The risk of becoming obese is higher in some families than in others. The risk (the lambda coefficient) is two to three fold for moderate obesity, but up to five to eight fold for severe obesity. Several genes exhibit mutations that can cause early onset severe obesity. These mutations are rare and account for only a small fraction of the cases of obesity. At this time, more than fifty genes have been shown in various studies to influence the energy balance, nutrient partitioning, or the age of onset of obesity. The results of these studies are generally disappointing and often contradictory. One approach is to scan the genome with a high number of polymorphic markers to identify chromosomal regions harboring genes implicated in the development of obesity. Such studies can be helpful in defining new targets to explore.
The objective of this review is to provide an overview of intermittent fasting regimens, summarize the evidence on the health benefits of intermittent fasting, and discuss physiological mechanisms by which intermittent fasting might lead to improved ...Read More
No abstract is provided for this article.
The concept of gene–environment interaction refers to a situation where the response or the adaptation to an environmental factor, a behavior, or a change in behavior is conditional on the genotype of the individual. Of particular interest for our understanding of the etiology of human obesity is the role played by genotype–nutrition and genotype–physical activity interactions. Evidence for the presence of such interaction effects affecting body mass and body composition comes from experimental studies undertaken with pairs of monozygotic twins and with nuclear families. These studies reveal that there are large individual differences in the responsiveness to well‐defined energy balance manipulations. Overfeeding as well as negative energy balance protocols indicate that the response to these standardized experimental treatments is strongly influenced by one's genetic background. The genes that are responsible for the individual differences in the sensitivity to alterations in energy balance remain to be fully identified. They are likely to be numerous considering the complexity of the biological systems that are involved in body weight regulation. A number of research designs and technologies are available to identify these genes and to delineate the nature and the extent of the genetic polymorphisms involved. It was the purpose of the workshop to define the conditions under which gene–behavior interaction effects of relevance to human obesity could be reliably identified.
Ten pairs of monozygotic twins of both sexes were submitted to a 20-wk endurance-training program, four and five times per week, 40 min per session, at an average of 80% of the maximal heart rate reserve. Testing and training were performed on cycle ergometers. Maximal aerobic power (MAP in ml O2.min1 kg−1) and ventilatory aerobic (VAT) and anaerobic (VANT) thresholds (ml O2.min−1.kg−1) were measured before and after the training program, as well as during the 7th and 14th week to adjust training to changes in maximal heart rate. Considering the 20 individuals as a group, training significantly (P≤0.01) increased MAP (from 44 ± 6 to 50 ± 6), VAT (25 ± 3 to 30 ± 4), and VANT (36 ± 5 to 42 ± 6). Thus, MAP improved by 12% of the pre-test value, while mean changes in VAT and VANT reached 20% and 17%, respectively. There were, however, considerable interindividual differences in training gains as exemplified by a range of about 0% to 41% for MAP. Differences in the MAP response to training were not distributed randomly among the twin pairs. Thus, intraclass correlations computed with the amount of improvement in MAP (ml O2.min−1.kg−1) reached 0.74 (P<0.01) indicating that members of the same twinpair yielded approximately the same response to training. The same coefficient reached 0.43 and 0.24 for VAT and VANT, respectively (P>0.05). These results suggest that there are considerable individual differences in the adaptive capacity to shortterm endurance training. Moreover, sensitivity of maximal aerobic power to such training is largely genotype-dependent.
