Aside from the physiological benefits from intermittent fasting don't you think eating this way could lead to binge eating for some people?
And please do post the studies regarding the benefits...not that I doubt you just that I've yet to see them.
my apologies guys, been super busy.
I have a ton here, this is random posting.I'll post more on the effects of hormesis later as it relates to IF.
[http://www.ajcn.org/content/86/1/7.full]
Paper highlights:
"Calorie restriction (CR), defined as a reduction in energy intake without malnutrition, has been shown to increase life span, improve numerous functional indexes, and reduce metabolic risk factors for chronic disease in several mammalian species (1, 2 "). "restricting daily energy intake by 15–40% has been shown in both animals and humans to improve glucose tolerance and insulin action, which indicates an enhancement in insulin sensitivity (7,

; to reduce blood pressure and the heart rate, which is consistent with benefits for cardiovascular health (9-11); and to reduce oxidative damage to lipids, protein, and DNA, which implies a protective effect against oxidative stress (12-15)" . Many other effects of CR have been documented, including increased average and maximal life span (12), reduced incidence of spontaneous and induced cancers (13), resistance of neurons to degeneration (14), lower rates of kidney disease (15), and prolongation of reproductive function (16). " Although the precise mechanisms responsible for such effects are still not clear, several general hypotheses have been proposed—most prominent are the stress resistance hypothesis, the oxidative stress hypothesis, and the induction of a scarcity program hypothesis (3, 17-19). The first hypothesis suggests that, after prolonged dietary restriction, increased resistance to different types of stressors occurs, which permits the cells of many tissues to resist injury induced by genotoxic, metabolic, or oxidative insults (20-22) The second hypothesis proposes more specifically that fewer free radicals are produced in the mitochondria of cells, because dietary restriction generally limits energy utilization, which results in less cellular oxidative damage (3). The third hypothesis proposes that CR induces intrinsic cellular and organismal programs for adaptation to scarcity, which result in the slowing of metabolic processes such as cell proliferation that contribute to senescence; this hypothesis has been strengthened by findings in yeast (19). The effects of ADF on these proposed mechanisms have not been explored as extensively as have the effects of CR, but some evidence has been generated, and that will be reviewed here. " To date, 12 studies using animal models have examined the effect of ADF on chronic disease risk (23-34; Table 1). Approximately half of these studies examined variables related to diabetes, such as fasting glucose and insulin concentrations, fat oxidation, degree of insulitis, and occurrence of type 2 diabetes. Fasting glucose concentrations have generally been reported to decrease in response to ADF in animal models. Three studies found reduced circulating glucose concentrations after a 20–24-wk intervention (27, 30), whereas one study reported no effect on glucose concentrations after a 16-wk treatment (24). In the trials that measured insulin concentrations, consistent reductions were noted after ADF regimens that lasted 20 (27) and 24 (28) wk. It is interesting that, in the study of Anson et al (27), both glucose and insulin concentrations decreased to a similar extent in the ADF and the 40% CR groups. Increases in fat oxidation in liver and muscle have also been observed after relatively short periods (8 wk) of ADF (33). Because impaired fat oxidation may contribute to ectopic accumulation of intracellular lipid and the development of insulin resistance (35), these increases in fat oxidation may increase insulin sensitivity. Also noted by Anson et al was a doubling of the plasma concentrations of ß-hydroxybutyrate in the ADF group but no change in the control group. In contrast, concentrations of this metabolite decreased in the 40% CR group but not in the control group (27). These results suggest that high rates of fatty acid oxidation leading to ketogenesis occurred with ADF but not with 40% CR. Moreover, reduced occurrence of insulin-dependent diabetes in response to ADF has been reported by Pedersen et al (30). These authors found that 77% of the BB rats fed ad libitum control diets developed diabetes, whereas only 52% of the animals fasted for 24 h on alternate days became diabetic. The degree of insulitis, however, was not affected, which suggested that the mechanism most likely did not involve modulation of this inflammatory variable (30).
Effect of intermittent fasting and refeeding on insulin action in healthy men
Nils Halberg,1 Morten Henriksen,1 Nathalie Söderhamn,1 Bente Stallknecht,1Thorkil Ploug,1 Peter Schjerling,2 and Flemming Dela1
1Copenhagen Muscle Research Centre, Department of Medical Physiology, The Panum Institute, University of Copenhagen, Denmark; and 2Copenhagen Muscle Research Center, Department of Molecular Muscle Biology, Rigshospitalet, Denmark
Submitted 9 June 2005 ; accepted in final form 22 July 2005
Insulin resistance is currently a major health problem. This may be because of a marked decrease in daily physical activity during recent decades combined with constant food abundance. This lifestyle collides with our genome, which was most likely selected in the late Paleolithic era (50,000–10,000 BC) by criteria that favored survival in an environment characterized by fluctuations between periods of feast and famine. The theory of thrifty genes states that these fluctuations are required for optimal metabolic function. We mimicked the fluctuations in eight healthy young men [25.0 ± 0.1 yr (mean ± SE); body mass index: 25.7 ± 0.4 kg/m2] by subjecting them to intermittent fasting every second day for 20 h for 15 days. Euglycemic hyperinsulinemic (40 mU·min–1·m–2) clamps were performed before and after the intervention period. Subjects maintained body weight (86.4 ± 2.3 kg; coefficient of variation: 0.8 ± 0.1%). Plasma free fatty acid and -hydroxybutyrate concentrations were 347 ± 18 and 0.06 ± 0.02 mM, respectively, after overnight fast but increased (P < 0.05) to 423 ± 86 and 0.10 ± 0.04 mM after 20-h fasting, confirming that the subjects were fasting. Insulin-mediated whole body glucose uptake rates increased from 6.3 ± 0.6 to 7.3 ± 0.3 mg·kg–1·min–1 (P = 0.03), and insulin-induced inhibition of adipose tissue lipolysis was more prominent after than before the intervention (P = 0.05). After the 20-h fasting periods, plasma adiponectin was increased compared with the basal levels before and after the intervention (5,922 ± 991 vs. 3,860 ± 784 ng/ml,P = 0.02). This experiment is the first in humans to show that intermittent fasting increases insulin-mediated glucose uptake rates, and the findings are compatible with the thrifty gene concept.
Prostate Cancer Prostatic Dis. 2010 Dec;13(4):350-5. Epub 2010 Aug 24.
Effect of intermittent fasting on prostate cancer tumor growth in a mouse model.
Thomas JA 2nd, Antonelli JA, Lloyd JC, Masko EM, Poulton SH, Phillips TE, Pollak M, Freedland SJ.
Source
Division of Urologic Surgery, Department of Surgery, Duke Prostate Center, Duke University Medical Center, Durham, NC 27710, USA.
Abstract
Caloric restriction (CR) has been shown to have anti-cancer properties. However, CR may be difficult to apply in humanssecondary to compliance and potentially deleterious effects. An alternative is intermittent CR, or in the extreme caseintermittent fasting (IF). In a previous small pilot study, we found 2 days per week of IF with ad libitum feeding on the other days resulted in trends toward prolonged survival of mice bearing prostate cancer xenografts. We sought to confirm these findings in a larger study. A total of 100 (7- to 8-week-old) male severe combined immunodeficiency mice were injected subcutaneously with 1 × 10(5) LAPC-4 prostate cancer cells. Mice were randomized to either ad libitum Western Diet (44% carbohydrates, 40% fat and 16% protein) or ad libitum Western Diet with twice-weekly 24 h fasts (IF). Tumor volumes and mouse bodyweights were measured twice weekly. Mice were killed when tumor volumes reached 1000 mm(3). Serum and tumor were collected for analysis of the insulin/insulin-like growth factor 1 (IGF-1) hormonal axis. Overall, there was no difference in mouse survival (P=0.37) or tumor volumes (P ≥ 0.10) between groups. Mouse body weights were similar between arms (P=0.84). IF mice had significantly higher serum IGF-1 levels and IGF-1/IGFBP-3 ratios at killing (P<0.001). However, no difference was observed in serum insulin, IGFBP-3 or tumor phospho-Akt levels (P ≥ 0.39). IF did not improve mouse survival nor did it delay prostate tumor growth. This may be secondary to metabolic adaptations to the 24 h fastingperiods. Future studies are required to optimize CR for application in humans
Int J Obes (Lond). 2011 May;35(5):714-27. Epub 2010 Oct 5.
The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women.
Harvie MN, Pegington M, Mattson MP, Frystyk J, Dillon B, Evans G, Cuzick J, Jebb SA, Martin B, Cutler RG, Son TG, Maudsley S,Carlson OD, Egan JM, Flyvbjerg A, Howell A.
Source
Genesis Prevention Centre, University Hospital of South Manchester NHS Foundation Trust, Manchester, UK. michelle.harvie@manchester.ac.uk
Abstract
BACKGROUND:
The problems of adherence to energy restriction in humans are well known.
OBJECTIVE:
To compare the feasibility and effectiveness of intermittent continuous energy (IER) with continuous energy restriction (CER) for weight loss, insulin sensitivity and other metabolic disease risk markers.
DESIGN:
Randomized comparison of a 25% energy restriction as IER (∼ 2710 kJ/day for 2 days/week) or CER (∼ 6276 kJ/day for 7 days/week) in 107 overweight or obese (mean (± s.d.) body mass index 30.6 (± 5.1) kg m(-2)) premenopausal women observed over a period of 6 months. Weight, anthropometry, biomarkers for breast cancer, diabetes, cardiovascular disease and dementia risk; insulin resistance (HOMA), oxidative stress markers, leptin, adiponectin, insulin-like growth factor (IGF)-1 and IGF binding proteins 1 and 2, androgens, prolactin, inflammatory markers (high sensitivity C-reactive protein and sialic acid), lipids, blood pressure and brain-derived neurotrophic factor were assessed at baseline and after 1, 3 and 6 months.
RESULTS:
Last observation carried forward analysis showed that IER and CER are equally effective for weight loss: mean (95% confidence interval ) weight change for IER was -6.4 (-7.9 to -4.

kg vs -5.6 (-6.9 to -4.4) kg for CER (P-value for difference between groups = 0.4). Both groups experienced comparable reductions in leptin, free androgen index, high-sensitivity C-reactive protein, total and LDL cholesterol, triglycerides, blood pressure and increases in sex hormone binding globulin, IGF binding proteins 1 and 2. Reductions in fasting insulin and insulin resistance were modest in both groups, but greater with IER than with CER; difference between groups for fasting insulin was -1.2 (-1.4 to -1.0) μU ml(-1) and for insulin resistance was -1.2 (-1.5 to -1.0) μU mmol(-1) l(-1) (both P = 0.04).
CONCLUSION:
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.