LOL, hippy science. Granted the research is fairly lacking, but it has been done in humans and in mammals and more studies are being done and there is undoubtedly positive results so far.
Fasting: Molecular Mechanisms and Clinical Applications
Fasting has been practiced for millennia, but only recently studies have shed light on its role in adaptive cellular responses that reduce oxidative damage and inflammation, optimize energy metabolism and bolster cellular protection. In lower eukaryotes, chronic fasting extends longevity in part by reprogramming metabolic and stress resistance pathways. In rodents intermittent or periodic fasting protects against diabetes, cancers, heart disease and neurodegeneration, while in humans it helps reduce obesity, hypertension, asthma and rheumatoid arthritis. Thus, fasting has the potential to delay aging and help prevent and treat diseases while minimizing the side effects caused by chronic dietary interventions.
Among the major effects of fasting relevant to aging and diseases are changes in the levels of IGF-1, IGFBP1, glucose, and insulin. Fasting for 3 or more days causes a 30% or more decrease in circulating insulin and glucose, as well as rapid decline in the levels of insulin-like growth factor 1 (IGF-1), the major growth factor in mammals, which together with insulin is associated with accelerated aging and cancer (Fontana et al., 2010). In humans, five days of fasting causes an over 60% decrease in IGF-1and a 5-fold or higher increase in one of the principal IGF-1-inhibiting proteins: IGFBP1 (Thissen et al., 1994a). This effect of fasting on IGF-1is mostly due to protein restriction, and particularly to the restriction of essential amino acids, but is also supported by calorie restriction since the decrease in insulin levels during fasting promotes reduction in IGF-1(Thissen et al., 1994a). Notably, in humans, chronic calorie restriction does not lead to a decrease in IGF-1unless combined with protein restriction (Fontana et al., 2008).
Fasting has the potential for applications in both cancer prevention and treatment. Although no human data are available on the effect of IF or PF in cancer prevention, their effect on reducing IGF-1, insulin and glucose levels, and increasing IGFBP1 and ketone body levels could generate a protective environment that reduces DNA damage and carcinogenesis, while at the same time creating hostile conditions for tumor and pre-cancerous cells (Figure 5). In fact, elevated circulating IGF-1 is associated with increased risk of developing certain cancers (Chan et al., 2000; Giovannucci et al., 2000) and individuals with severe IGF-1deficiency caused by growth hormone receptor deficiency, rarely develop cancer (Guevara-Aguirre et al., 2011; Shevah and Laron, 2007; Steuerman et al., 2011). Furthermore, the serum from these IGF-1deficient subjects protected human epithelial cells from oxidative stress-induced DNA damage. Furthermore, once their DNA became damaged, cells were more likely to undergo programmed cell death (Guevara-Aguirre et al., 2011). Thus, fasting may protect from cancer by reducing cellular and DNA damage but also by enhancing the death of pre-cancerous cells.
Effect of intermittent fasting and refeeding on insulin action in healthy men | Journal of Applied Physiology
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).
The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overwei... - PubMed - NCBI
IER is as effective as CER with regard to weight loss, insulin sensitivity and other health biomarkers, and may be offered as an alternative equivalent to CER for weight loss and reducing disease risk.
Glucose tolerance and skeletal muscle gene expression in response to alternate day fasting. - PubMed - NCBI
Alternate day fasting may adversely affect glucose tolerance in nonobese women but not in nonobese men. The gene expression results indicate that fatty acid oxidation and mitochondrial biogenesis are unaffected by alternate day fasting. However, the increased expression in SIRT1 suggests that alternate day fasting may improve stress resistance, a commonly observed feature of calorie-restricted rodents.
Alternate-day fasting in nonobese subjects: effects on body weight, body composition, and energy metabolism
In conclusion, alternate-day fasting is feasible in nonobese subjects for short time periods, although unlike rodents, the subjects were unable to maintain their body weight. Furthermore, fat oxidation was increased and translated into fat mass loss.
Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? - PubMed - NCBI
Accordingly, this review examines the effects of daily CR versus intermittent CR on weight loss, fat mass loss and lean mass retention in overweight and obese adults. Results reveal similar weight loss and fat mass loss with 3 to 12 weeks' intermittent CR (4-8%, 11-16%, respectively) and daily CR (5-8%, 10-20%, respectively). In contrast, less fat free mass was lost in response to intermittent CR versus daily CR. These findings suggest that these diets are equally as effective in decreasing body weight and fat mass, although intermittent CR may be more effective for the retention of lean mass.
Meal frequency and timing in health and disease
When organisms ingest regular meals, their cells receive a relatively steady supply of nutrients and so remain in a "growth mode" in which protein synthesis is robust and autophagy is suppressed (68). The nutrient-responsive mTOR pathway negatively regulates autophagy. Accordingly, fasting inhibits the mTOR pathway and stimulates autophagy in cells of many tissues, including liver, kidney, and skeletal muscle (69-71). In this way, fasting "cleanses" cells of damaged molecules and organelles.