11 research outputs found

    Energy expenditure during overfeeding

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    The large inter-individual variation in weight gain during standardized overfeeding together with a weight gain that is often less than theoretically calculated from the energy excess suggest that there are differences between persons in the capacity to regulate energy expenditure and hence metabolic efficiency. Adaptive thermogenesis is defined as the regulated production of heat in response to environmental changes in temperature and diet, resulting in metabolic inefficiency. The question is whether adaptive thermogenesis can be identified in overfeeding experiments. From the numerous human overfeeding experiments we selected those studies that applied suitable protocols and measurement techniques. Five studies claimed to have found evidence for adaptive thermogenesis based on weight gains smaller than expected or unaccounted increases in thermogenesis above obligatory costs. Results from the other 11 studies suggest there is no adaptive thermogenesis as weight gains were proportional to the amount of overfeeding and the increased thermogenesis was associated with theoretical costs of an increased body size and a larger food intake. These results show that in humans, evidence for adaptive thermogenesis is still inconsistent. However, they do not rule out the existence, but emphasize that if present, adaptive changes in energy expenditure may be too small to measure considering measurement errors, errors in assumptions made and small (day-to-day) differences in physical activity. In addition, it is not clear in which component or components of total energy expenditure adaptive changes can occur and whether components can overlap due to measurement limitations

    Heritability and genetic etiology of habitual physical activity: a twin study with objective measures

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    Twin studies with objective measurements suggest habitual physical activity (HPA) are modestly to highly heritable, depending on age. We aimed to confirm or refute this finding and identify relevant genetic variants using a candidate gene approach. HPA was measured for 14 days with a validated triaxial accelerometer (Tracmor) in two populations: (1) 28 monozygotic and 24 dizygotic same-sex twin pairs (aged 22 ± 5 years, BMI 21.8 ± 3.4 kg/m(2), 21 male, 31 female pairs); (2) 52 and 65 unrelated men and women (aged 21 ± 2 years, BMI 22.0 ± 2.5 kg/m(2)). Single nucleotide polymorphisms (SNPs) in PPARD, PPARGC1A, NRF1 and MTOR were considered candidates. Association analyses were performed for both groups separately followed by meta-analysis. Structural equation modeling shows significant familiality for HPA, consistent with a role for additive genetic factors (heritability 57 %, 95 % CI 32-74 %, AE model) or common environmental factors (47 %, 95 % CI 23-65 %, CE model). A moderate heritability was observed for the time spent on low- and high-intensity physical activity (P ≤ 0.05), but could not be confirmed for the time spent on moderate-intensity physical activity. For PPARD, each additional effect allele was inversely associated with HPA (P ≤ 0.01; rs2076168 allele C) or tended to be associated with HPA (P ≤ 0.05; rs2267668 allele G). Linkage disequilibrium existed between those two SNPs (alleles A/G and A/C, respectively) and meta-analysis showed that carriers of the AA GC haplotype were less physically active than carriers of the AA AA and AA AC haplotypes combined (P = 0.017). For PPARGC1A, carriers of AA in rs8192678 spent more time on high-intensity physical activity than GG carriers (P = 0.001). No associations were observed with SNPs in NRF1 and MTOR. In conclusion, HPA may be modestly heritable, which is confirmed by an association with variants in PPARD.status: publishe

    Dietary biomarkers: advances, limitations and future directions

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    <p>Abstract</p> <p>The subjective nature of self-reported dietary intake assessment methods presents numerous challenges to obtaining accurate dietary intake and nutritional status. This limitation can be overcome by the use of dietary biomarkers, which are able to objectively assess dietary consumption (or exposure) without the bias of self-reported dietary intake errors. The need for dietary biomarkers was addressed by the Institute of Medicine, who recognized the lack of nutritional biomarkers as a knowledge gap requiring future research. The purpose of this article is to review existing literature on currently available dietary biomarkers, including novel biomarkers of specific foods and dietary components, and assess the validity, reliability and sensitivity of the markers. This review revealed several biomarkers in need of additional validation research; research is also needed to produce sensitive, specific, cost-effective and noninvasive dietary biomarkers. The emerging field of metabolomics may help to advance the development of food/nutrient biomarkers, yet advances in food metabolome databases are needed. The availability of biomarkers that estimate intake of specific foods and dietary components could greatly enhance nutritional research targeting compliance to national recommendations as well as direct associations with disease outcomes. More research is necessary to refine existing biomarkers by accounting for confounding factors, to establish new indicators of specific food intake, and to develop techniques that are cost-effective, noninvasive, rapid and accurate measures of nutritional status.</p
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