Restricting caloric intake to 60–70% of normal adult weight maintenance requirement prolongs lifespan 30–50% and confers near perfect health across a broad range of species. Every other day feeding produces similar effects in rodents, and profound beneficial physiologic changes have been demonstrated in the absence of weight loss in ob/ob mice. Since May 2003 we have experimented with alternate day calorie restriction, one day consuming 20–50% of estimated daily caloric requirement and the next day ad lib eating, and have observed health benefits starting in as little as two weeks, in insulin resistance, asthma, seasonal allergies, infectious diseases of viral, bacterial and fungal origin (viral URI, recurrent bacterial tonsillitis, chronic sinusitis, periodontal disease), autoimmune disorder (rheumatoid arthritis), osteoarthritis, symptoms due to CNS inflammatory lesions (Tourette’s, Meniere’s) cardiac arrhythmias (PVCs, atrial fibrillation), menopause related hot flashes. We hypothesize that other many conditions would be delayed, prevented or improved, including Alzheimer’s, Parkinson’s, multiple sclerosis, brain injury due to thrombotic stroke atherosclerosis, NIDDM, congestive heart failure.
Our hypothesis is supported by an article from 1957 in the Spanish medical literature which due to a translation error has been construed by several authors to be the only existing example of calorie restriction with good nutrition. We contend for reasons cited that there was no reduction in calories overall, but that the subjects were eating, on alternate days, either 900 calories or 2300 calories, averaging 1600, and that body weight was maintained. Thus they consumed either 56% or 144% of daily caloric requirement. The subjects were in a residence for old people, and all were in perfect health and over 65. Over three years, there were 6 deaths among 60 study subjects and 13 deaths among 60 ad lib-fed controls, non-significant difference. Study subjects were in hospital 123 days, controls 219, highly significant difference. We believe widespread use of this pattern of eating could impact influenza epidemics and other communicable diseases by improving resistance to infection. In addition to the health effects, this pattern of eating has proven to be a good method of weight control, and we are continuing to study the process in conjunction with the NIH.

http://www.proteinpower.com/drmike/intermittent-fasting/fast-way-to-better-health/

http://en.wikipedia.org/wiki/Brain-derived_neurotrophic_factor

Yup

Interesting.  A lab I collaborate with just found data that IF in rodents pretty much replicates the long term calorie restriction as far as lifespan, lipid markers, etc.  I like it.  IF is MUCH easier than long term calorie restriction. 

Hah.  That's tough.  First off, it's really difficult to try to establish a mechanism for WHY calorie restriction slows down ageing when we are not even in agreement as to what the mechanism of ageing is.  This was discovered in the 1930's (that CR extends lifespan in rodents) and since then the proposed mechanism has changed as research into ageing has progressed. 

Although there are many proposed mechanisms for the effect of CR you can put most of the mechanism into two camps.

1) Metabolism is very bad. 

This camp basically points to the fact that with less food, you invariably have a lower metabolic rate, less oxidative damage, less inflammation, less plasma glucose, lower body temperature.   These results are pretty well established.  The story most biologists will give you is the story of blood glucose metabolism.   We know if blood glucose is high then mitochondria operate poorly and generate more superoxide (a free radical implicated in ageing).  If blood glucose is too high for too long we know cells eventually become insulin resistant which results in a increased glycation of proteins, higher probability of infection (bugs eat sugar), and what we call metabolic syndrome or type II diabetes. 


2) Metabolism is not necessarily bad, but the lack of metabolism "trains" the body and this adaptation increases lifespan.

This camp really turns the idea of "free radical damage" on it's head.  Most of the research in this camp is less than 5 years old.  It's been shown in nematode that small increases in oxidative stress lead to increased resistance to further oxidative stress.  Basically, it's the idea that the free radical damage actually trains the cell to be robust to further damage.  It's believed that the low-intensity biological stress of calorie restriction A) Causes changes in cell physiology which make it more robust in the face of   stress  B) Cause transcription of "longevity genes" which turn on protective proteins like heat-shock protein. 


********************

In all likelihood, its probably a combination of factors from both camps and a few unmentioned factors.  But....the reason why the studies about intermittent fasting are so encouraging is because they shift the likelihood that camp 2 is playing a major role in the increased longevity.  If IF == CR as far as results, it's not simply the lack of calories.  It's a poor analogy, but I would describe Camp 1 is sort of like saying you will live longer if you do less because by doing less you accumulate less damage.  To effectively calorie restrict activity must be kept to a minimum which is not what people who love to train want to hear!  Camp 2 can be summarized as saying "just like you train your your muscles (with progressive overload) and they supercompensate so to must you train your cells (by intermittently reducing the amount of energy you provide to them)  so they will supercompensate and become efficient
at glucose metabolism and ready to withstand all the stresses of life!

Now that's something we can all get behind!  Hope that made sense!