Okay, so here is a particularly exciting study - Effect of intermittent fasting and refeeding on insulin action in healthy men. It has an admittedly small cohort of 8 men, so take it for what it is (perhaps not statistically applicable to larger populations), but it is the first study I've found that actually looked at a cohort of healthy, active people, as opposed to obese/diabetic/etc populations.
I haven't fully analyzed the methodology of this study, but at first glance it's quite interesting. The following is taken from the Discussion section of the study as linked to above.
I haven't fully analyzed the methodology of this study, but at first glance it's quite interesting. The following is taken from the Discussion section of the study as linked to above.
It appears funding for this study came from a single grant from a Danish Diabetes Association, so it's hard to imagine that would skew the conclusions. Confirmation bias (preexisting ideology) is always a potential problem. And like I said, the sample size is admittedly small. Even so, it seems like a decent set of data, given what I'm trying to establish here."In the present study we have used a very simple intervention protocol with the aim of mimicking the perturbations in energy stores that are inherent in a physical active lifestyle with regular exercise sessions. In a wider perspective we have tried to unravel the significance of genes that may be responsible for an evolutionary selection process, i.e., the thrifty genes. In this context the used intervention seems inevitably small. Nevertheless, by subjecting healthy men to cycles of feast and famine we did change the metabolic status to the better, implying that the mismatch between our ancient genotype and the lifestyle of the westernized individual of today became smaller. To our knowledge this is the first study in humans in which an increased insulin action on whole body glucose uptake and adipose tissue lipolysis has been obtained by means of intermittent fasting. This result is in accordance with previously reported in rodents (2, 32). In these studies, fasting every second day increased the insulin sensitivity approximately sevenfold according to the homeostatic model assessment (2) and decreased the incidence of diabetes (32).
Prolonged fasting for 72 h with minimal physical activity has previously been shown to increase IMTG levels in humans (46). With the present fasting protocol and maintenance of habitual daily physical activity in the fasting periods, we had expected to detect a decrease in IMTG content in the skeletal muscle. The fact that this was not seen and that muscle glycogen content was unchanged could suggest that skeletal muscle is not immediately involved in recognition of acute energy oscillations. There is no doubt, however, that fasting for 20 h while maintaining normal daily physical activity must cause a temporary negative energy balance larger than normally experienced in a daily basis. This is also indicated by our finding of decreased plasma glucose concentrations after 20-h fasting. We did not have the possibility to estimate the hepatic glycogen stores, but from animal studies (17) we must infer that liver glycogen probably also decreased considerably during the 20-h fasting periods. It has previously been suggested that usage of muscle energy depots during fasting would be an evolutionary disadvantage, because it would lessen the capacity for physical performance and hence the ability to provide food (i.e., to hunt and gather) during periods of fasting (6, 45). The present findings support this view.
In contrast to the findings in skeletal muscle, the adipose tissue responded to the changes in energy balance as intermittent fasting changed the plasma concentrations of the adipocyte-specific hormones leptin and adiponectin. However, because we did not measure the energy stores in the adipose tissue during the intervention (e.g., by fat cell size), we cannot determine whether the change in adipokine release is merely a secondary response to intermittent fasting or whether the adipose tissue is an active recognizer of energy oscillations.
...
In conclusion, the findings that intermittent fasting increases insulin sensitivity on the whole body level as well as in adipose tissue support the view that cycles of feast and famine are important as an initiator of thrifty genes leading to improvements in metabolic function (6). We suggest that a fasting-induced increase in circulating adiponectin is at least partly responsible for this finding. The change in adiponectin, together with changes in plasma leptin with fasting, underlines the important role of the adipose tissue in recognizing the oscillation in energy stores. Finally, the data indicate that intermittent fasting and physical training may increase insulin action via different mechanisms because muscle energy stores did not change with the present fasting intervention."
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