No abstract is provided for this article.
The model developed by Forbes (1987) of how body fat mass (FM) and fat-free mass (FFM) change during periods of weight loss or gain (Δ body weight (BW)) assumed that they change in relationship to a constant C = 10·4, where ΔFFM/ΔBW = 10·4/(10·4+FM). Forbes derived C based on aggregated, cross-sectional data from a small sample of women. The objective of the present study was to reanalyse the relationship described by Forbes and to explore whether this relationship is consistent across ethnicity and sex groups using cross-sectional data from a large sample of white and African-American men and women. Baseline data from white and African-American men and women aged 18–60 years, who participated in a clinical study at the Pennington Biomedical Research Center since 2001 and who underwent dual-energy X-ray absorptiometry scans, were available for analysis. To overcome differences in BMI distributions among the ethnicity-by-sex groups, a stratified random sample of participants was selected within each group such that numbers in each BMI category ( < 25, 25–29·9, 30–34·9, 35–39·9, 40+ kg/m 2 ) were proportional to those within the group with the smallest sample size, yielding a sample of 1953 individuals. Linear regression models assessed the FM–FFM relationship across the four ethnicity-by-sex groups. The FM–FFM relationship varied little by ethnicity ( P = 0·57) or by sex ( P = 0·26). The constant describing the FM–FFM relationship was estimated to be 9·7 (95 % CI 9·0, 10·3). In conclusion, results from our large, biethnic sample of men and women found a FM–FFM relationship very close to that originally described by Forbes, absent of significant variability by ethnicity or sex.
To investigate the relationship between sleep duration and subsequent body weight and fat gain.Six-year longitudinal study.Community setting.Two hundred seventy-six adults aged 21 to 64 years from the Quebec Family Study. More than half of the sample is drawn from families with at least 1 parent and 1 offspring with a body mass index of 32 kg/m2 or higher.Body composition measurements and self-reported sleep duration were determined. Changes in adiposity indices were compared between short- (5-6 hours), average- (7-8 hours), and long- (9-10 hours) duration sleeper groups. After adjustment for age, sex, and baseline body mass index, short-duration sleepers gained 1.98 kg (95% confidence interval: 1.16-2.82) more and long-duration sleepers gained 1.58 kg (95% CI: 1.02-2.56) more than did average-duration sleepers over 6 years. Short- and long-duration sleepers were 35% and 25% more likely to experience a 5-kg weight gain, respectively, as compared with average-duration sleepers over 6 years. The risk of developing obesity was elevated for short- and long-duration sleepers as compared with average-duration sleepers, with 27% and 21% increases in risk, respectively. These associations remained significant after inclusion of important covariates and were not affected by adjustment for energy intake and physical activity participation.This study provides evidence that both short and long sleeping times predict an increased risk of future body weight and fat gain in adults. Hence, these results emphasize the need to add sleep duration to the panel of determinants that contribute to weight gain and obesity.
No abstract is provided for this article.
The data reviewed in this paper reveal that individual differences in the response to alterations in energy balance induced by diet or exercise are ubiquitous. These differences are observed in a variety of obesity-related phenotypes, including body weight, body fatness, and abdominal visceral fat. Although little is known about the causes of the heterogeneity in responsiveness to dietary habits or to regular exercise, the evidence accumulated so far suggests that genetic factors may play an important role in determining the response of body mass and body fat stores to chronic alterations in energy balance. It is likely that genetic variation at several genes contributes to this heterogeneity of responses and thus to the susceptibility to obesity. Research on the genetic and molecular basis of gene-environment interactions has become a major area of investigation. One can, therefore, anticipate that major advances will occur in the coming years with respect to the identification of the genetic and molecular causes of the susceptibility to the most common diseases, including obesity.
This brief review constitutes a synthesis of some of the research conducted in our laboratory about the role of inheritance in human variation observed for subcutaneous fat, total fat mass and subcutaneous fat distribution. Our first studies were of the genetic epidemiology type and were conducted on a cohort of 1,698 subjects from 409 families of French descent living in the greater Québec city area. These studies have shown that heritability of the amount of subcutaneous fat was almost zero, while the additive genetic effect reached about 25% of human variation, after statistical control over the effects of age and gender, for total fat mass and regional subcutaneous fat distribution. On the other hand, there are considerable individual differences in the response to overfeeding and those that pertain to body weight and body composition, and the various components of daily energy expenditure in subjects kept inactive, are mainly determined by the genotype. These findings come from a study on the response to chronic overfeeding, sustained for 22 consecutive days, undertaken with 6 pairs of identical twins. In general, our research shows that there are individuals who are more at risk of becoming obese because of undetermined genetic characteristics but that are apparently associated somehow with the various components of habitual energy expenditure.
Large interindividual variation in work capacities and powers are often reported in the literature. The variations are attributed to such varied factors as age, sex, exercise training, and heredity, among others. Ethnic/racial origin as a putative causal factor of such variations has also been considered. Studies of subjects from various countries report aerobic power generally between 40 and 50 mL O2/kg.min-1, with a mean around 45 mL. Differences between groups are generally small and genuine racial differences in maximal aerobic power are lacking when allowance is made for other factors. There are, on the other hand, differences between racial groups in submaximal work efficiency and endurance performance. These differences, however, appear to result from differences in mechanical efficiency owing to test mode and/or level of habituation to the ergometer. Performances on maximal tests of short duration demonstrate some variation among racial groups, but again differences in mechanical efficiency cannot be ruled out. Thus there does not appear to be valid and reliable evidence to support the concept of clear racial differences in work capacities and powers.
No abstract is provided for this article.
BOUCHARD, C., and T. RANKINEN. Individual differences in response to regular physical activity. Med. Sci. Sports Exerc., Vol. 33, No. 6, Suppl., 2001, pp. S446–S451. Purpose: The purpose of this review was to address the question of interindividual variation in responsiveness to regular exercise training and to define the contributions of age, sex, race, and pretraining phenotype level to this variability. Methods: A literature review was conducted of the studies reporting interindividual variation in responsiveness to standardized and controlled exercise-training programs, and included an analysis of the contribution of age, sex, race, and initial phenotype values to the heterogeneity in V̇O2max, high-density lipoprotein (HDL)-C and submaximal exercise, heart rate (HR), and systolic blood pressure (SBP) training responses in subjects from the HERITAGE Family Study. Results: Several studies have shown marked individual differences in responsiveness to exercise training. For example, V̇O2max responses to standardized training programs have ranged from almost no gain up to 100% increase in large groups of sedentary individuals. A similar pattern of heterogeneity has been observed for other phenotypes. Data from the HERITAGE Family Study show that age, sex, and race have little impact on interindividual differences in training responses. On the other hand, the initial level of a phenotype is a major determinant of training response for some traits, such as submaximal exercise heart rate and blood pressure (BP) but has only a minor effect on others (e.g., V̇O2max, HDL-C). The contribution of familial factors (shared environment and genetic factors) is supported by data on significant familial aggregation of training response phenotypes. Conclusions: There is strong evidence for considerable heterogeneity in the responsiveness to regular physical activity. Age, sex, and ethnic origin are not major determinants of human responses to regular physical activity, whereas the pretraining level of a phenotype has a considerable impact in some cases. Familial factors also contribute significantly to variability in training response.
A considerable amount of research on the genetics of obesity has been reported in the past few years. Despite evidence that genetic factors play a significant role in the etiology of this nutritional disease and the increasing number of obesity genes identified, relatively little is known about the role of genes in the response of obesity phenotypes to alterations in energy balance or diet composition. This is especially true for dietary fat, which is known to be associated with obesity at the population level. The aim of this review was to summarize the evidence currently available about the role of gene-nutrient interactions in human obesity. Evidence from both genetic epidemiology and molecular epidemiology studies suggests that genetic factors are involved in determining the susceptibility to gaining or losing fat in response to diet or the risk of developing some of the comorbidities generally observed in obese individuals. Recent evidence suggests that quantitative trait loci identified from animal models of diet-induced obesity could influence body fat in humans. Despite the limited number of studies, the evidence on gene-diet interactions in obesity is convincing. More research is needed to identify the genes responsible for these interaction effects, and the use of animal models of diet-induced obesity represents a promising approach. Finally, data on children are needed to allow assessment of the tracking of nutrient intake between childhood and adulthood. In addition, gene-diet interactions in children need to be investigated to determine whether the genes involved are the same as those found in adults.
