Background: The daily energy imbalance gap associated with the current population weight gain in the obesity epidemic is relatively small. However, the substantially higher body weights of populations that have accumulated over several years are associated with a substantially higher total energy expenditure (TEE) and total energy intake (TEI), or energy flux (EnFlux = TEE = TEI).
Objective: The objective was to develop an equation relating EnFlux to body weight in adults for estimating the rise in EnFlux associated with the obesity epidemic.
Design: Multicenter, cross-sectional data for TEE from doubly labeled water studies in 1399 adults aged 5.9 ± 18.8 y (mean ± SD) were analyzed in linear regression models with natural log (ln) weight as the dependent variable and ln EnFlux as the independent variable, adjusted for height, age, and sex. These equations were compared with those for children and applied to population trends in weight gain.
Results: ln EnFlux was positively related to ln weight (β = 0.71; 95% CI: 0.66, 0.76; R2 = 0.52), adjusted for height, age, and sex. This slope was significantly steeper than that previously described for children (β = 0.45; 95% CI: 0.38, 0.51).
Conclusions: This relation suggests that substantial increases in TEI have driven the increases in body weight over the past 3 decades. Adults have a higher proportional weight gain than children for the same proportional increase in energy intake, mostly because of a higher fat content of the weight being gained. The obesity epidemic will not be reversed without large reductions in energy intake, increases in physical activity, or both.
Marie-Pierre St-Onge, Kathleen L Keller, Steven B Heymsfield
Dec 1, 2003; 78:1068-1073
Background: The major drivers of the obesity epidemic are much debated and have considerable policy importance for the population-wide prevention of obesity.
Objective: The objective was to determine the relative contributions of increased energy intake and reduced physical activity to the US obesity epidemic.
Design: We predicted the changes in weight from the changes in estimated energy intakes in US children and adults between the 1970s and 2000s. The increased US food energy supply (adjusted for wastage and assumed to be proportional to energy intake) was apportioned to children and adults and inserted into equations that relate energy intake to body weight derived from doubly labeled water studies. The weight increases predicted from the equations were compared with weight increases measured in representative US surveys over the same period.
Results: For children, the measured weight gain was 4.0 kg, and the predicted weight gain for the increased energy intake was identical at 4.0 kg. For adults, the measured weight gain was 8.6 kg, whereas the predicted weight gain was somewhat higher (10.8 kg).
Conclusions: Increased energy intake appears to be more than sufficient to explain weight gain in the US population. A reversal of the increase in energy intake of 2000 kJ/d (500 kcal/d) for adults and of 1500 kJ/d (350 kcal/d) for children would be needed for a reversal to the mean body weights of the 1970s. Alternatively, large compensatory increases in physical activity (eg, 110–150 min of walking/d), or a combination of both, would achieve the same outcome. Population approaches to reducing obesity should emphasize a reduction in the drivers of increased energy intake.
Background: The prominent clinical feature of cachexia has traditionally been understood to be weight loss; however, in recognition of the potential for divergent behavior of muscle and adipose tissue, cachexia was recently defined as loss of muscle with or without loss of fat mass. Detailed assessments are required to verify body composition in patients with cancer cachexia.
Design: We adopted a population-based approach to study body composition in patients with cancer, with the use of diagnostic computed tomography images acquired for cancer diagnosis and follow-up. A prospective cohort of 441 patients with non–small cell lung cancer, who were referred consecutively to a regional medical oncology service in Alberta, Canada, was evaluated.
Results: At referral (median time to death: 265 d), mean body mass index (BMI; in kg/m2) was 24.9, with 47.4% of patients being overweight or obese. Only 7.5% overall were underweight as conventionally understood (BMI < 18.5). Analysis of computed tomography images showed extremely high heterogeneity of muscle mass within all strata of BMI. The overall prevalence of severe muscle depletion (sarcopenia) was 46.8% and was present in patients in all BMI categories. A much higher proportion of men (61%) than women (31%) met the criteria for sarcopenia.
Conclusions: Wasting of skeletal muscle is a prominent feature of patients with lung cancer, despite normal or heavy body weights. The significance of muscle wasting in normal-weight, overweight, and obese patients as a nutritional risk factor, as a prognostic factor, and as a predictor of cancer treatment toxicity is discussed in this article.