All energy production in the earliest primordial times was fermentative and anaerobic. These two nutrients eventually established the basis and driving force behind reproduction for all organisms, and, consequently, behind aging and life span.
The first living cells were prokaryotic in nature; each one was identical to the next, much like bacteria, lacking a nucleus and feeding anaerobically on sugars.
Later, development of an oxygen-based atmosphere allowed for evolution into eukaryotic cells (possessing a nucleus), which allowed for cellular differentiation into organs, eyes, skin, and other tissues, making higher organisms possible. The developing presence of oxygen—essentially among the first waste products of Earth's earliest life-forms—eventually allowed for the use of fat as a nutrient for the first time. Eukaryotic cells are fueled aerobically and use fatty acids and ketones for this purpose, just as most human and other mammalian cells do today. Fat is an aerobic nutrient and forms the basis of aerobic metabolism. Herein lies the dis- tinction between the two energy sources: aerobic and anaerobic forms.
One theory of how cancers develop involves the idea that an excessively fermentative, acidic, sugar-rich, and anaerobic environment (known to be friendly to cancer growth) somehow simulates our earliest primordial environment and stimulates the reversion of some cells to their primordial, prokaryotic state. Tumors are basically masses of undifferentiated, identical cells with a weak protein matrix that feed exclusively on sugars. In other words, when the environment is ripe—when the availability of sugar is high and a fermentative, acidic, and anaerobic environment is allowed to take hold—this primordial component of our genetic makeup is somehow triggered and stimulates cells into an unhealthy, abnormal, and exceedingly primitive form of cellular proliferation. Healthy cellular differentiation cannot occur in a fermentative environment. This certainly presents a plausible model for carcinogenesis as well as other unhealthy forms of cellular proliferation.
The development of an oxygen-based atmosphere eventually allowed for the use of fat as an important energy source. In the evolution of more-complex organisms such as mammals, it is fat that serves as the primary, most efficient source of fuel. Leptin, which is the key fat sensor in the body, then controls and regulates all our energy stores via the hypothalamus, which manages the signals given to every other hormone in the body.
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Evidence of the effects of caloric restriction in slowing aging and extending youth can be found in its abilities to prevent the immune dysfunctions of old age, improve DNA repair abilities, reduce damaging free-radical activity, lower glucose and insulin levels, maintain fertility at advanced ages, boost energy levels, increase protein synthesis, reduce the accumulation of damaged proteins, inhibit the inflammatory responses of aging, lower the levels of cholesterol and triglycerides in the blood, counteract neural degeneration, and prevent the age-related decline in the health-building hormone dehydroepiandrosterone (DHEA).
Caloric restriction also prevents or postpones the incidence of and reduces the severity of diseases such as cancer, kidney disease, and cardio-vascular disease (Masoro 2003).
It is also known today to be additionally important that adequate vitamins, minerals, and nutrients be supplied or added to caloric restriction approaches to avoid nutrient deficiencies. The idea is to limit calories, not nutrients (Nicolas et al. 1999). Therefore, nutrient density also plays a very important role.
Longevity enthusiasts who attempt to apply the earlier caloric restriction research by attempting to sustain themselves each day on a single kumquat and a tablespoon of oatmeal are gravely missing the point, to say nothing of living an unnecessarily stress-inducing, deprivation-oriented life. No such thing is necessary, nor is it really helping them arrive at their hoped-for objective. Recently popularized raw-food vegan diets can achieve temporary improvements by essentially down-regulating insulin and mTOR (and through such diets being generally detoxifying). The problem here is multifold, however. In addition to the fact that we as humans lack four stomachs and cud-chewing ruminant tendencies to maximize the use of plant-based foods to meet all our needs, such a diet ' completely fails to provide many essential animal-source nutrients needed, for long-term maintenance of our health, our brain, our nervous system, and our vitality. Without adequate fat to normalize leptin (among countless other things) or complete protein sources to allow for critical rebuild¬ing and maintenance, such dietary approaches ultimately do far more depletive harm than good in the long run.
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Modern studies of healthy human centenarians, those people who are one hundred years old and older, have revealed the presence of a certain class of genes that seem to be activated in these individuals. Called sirtuins, they have come to be known as our longevity genes. In mammals, one of these genes is referred to as SIRT-I (in worms, it is called SIR-2 In certain fortunate people who appear to age unusually gracefully and remain vital to extremely old age, the SIRT-1 gene just sort of seems to inherently activated, for unknown lucky reasons. This is why certain lived people can claim not to have taken particular care of their health and still seem to make it to very old age. [...] Recently, a nutrient found in red wine called resveratrol was shown to have the effect of activating this gene. It has also been clearly demonstrated that calorie restriction similarly activates these genes in all organisms and has all the same beneficial effects.
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The newly discovered genes are called SIRT-3 and SIRT-4. Like SIRT-1, they are part of the larger class of sirtuins. The newly discovered role of SIRT-3 and SIRT 4 confirmed the particular importance of mitochondria as vital for sustaining the health and longevity of a cell.
Mitochondria, cellular organs that are found in the cytoplasm, are often considered to be the cell's battery packs or energy-producing factories. When mitochondria become compromised by particular stressors, energy is drained out of a cell and its days are numbered. This, in turn, compromises our energy production, health, and metabolic efficiency. Sinclair and his colleagues discovered that SIRT-3 and SIRT-4 play a vital role in a longevity network that maintains the vitality of the mitochondria and keeps cells healthy when they would otherwise die. The most powerful method found of activating these life-saving and life-extending genes is caloric restriction.
When cells undergo caloric restriction, signals sent in through the cell membrane activate an enzyme called nicotinamide phosphoribosyl-transferase (NAMPT). As levels of NAMPT ramp up, a small molecule called nicotinamide adenine dinucleotide (NAD+) begins to amass in the mitochondria. This, in turn, causes the activity of enzymes created by the SIRT-3 and SIRT-4 genes—enzymes that live in the mitochondria—to increase as well. As a result, the mitochondria grow stronger, energy out¬put increases, and the cell's aging process slows down significantly.
In laboratory experiments, certain animal subjects have had their healthy life span extended by 30-60 percent—sometimes even by 300¬400 percent—using methods of optimized caloric restriction! The impli¬cations are staggering. The same basic mechanism seems to exist across all species studied, from yeast to even primates (like us).
But Why Does Caloric Restriction Work?
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Insulin in these simple life-forms has nothing to do with blood sugar regulation, but instead is entirely designed to regulate reproduction and actual life span. Subsequent research has confirmed this role of insulin across all species, including primates.
How much insulin we produce over the course of our lives controls how long we live! And it turns out, the less insulin we need, the better.
Studies looking at the effects of insulin levels on human health and longevity are emerging, and the picture is quite clear. One study showed that over a ten-year period, the risk of dying was almost twice as great for people with the highest insulin levels than for those with the lowest levels. The study authors stated that excess insulin, or hyperinsulinemia, associated with increased all-cause and cardiovascular mortality, independent of other risk factors (Dekker et al. 2005). High levels of serum insulin promote high blood pressure by impairing sodium balance. Prolonged exposure to excess insulin can severely compromise the vascular system. By acting as a catalyst in promoting cellular proliferation, excess insulin also increases the risk for and progression of certain cancers. High insulin levels promote the formation of beta-amyloid in brain cells and may contribute to the development of Alzheimer's disease. Overproduction of insulin even contributes to prostate enlargement by helping to promote the overgrowth of prostate cells. Insulin resistance, a by-product of chronic excess insulin production, is associated with the development of abdominal obesity and health problems such as atherosclerosis and impotence. Furthermore, insulin resistance and obesity are risk factors for type 2 diabetes mellitus. Hyperinsulinemia is, in fact, a predictive factor for type 2 diabetes mellitus.
It turns out that insulin is an extremely ancient molecule and exists in identical form in everything from yeast cells to humans. Far from its formerly perceived, limited role in nutrient storage or even blood sugar control (a trivial sideline for insulin), insulin is now being understood as something far more important and fundamental to the very underlying mechanisms of our health and longevity. In monitoring our energy availability, while leptin oversees the actual energy stores, it is insulin that switches on and off the extremely ancient mechanisms that allow us to outlive what our body thinks is an apparent famine.
That's the clue to as to how we beat Mother Nature at her own game. The down-regulation of insulin (and mTOR) triggers the up-regulation of repair and maintenance on a cellular level that allows us to remain healthy until food becomes more available and we can finally reproduce. Bingo.
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Research across the board has shown that long-lived individuals (animals and humans) share the following characteristics:
• low fasting insulin levels
• low fasting glucose levels
• optimally low leptin levels
• low triglyceride levels
• low percentage of visceral body fat
• lower body temperature
• reduced thyroid levels
Low thyroid levels, you say? Isn't that a bad thing?
The idea here is that a reduced caloric load, which results in the almost exclusive use of fat for fuel and optimal nutrient intake, improves metabolic efficiency. [...] In a human clinical study article titled "Clinical Experience of a Diet Designed to Reduce Aging," the authors remarked, "It has been stated that the reduction in T3 and body temperature could alter the aging process by reflecting a reducing metabolic rate, oxidative stress and systemic inflammation" (Rosedale et al. 2009).
{Description about a twenty-year study on the effects of caloric restriction on primates published on "Science". The primates were rhesus monkeys which are very similar to humans even in terms of diet.}
Twenty years later, only 63 percent of the monkeys that ate as much as they wanted were still alive. Thirty-seven percent of them had died from age-related causes. And the caloric-restriction group? Eighty-seven per-cent of them were still alive, and only 13 percent had died of age-related causes. Throughout their lives, the calorically restricted group maintained superior health and aging-related biomarkers in every area: brain health, metabolic health and rate, insulin sensitivity, and cardiovascular vitality. The monkeys in the caloric-restriction group enjoyed a threefold reduction in age-related disease! Also, they lost fat weight but maintained healthy levels of lean tissue mass. They also retained greater brain volume, which nor¬mally shrinks with age and glycation, but more than that, they retained superior cognitive function. The cardiovascular disease rate of the caloric-restriction group was fully half the rate of the control group. Forty percent of the monkeys in the control group developed diabetes or prediabetes. Not one single monkey in the calorically restricted group developed either.
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Another area of human longevity research getting a lot of publicity these days involves manipulating the length of something called a telom-ere. Telomeres are sequences of nucleic acids extending from the ends of chromosomes that act to maintain chromosomal integrity. Every time our cells divide, telomeres are shortened, leading to cellular damage and cellular death associated with aging. Shorter telomeres have been associated with significantly higher cancer incidence. In fact, a recent Italian study showed that people with shorter telomeres have ten times the cancer risk of those with longer telomeres (and those with short telomeres were twice as likely to die from cancer) (Armanios et al. 2009).
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Drug companies, of course, are looking for ways to enhance telomerase any way they can. In fact, look for other upcoming supplements and, possibly, life extension—related media¬tions claiming to do just this. What they won't tell you, however, is that caloric restriction also preserves and may even also reverse telomere length.
[If] you apply the caloric-restriction model in a way that does not leave you hungry, which is exactly what this book tells you how to do. Just follow the simple, most basic dietary guidelines outlined here to eat optimally well, and you will feel fully satisfied, live healthier and longer, and even save some real money along the way! Even while buying the best-quality produce, grass-fed meats, and wild-caught fish, you can find yourself saving considerable money on groceries. The basic guideline to remember is this: Greatly restrict or eliminate sugar and starch (preferably eliminating gluten completely); keep your protein intake adequate (roughly the RDA: 44-56 g per day or 0.8 g of protein/ kg of ideal body weight), amounting to a total of approximately 6 to 7 ounces of organic eggs, grass-fed, or wild-caught meat or seafood per day; eat as many fibrous, "aboveground," nonstarchy vegetables and greens as you like; and eat as much fat (from fattier cuts of meat or fish, nuts, seeds, avocados, coconut, butter or ghee, olives, olive oil, and other sources) as you need to satisfy your appetite. The bottom line here is that natural dietary fat is not at all our enemy and that, in the absence of dietary carbohydrate and with adequate protein, eating natural dietary fat can result in a far more satisfying, longer, and healthier life overall.
. I have also used grapeseed oil and like that as well, as long as it is the light colored one. The greenish grapeseed oil has a very strong taste. Have used olive oil and don't care for the taste.
