Calorie restriction is definitely good for you, provided that you maintain an optimal intake of micronutrients in your smaller diet. There is a tremendous weight of evidence for the benefits of calorie restriction in animals and a large weight of evidence for benefits in humans: it improves near all short term measures of health, slows down the progression of near every measure of degenerative aging, and extends healthy life in most species. Research publications are usually more understated in their evaluation of calorie restriction, of course. See this, for example:

Caloric Restriction: Implications for Human Cadiometabolic Health

Evidence from animal studies and a limited number of human trials indicates that calorie restriction has the potential to both delay cardiac aging and help prevent atherosclerotic cardiovascular disease via beneficial effects on blood pressure, lipids, inflammatory processes, and potentially other mechanisms.

The candidate list of mechanisms by which calorie restriction likely delivers its benefits include reduced visceral fat, increased levels of autophagy, altered mitochondrial function, and metabolic changes caused by reduced levels of methionine in the body. All of these on their own have been shown to extend life and improve measures of health in animal studies. Many other measurable changes result from calorie restriction, but identifying which of them are definitively primary and which are definitively secondary is still a work in progress.

Methionine is one of the essential amino acids that your metabolism doesn't manufacture. You have to obtain it in the diet, and it's an essential component for the cellular manufacture of new protein machinery. There are all sorts of studies in mice and rats showing that if you keep the same dietary calorie level but strip out much of the methionine then the animals involved live longer, and exhibit many of the same changes in metabolism as occur from reduced calorie levels. Here is a recent example:

Methionine restriction affects oxidative stress and glutathione-related redox pathways in the rat

Lifelong dietary methionine restriction (MR) is associated with increased longevity and decreased incidence of age-related disorders and diseases in rats and mice. A reduction in the levels of oxidative stress may be a contributing mechanistic factor for the beneficial effects of MR. To examine this, we determined the effects of an 80% dietary restriction of Met on different biomarkers of oxidative stress and antioxidant pathways in blood, liver, kidney and brain in the rat.

Male F-344 rats were fed control (0.86% methionine) or MR (0.17% methionine) diets for up to six months. Blood and tissues were analyzed for [levels of the natural antioxidant] glutathione (GSH). related enzyme activities and biomarkers of oxidative stress. MR was associated with reductions in oxidative stress biomarkers [and] erythrocyte protein-bound glutathione after one month with levels remaining low for at least six months.

Levels of free GSH in blood were increased after 1-6 months of MR feeding whereas liver GSH levels were reduced over this time. In MR rats, GSH peroxidase activity was decreased in liver and increased in kidney compared with controls. No changes in the activities of GSH reductase in liver and kidney and superoxide dismutase in liver were observed as a result of MR feeding. Altogether, these findings indicate that oxidative stress is reduced by MR feeding in rats, but this effect cannot be explained by changes in the activity of antioxidant enzymes.

You might compare the comments above with the two calorie restriction research papers I pointed out earlier today - you'll quickly see the similarities, such as the fact that the behavior of antioxidants and oxidants in metabolism is complex and hard to tie to the observed benefits in health and longevity. All in all it is convincing to argue that methionine sensing is at the heart of the metabolic changes that produce the benefits of calorie restriction:

• Calorie Restriction Versus Resveratrol Treatment
• Reviewing the Literature on Calorie Restriction and Oxidative Stress

From the practical standpoint of day to day effort and willpower, I'd say that that there isn't much difference between eating a calorie restricted diet and a methionine restricted diet. The latter is harder by far to organize, I think. You certainly couldn't do it without a lot of research, extra food preparation, and meal planning, and there are few resources out there to help you short-cut the process. Calorie restriction, on the other hand, just requires you to keep count and be sensible, plus of course to have a willingness to be hungry for some time every day. It's that latter item that most people find a challenge, in this age of ubiquitous, cheap, tasty food. Calorie restriction also has a far greater weight of supporting evidence for benefits to health in humans, which is probably the most important factor of those mentioned here, but every choice you make has trade-offs.

Source:
http://www.fightaging.org/archives/2013/06/a-little-methionine-restriction-research.php

Researchers here compare the effects of calorie restriction and dietary resveratrol on the pace of sarcopenia, the age-related loss of muscle mass and strength. What I take away from this is that calorie restriction produces meaningful results on this front, albeit modest in comparison to what we'd like to see, and resveratrol doesn't.

Aging is associated with a loss in muscle known as sarcopenia that is partially attributed to apoptosis. In aging rodents, caloric restriction (CR) increases health and longevity by improving mitochondrial function and the polyphenol resveratrol (RSV) has been reported to have similar benefits. In the present study, we investigated the potential efficacy of using short-term (6 weeks) CR (20%), RSV (50 mg/kg/day), or combined CR+RSV (20% CR and 50 mg/kg/day RSV), initiated at late-life (27 months) to protect muscle against sarcopenia by altering mitochondrial function, biogenesis, content, and apoptotic signaling in both glycolytic white and oxidative red gastrocnemius muscle (WG and RG, respectively) of male Fischer 344 x Brown Norway rats.

CR but not RSV attenuated the age-associated loss of muscle mass in both mixed gastrocnemius and soleus muscle, while combined treatment (CR+RSV) paradigms showed a protective effect in the soleus and plantaris muscle. Sirt1 protein content was increased by 2.6-fold in WG but not RG muscle with RSV treatment, while CR or CR+RSV had no effect. PGC-1? levels were higher (2-fold) in the WG from CR-treated animals when compared to ad-libitum (AL) animals but no differences were observed in the RG with any treatment.

These data suggest that short-term moderate CR, RSV, or CR+RSV tended to modestly alter key mitochondrial regulatory and apoptotic signaling pathways in glycolytic muscle and this might contribute to the moderate protective effects against aging-induced muscle loss observed in this study.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23747682

Source:
http://www.fightaging.org/archives/2013/06/calorie-restriction-versus-resveratrol-treatment.php

Oxidative theories of aging place the blame for the damage of aging on reactive oxidizing molecules, generated most notably in the mitochondria of your cells, and which tend to break the protein machinery they react with. Oxidative stress is the term given to ongoing damage (and efforts to repair it) caused by the presence of oxidative molecules in and around cells. Levels of oxidative stress can alter as a result of heat, exposure to ionizing radiation, the details of diet, and all sorts of other environmental influences.

The relationship between oxidative stress and the pace of aging is far from straightforward, however. There is more oxidative stress with age, but this is an expected result of carrying a high level of cellular and molecular damage. Some very long-lived species, such as naked mole rats, show very high levels of oxidative stress but don't appear to be particularly harmed by it. Mild oxidative stress can be beneficial, triggering increased cellular maintenance for a time to produce a net benefit. Oxidative compounds are also widely used in our biochemistry for necessary signaling purposes.

You can see the nature of this complex relationship between oxidative stress and aging by looking at what happens in interventions that reliably slow aging and extend life, such as calorie restriction in rodents:

Oxidative stress is observed during aging and in numerous age-related diseases. Dietary restriction (DR) is a regimen that protects against disease and extends lifespan in multiple species. However, it is unknown how DR mediates its protective effects. One prominent and consistent effect of DR in a number of systems is the ability to reduce oxidative stress and damage. The purpose of this review is to comprehensively examine the hypothesis that dietary restriction reduces oxidative stress in rodents by decreasing reactive oxygen species (ROS) production and increasing antioxidant enzyme activity, leading to an overall reduction of oxidative damage to macromolecules.

The literature reveals that the effects of DR on oxidative stress are complex and likely influenced by a variety of factors, including sex, species, tissue examined, types of ROS and antioxidant enzymes examined, and duration of DR. [In] a majority of studies, dietary restriction had little effect on mitochondrial ROS production or antioxidant activity. On the other hand, DR decreased oxidative damage in the majority of cases. Although the effects of DR on endogenous antioxidants are mixed, we find that glutathione levels are the most likely antioxidant to be increased by dietary restriction, which supports the emerging redox-stress hypothesis of aging.

While thinking about antioxidants and their effect on aging, it's important to remember that location matters immensely. Ingested antioxidants of the sort you can buy in the store are convincingly demonstrated to do nothing for your health, and there is evidence to suggest that they are actually mildly harmful - for example by blocking some of the oxidant-based signaling mechanisms the body uses to dial up cellular housekeeping and muscle growth responses after exercise. Meanwhile researchers are demonstrating benefits in mice by targeting designed antioxidant compounds to the mitochondria in cells, the place that most oxidants are generated. Those antioxidants are not yet available for the rest of us, however. The antioxidant pills from the store don't deliver their contents to your mitochondria, and are thus not terribly helpful.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23743291

Source:
http://www.fightaging.org/archives/2013/06/reviewing-the-literature-on-calorie-restriction-and-oxidative-stress.php

It is usually the case that the first knee-jerk reaction in opposition to increased human longevity is based on the mistaken belief that life extension technologies would lead to people being ever more frail and decrepit for a very long time. This is far from the case, and it's probably not even possible to cost-effectively engineer a society of long-lived frail people - even if that was the goal to hand. If you are frail and decrepit then you have a high mortality rate due to the level of age-related cellular and molecular damage that is causing the failure and degeneration of your body and its organs. You won't be around for long. No, the only way to engineer longer healthy life is extend the period of youth and vitality, a time in which you have little age-related damage and your mortality rate is very low. Most present strategies are aimed to prolong that period of life, either by slowing the rate at which damage occurs (not so good) or finding ways to periodically repair the damage and thus rejuvenate the patient (much better).

Once people grasp that longevity science is the effort to make people younger for far longer, then the second knee-jerk objection arises. This is the belief that a very long-lived individual would become overwhelmed by boredom: they would run out of interest and novelty. This is by far the sillier objection, and there is absolutely no rational basis for it. Even a few moments of thought should convince you that there is far more to do and learn that you could achieve in a thousand life spans - and it's a little early in the game to be objecting to enhanced longevity on the basis that you can't think of what to do with life span number number 1001.

Considering boredom, futility, meaningless, and related matters, I noticed what appears to be an argument by induction in the article below. Mathemetical induction is a tool used in formal proofs wherein if you can prove that something is generally true for n and n+1 (where n is a natural number), and then show that it is true for 1, then you can conclude it must be true for all natural numbers. If it is true for 1, then it must be true for 1+1 = 2, and true for 2+1 = 3, and so on.

Life Extension Leads to Meaningless Days? NO!

Person X lives a fulfilling and meaningful life for X number of years before that life is terminated by a sudden, massive heart attack.Now, imagine another person whom we shall label (not too creatively) 'Person 2?. Person 2?s life follows the same general path as person 1 with one exception: It is one day longer than person 1?s was. Now ask yourself: Is there any reason to suppose that this day, let us assume it is aTuesday, strikes person 2 as being meaningless despite the fact that all Tuesdays (and indeed every other day in person 2?s past) seemed worth living?

OK, so now imagine yet another person who goes by the label of... yes, you guessed it, Person 3. You can probably also guess that Person 3 lives one day longer than person 2. Once again, I can think of no reason why, where we have two people who live meaningful lives but one lives one day longer, that extra day would not seem worth experiencing. Put another way: If possible would persons 2 and 1 rather not be dead on Wednesday (the last day for person 3) when Monday and all preceding days were worth experiencing? So far as I can see, the answer to that question is, 'yes'. There seems to be no reason why this argument should not hold for any number of hypothetical people, each one of which lives one day longer than the last.

Unfortunately you can't prove conjectures about aspects of human nature with induction (or not yet, at least). What you can do is use it, as above, to mount a more convincing argument. This one is somewhat akin to one of the standard lines in any debate between a person who is in favor of greatly extending healthy life versus someone who isn't.

Advocate: So you are fine with aging and dying?

Deathist: Yes.

Advocate: So you are fine with dying right now, done and finished?

Deathist: Well, no.

Advocate: Why would you think any differently ten days, or a hundred days, or decades from now, if you still had your health and vigor?

Deathist: Um...

There seems to be a strange disconnect in many people's minds, in which they are vigorously in favor of being alive right this instant or next week, but they nonetheless believe that their future self of years ahead will be of a different opinion and want to die. Now if you're on the downhill slope of aging, in great pain, and your body is falling apart, desiring a stopping point is not unreasonable. (With the best of present options for those in that position being cryonics). But in a world of rejuvenation therapies, in which older life is just as healthy, low-risk, and full of possibility as younger life, what mysterious thing is going make people want to die?

Source:
http://www.fightaging.org/archives/2013/06/arguing-by-induction-for-an-absence-of-boredom-in-an-ageless-greatly-extended-healthy-life.php

Young mammals, and occasionally adults, can regenerate lost fingertips. This seems like a good place to learn more about the mechanisms of regeneration, gaining insight into why it is that mammals cannot replicate the feats of limb and organ regeneration exhibited by species such as salamanders and zebrafish. More importantly, researchers hope to find that it is practical to adjust human biology to allow this sort of exceptional regeneration:

If a salamander loses its leg, it can grow a new one. Humans and other mammals are not so fortunate, but we can regenerate the tips of our digits, as long as enough of the nail remains. This was first shown some 40 years ago; today researchers finally reveal why it is that nails are necessary. Working with mice, [researchers] have identified a population of stem cells lying beneath the base of the nail that can orchestrate the restoration of a partially amputated digit. However, the cells can do so only if sufficient nail epithelium - the tissue that lies immediately below the nail - remains.

The process is limited compared with the regenerative powers of amphibians, but the two share many features, from the molecules that are involved to the fact that nerves are necessary. "I was amazed by the similarities. It suggests that we partly retain the regeneration mechanisms that operate in amphibians."

The nail base contains a small population of self-renewing stem cells, which sustain the nail's continuous growth. This ongoing growth depends on signals carried by the Wnt family of proteins - if this signalling pathway is disrupted, mouse nails cannot form. The team found that the same pathway is involved in the regeneration of lost mouse toe tips. After amputation, the Wnt pathway is activated in the epithelium underlying the remaining nail and attracts nerves to the area. Through a protein called FGF2, the nerves drive the growth of mesenchymal cells, which restore tissues such as bone, tendons and muscle. Within five weeks, the digit is good as new.

However, none of this can happen if the digit is amputated too far back, and too much nail epithelium is lost. In such cases, the Wnt pathway is never activated, the nerves do not extend and the other tissues cannot regenerate.

Link: http://www.nature.com/news/how-nails-regenerate-lost-fingertips-1.13192

Source:
http://www.fightaging.org/archives/2013/06/investigating-fingertip-regeneration-in-mammals.php