICC International Cancer Technology Transfer Fellowship (ICRETT) to Ms Hemali Mehta for collaborative work conducted with Drs Hebert and Ebbeling at the University of Massachusetts Medical School in 1998. European Journal of Clinical Nutrition (2000) 54, 479–486