Friday, June 4, 2010

Do antiaging nutrients work? Part two by Jerry Brainum

As discussed in part one, the only possible means of life extension deemed plausible by most gerontologists, or scientists who study aging, is caloric restriction (CR). This involves an average reduction in daily caloric intake of about 30-40 percent. CR works quite well in short-lived species, such as mice. Mice on diets that have a reduced calorie content of 30% or more, along with supplemented nutrients that may be in short supply with such food restriction, live up to 50 percent longer than their normally eating littermates. But more importantly, they seem to be protected from nearly all degenerative disease, including cardiovascular disease, cancer, type-2 diabetes, and Alzheimer's disease. One theory of why CR works is that energy that is normally used to support growth and reproduction is instead shifted on a CR regime to mechanisms involving cellular survival. These would include such as aspects as increased heat shock protein production, and increased survival of cellular mitochondria.
     It's difficult to say whether CR would work as well in humans as it does in animals and insects, which are much more short-lived compared to humans. Studies with monkeys, a close biological relative of humans, have shown that the monkeys on a 30% CR regime for 10 years or more also show a lack of the usual fatal diseases mentioned earlier. Humans who follow CR regimes consume mostly vegetables, and the results of their medical tests are impressive. They show low risk factors for all degenerative diseases, although they also appear gaunt, often feel cold, show poor wound healing, and may be infertile. From a muscular perspective, they are in a relative catabolic state. I say "relative" because they show paradoxical effects in this area. Their muscle mitochondria is better preserved, which maintains muscle with age. Interestingly, the levels of one anabolic hormone in CR humans, IGF-1, is similar to that of people who eat normally. In animals on CR regimes, IGF-1 levels decline significantly.
      The reason that IGF-1 levels are maintained in CR humans is that they eat a good amount of protein, despite being on vegetarian diets. The levels of IGF-1 bear a direct relationship to both total caloric intake, as well as protein intake. But it turns out that a lack of protein may be the key to success in animals on CR regimes. It has to do with a protein synthesis signaling factor called mTOR that is stimulated by protein, or more specifically, amino acid intake. Animals that eat a lot of calories, but restrict protein intake, show the same benefits as CR in relation to life extension. mTor, which stands for "mammalian target of rapamycin," promotes cell growth, and diverts calories to be used for that purpose, rather than to maintain cellular longevity reactions. In fact, mTor seems to promote cancer, and drugs that interfere with Mtor activity appear to prevent cancer. Again, it relates to cell growth, and cancer is a process involving uncontrolled cell growth.
      Studies with rapamycin, an antibiotic that was discovered on Easter island, show that it extends life in mice. It does so by blocking Mtor, But rapamycin is also a potent immune suppressant, so using it in humans would likely result in a shortened lifespan due to aquiring a disease through lack of immune response. Another drug that also interferes with Mtor is metformin. Metformin is a popular drug used to treat insulin resistance and diabetes. Various studies show that it seems to prevent many types of cancer, including both lung and pancreatic cancers though blocking Mtor cell stimulation. The implications of all this are bad news for anyone interested in building muscle.
     Mtor plays a pivotal role in muscle protein synthesis reactions that result in increased muscle size and strength. The branched-chain amino acids provide most of their anabolic effects in muscle by interacting and promoting the activity of Mtor. The implications of the emerging studies show that consuming a high protein diet stimulates Mtor, which does good things for muscle building, but bad things for longevity. Other studies show that one amino acid in particular, methionine, may play a key role in longevity, since restricting it in animals leads to longevity in some species. But methionine is an essential amino acid, a major methyl donor. This means that it's involved in the synthesis of other nutrients, including creatine and choline. A lack of methionine can result in fatty liver, the first stage of liver failure. If the animal findings about Mtor and longevity prove true in humans, the best diet for longevity would involve a vegan diet with low to moderate protein intake. But attempting to build much muscle on such a diet would prove challenging, particularly if the diet also featured a CR design. Then the choice may come down to: do you want to live longer, or be more muscular?

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited

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