test your knowledge
How the world got lost on
the road to an anti-aging pill
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May 17, 2010: by Bill Sardi
A news story published in The London Times says so-called “Methuselah” genes have been found which increase the chance of living 100 years and beyond. An anti-aging pill is just 2 years away from being tested, says the report.
The report goes on to say that “the secret of longevity probably lies in have the right ‘suite’ of genes.” “Centenarians (those individuals who do live 100 years or more) have a high chance of having several such genes embedded in their DNA.” One researcher is quoted to say that “Longevity is strongly genetic and inherited.”
Can only those individuals fortunate enough to carry certain genes expect to live long? Might as well eat, drink and be merry, and live out the number of days your genes have destined you to live?
Eline Slagboom of Leiden University says “People who live to a great age metabolize fats and glucose differently, their skin ages more slowly and they have lower prevalence of heart disease, diabetes and hypertension. These factors are all under strong genetic control, so we see the same features in the children of very old people.”
However, it’s not quite like that. Every human has the same set of genes. A gene may be mutated, that is one of the nucleotide proteins on the DNA ladder may be missing or substituted for, but we have the same set of ~25,000 genes. You have the same sets of genes as groups of people who are known to live long.
Genes are not static. They are influenced by their environment – such as solar radiation, temperature, food or lack of food. Genes that are “switched on” make proteins (called gene expression) and genes that are “switched off” are not making proteins (called gene silencing).
Professor Slagboom along with Nir Barzilai and colleagues, report that two genes, ADIPOQ and CETP, are found in about 10% of young people, but about 20-30% of centenarians. Let’s examine these two genes a bit further.
ADIPOQ is a gene responsible for the production of a protein-based hormone, adiponectin, that is exclusively secreted by fat cells (adipocytes) that regulates the metabolism of lipids and glucose; and the CETP gene, or cholesterol ester transfer protein gene, which is linked with the production of HDL (high-density lipoprotein) “good” cholesterol.
Whatever protective effect the ADIPOQ gene affords, for unknown reasons it vanishes when blood pressure rises over 140/90.
There are reasons why resveratrol doesn’t need to activate the CETP gene. For example, resveratrol facilitates the efflux (outflow) of cholesterol from cells, rather than inhibit the production of cholesterol in the liver as statin drugs do. Resveratrol doesn’t limit the amount of cholesterol that is produced in the liver, it just inhibits cholesterol from sticking to artery walls. The cholesterol number remains the same, but the plaque doesn’t form.
Geneticists often don’t explain why twins differ in their rate of aging, even though they have the same set of genes and childhood environment. The concordance of hair graying, balding and need for reading glasses is not particularly high between twins. The difference in longevity between twins was found to be 6.65 years in one study.
Biologists do not provide adequate answers for why biological aging does not begin till full physical growth is achieved, and then slowly progresses through middle age, with the rate of aging slowing in late life. Only the overmineralization theory of aging explains these three “speeds” of human aging.
The overmineralization theory of aging asserts that major minerals, such as calcium, iron and copper, are being shuttled to make new bone, red blood cells and connective tissue during childhood growth. Once growth ceases, there is a slight excess of these minerals leading to progressive calcification and rusting. Women escape this fate for a time, donating minerals to their offspring and losing iron and copper in their monthly menstrual flow.
Let’s see how this theory of aging holds up in regard to the ADIPOQ gene.
First, among markers that foretell diabetes, both adiponectin and ferritin (iron storage protein) are among 4 of 31 highly-predictable factors. Another study reveals that a high ferritin (iron storage) count in blood serum strongly correlates with lower production of adiponectin. This is confirmed in other studies. The higher the iron count the lower the adiponectin production. Healthy metabolism of sugars and fats would be compromised.
Higher ferritin levels have been correlated with progressive aging. The progressive accumulation and storage of iron is associated with accelerated rates of aging.
What about copper and aging? Copper is what resveratrol chelates (kee-lay-ts) or binds to. Copper overload can switch on disease genes and copper removal (chelation) can switch them off.
Reuters published another news headline which says “New Way Found To Boost Good Cholesterol in Mice.” But cholesterol only represents a small portion (3%) of arterial plaque. Most arterial plaque is comprised of calcium. Drugs that boost so-called “good” HDL cholesterol are a misdirection. Pfizer drug found this out as its highly touted HDL cholesterol-boosting drug fizzled. But we are greeted with the headline again and again that a pill to boost HDL cholesterol would prolong human life.
First, there already is such a pill that boosts HDL cholesterol – niacin, and it hasn’t been shown to significantly reduce coronary artery disease mortality rates. Second, HDL cholesterol appears to be nothing more than a marker of arterial calcification, which is the primary cause of arterial disease.
So much for banking on news reports to find an anti-aging pill. Most news reports are driven by commercial interests, usually pharmaceutical companies.