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Excess adiposity is the main phenotypic feature that defines human obesity and that plays a pathophysiological role in most chronic diseases. Measuring the amount of fat mass present is thus a central aspect of studying obesity at the individual and population levels. Nevertheless, a consensus is lacking among investigators on a single accepted 'reference' approach for quantifying fat mass in vivo. While the research community generally relies on the multi-component body volume class of 'reference' models for quantifying fat mass, no definable guide discerns among different applied equations for partitioning the four (fat, water, protein and mineral mass) or more quantified components, standardizes 'adjustment' or measurement system approaches for model-required labelled water dilution volumes and bone mineral mass estimates, or firmly establishes the body temperature at which model physical properties are assumed. The resulting differing reference strategies for quantifying body composition in vivo leads to small, but under some circumstances, important differences in the amount of measured body fat. Recent technological advances highlight opportunities to expand model applications to new subject groups and measured components such as total body protein. The current report reviews the historical evolution of multi-component body volume-based methods in the context of prevailing uncertainties and future potential.

Energy intake (EI) and physical activity energy expenditure (PAEE) are key modifiable determinants of energy balance, traditionally assessed by self-report despite its repeated demonstration of considerable inaccuracies. We argue here that it is time to move from the common view that self-reports of EI and PAEE are imperfect, but nevertheless deserving of use, to a view commensurate with the evidence that self-reports of EI and PAEE are so poor that they are wholly unacceptable for scientific research on EI and PAEE. While new strategies for objectively determining energy balance are in their infancy, it is unacceptable to use decidedly inaccurate instruments, which may misguide health-care policies, future research and clinical judgment. The scientific and medical communities should discontinue reliance on self-reported EI and PAEE. Researchers and sponsors should develop objective measures of energy balance.

Objective The heritability of food neophobia, the tendency to avoid new foods, was tested in 4- to 7-year-old twins. We also examined whether food neophobia is associated with parent-child feeding relations or child body fat. Design and Methods We studied sixty-six same-sex twin pairs, including 37 monozygotic (MZ) and 29 dizygotic (DZ) pairs. Food neophobia was assessed by parent questionnaire (Child Food Neophobia Scale, CFNS), as were child feeding practices and “division of responsibility” feeding relations. Child anthropometry and percent body fat were directly measured. Results MZ and DZ twin pair correlations for food neophobia were r=0.71 and r= −0.01, respectively; heritability= 72%. Greater food neophobia was associated with reduced child eating compliance of prompted foods (p< 0.001) reduced eating compliance of initially refused foods (p< 0.001), and – among girls only – fewer parental food demands (p= 0.01). Interestingly, the correlation between maternal BMI and child BMI z-score was significant only for children high (p=0.03), but not low (p=0.55), in food neophobia. Conclusions Child food neophobia, a highly heritable trait previously linked to emotionality, was associated with less compliant parent-child feeding relations. Strategies to combat food neophobia and foster more harmonious feeding relationships may have a role in obesity prevention.

Obesity is associated with risk of pulmonary disease, and adversely affects lung function. The parallel increase in obesity and asthma suggests the two conditions are linked; indeed, they can worsen each other. Obesity and inadequate asthma control are associated with poor quality of life, and place a high economic burden on public health. Although the obesity-lung interaction is a major issue for basic research and clinical studies, various questions remain unanswered. Do intrauterine and early life factors impact on the development of obesity and lung disease? If so, can this be prevented? Asthma is generally more severe in obese subjects, but is adiposity a driver of a new asthma phenotype that features greater morbidity and mortality, worse control and decreased response to medications? Obese individuals have small lung volumes, hence their airway calibre is reduced and airway resistance is increased. What puzzles physicians is whether peripheral airways undergo remodelling, which would increase bronchoconstriction. Obese asthmatics respond suboptimally to anti-inflammatory treatment, which raises the question: 'what drug for what patient?' Life expectancy is decreased in obesity and in chronic pulmonary disorders, but does obesity protect against or trigger chronic obstructive pulmonary disease? The time has come to find answers to these questions.

Although Quetelet first reported in 1835 that adult weight scales to the square of stature, limited or no information is available on how anatomical body compartments, including adipose tissue (AT), scale to height.We examined the critical underlying assumptions of adiposity-body mass index (BMI) relations and extended these analyses to major anatomical compartments: skeletal muscle (SM), bone, residual mass, weight (AT+SM+bone), AT-free mass, and organs (liver, brain).This was a cross-sectional analysis of 2 body-composition databases: one including magnetic resonance imaging and dual-energy X-ray absorptiometry (DXA) estimates of evaluated components in adults (total n=411; organs=76) and the other a larger DXA database (n=1346) that included related estimates of fat, fat-free mass, and bone mineral mass.Weight, primary lean components (SM, residual mass, AT-free mass, and fat-free mass), and liver scaled to height with powers of approximately 2 (all P0.001); bone and bone mineral mass scaled to height with powers2 (2.31-2.48), and the fraction of weight as bone mineral mass was significantly (P0.001) correlated with height in women. AT scaled weakly to height with powers of approximately 2, and adiposity was independent of height. Brain mass scaled to height with a power of 0.83 (P=0.04) in men and nonsignificantly in women; the fraction of weight as brain was inversely related to height in women (P=0.002).These observations suggest that short and tall subjects with equivalent BMIs have similar but not identical body composition, provide new insights into earlier BMI-related observations and thus establish a foundation for height-normalized indexes, and create an analytic framework for future studies.

Waist circumferences (WCs) in white men and women that represent a risk of cardiovascular disease (CVD) equivalent to that of body mass indexes (BMIs; in kg/m2) of 25 and 30 have been identified. However, WC cutoffs for other race-ethnicity groups remain unknown.The objective was to determine WC cutoffs for CVD risk in non-Hispanic blacks (blacks), Mexican Americans (MA), and non-Hispanic whites (whites).Data from 10,969 participants in the third National Health and Nutrition Examination Survey (1988-1994) were analyzed. The presence of CVD risk factors was the main outcome. Sex- and race-ethnicity-specific WC cutoffs were determined with logistic regression models by linking WC cutoffs with equivalent CVD risk based on BMI cutoffs for overweight and obesity. WC cutoffs for metabolic syndrome risk factors were similarly calculated.Correlations between WC and lipid profiles, blood pressure, and glucose were significantly higher than those between BMI and these same variables in all groups. The WC cutoffs were approximately 5-6 cm greater for white than for black men at BMIs between 25 and 40, and those for MA were intermediate. In women, few differences in WC cutoffs were observed between the groups. Simplified WC cutoffs corresponding to BMIs of 25 and 30, largely independent of age, for the 3 race-ethnicity groups were 89 and 101 cm for men and 83 and 94 cm for women. Minimal distances in receiver operating characteristic curves tended to be shorter when WC cutoffs rather than BMI cutoffs were used.WC is a better indicator of CVD risk than is BMI in the 3 race-ethnicity groups studied. The proposed WC cutoffs are more sensitive than are BMI cutoffs in predicting CVD risk.