Early old age without vitamins and minerals

January 15, 2007

Without sufficient vitamins and minerals, old age comes too early. This is because the organism ignores the future when resources are limited. If it needs to, it does what is best for the present.

Keep an eye on Bruce Ames, the American biochemist and professor from Berkeley University. He is the man behind the worldwide renown Ames test, a quick method of establishing whether or not substances in food and the environment are cancerous, which is to say whether or not they cause mutation. He is also the author of uncountable numbers of scientific articles and has proposed some very important hypothesises in the field of nutrition. In 1999 President Clinton handed him the “American Nobel prise,” the National Medal of Science, for his contributions. At an age of 78, Ames is still extremely active.

Ames is among those who insist that there is, in uncountable ways, relationships between shortages of vitamins and minerals and cancer, mutations, and aging. But earlier than others, he also sought to explain these relationships bio chemically. It is highly important that we turn to long term studies involving thousands of people for these biomechanical mechanisms to be tested. When Ames invented his mutation test, he simplified detection of cancerous substances with one blow. Long term animal studies became unnecessary. Now he also wants to make long term human studies unnecessary in the study of nutritional deprivation.

The relationship between nutritional deprivation and cancer has been documented with extensive references in last November’s Proceedings of the National Academy of Science. For example, mutations, cancer, and early aging are seen early in association with magnesium deficiency. Vitamin D deficiency is believed to be the reason for 29% of all cancer in men. There is a relationship between deficiency of n-3 fatty acids from fish oil and malignant melanoma (skin caner), between selenium deficiency and cancer, and between potassium deficiency and heart disease. Lack of the B vitamin folic acid, vitamin B12, thiamine, and niacin also are associated with mutations and cancer. Even iron deficiency leads to mutations.

If all of this, and more, is an expression of a causal relationship, then nutrient deficiency should naturally be combated. Deficiency is, as we all know, extremely widespread. We receive large amounts of carbohydrates and fats, but few vitamins and minerals. One in every two Americans receive less magnesium than recommended, 90% receive too little vitamin E, 30% receive too little vitamin C, and so on… and so on.

Mutations can wait
If these many nutrient deficiencies are really the reasons for cancer, aging, and mutation, than what is the explanation? According to Ames, cells, and therefore the organs that they compose, prioritise when they temporarily or permanently lack something. A cell which as a result of a deficiency cannot accomplish all of its tasks, choose, for example, to prioritise the production of energy over the reparation of mutations. Correspondingly, scarce resources cause the organism to prioritise the production of red blood cells over the production of white blood cells, which is to say over immune system maintenance. The principle behind this is the same as when blood is directed to vital organs, such as the heart and lung, after blood loss. The organism must survive now, even though the price is weakening in the long term.

Prioritising is nonetheless only one reason for mutation and aging. A more direct connection is that nutrient deficiencies cause problems for the cells’ energy factories, the mitochondria. They are weakened by vitamin B (biotin) deficiency, pantoic acid deficiency, riboflavin deficiency, B6 deficiency, among others. Without these nutrients, the mitochondria cannot produce the enzymes necessary for energy production. Without energy nothing works in the cell, including the defence against mutation

Ames and others are now trying to find out how much nutrients we need to hold the number of mutations to a minimum and to keep the our mitochondria intact. This is not easy, but it is easier than undertaking expensive, and in many ways, uncertain, decade(s) long population studies. Also, who would finance such expensive studies?

In recent years we have seen a number of studies of supplementary vitamins E and C, selenium, beta-carotene, and vitamin A. Many of these were poorly done, more have been misinterpreted, and some have been proven. Few have become wiser. Is this the way forward? Or has Ames again shown a better shortcut?

While we wait for better knowledge, we should, according to Ames, take reasonable supplements of vitamins and minerals. Everything points towards that this is wise. And there are no risks.

By: Niels Hertz, MD

Reference:
Ames B. Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. PNAS 2006; 103:17589-94.

www.pnas.org

Vitamins against aging

January 9, 2006

The need for many vitamins increases with age. A deficiency can be compared to radiation exposure, which causes mutations, decreased energy production, cancer, and age-related changes in the body, according to one of the World’s leading nutrition scientists.

When Bruce Ames was 70, President Clinton surprised him with U.S.A.’s highest scientific recognition, The National Medal of Science, for his research in nutrition, cancer, and aging.

Today he is 77, but still an almost incomprehensibility active researcher and professor at the famous Berkeley University in California. He is also the man behind the world renown Ames test, a lightning fast method to find out whether a specific chemical can cause mutations, and thereby cancer.

This introduction shows that Ames it a researcher to be listen to, and therefore we have decided to discuss one of Ames’s latest and most important scientific articles.

The article was published in a periodical for the European organization of molecular biologists (EMBO reports). It describes how it is possible to reduce the tendency for cancer and aging by taking more than the recommended dose of diverse vitamins and other important substances.

How does it do this? In his study Ames found that deficiencies of vitamins C, E, B6, and B12 as well as of folic acid and zinc can have exactly the same effect on cells as radioactivity. This means that such deficiency causes mutations, for example as a result of breakage of the chromosomes.

Folic acid deficiency causes such breakage because it leads to the introduction of a wrong substance (uracil) in uncountable places along the DNA molecules. These mutations affect the cells the same way as a virus affects a computer. In the worst cases, the system beaks down.

But deficiency does not only lead to mutations. Another result is weakening of the energy producing mitochondria, otherwise known as the cells’ power plants. In order for the mitochondria to function, they must have access to certain enzymes, which can be regarded as the power plant’s machinery. The enzymes work together so that the product from one “machine” is processed further by the next in a chain of reactions which result in the conversation of oxygen and hydrogen into water, and the production of energy. But where do the enzymes come from? Without the necessary building blocks they do not exist at all!

Ames has among other things proven that deficiencies of zinc or the B vitamins biotin and pantothenic acid weaken the fourth reaction in this chain of reactions. They are the building blocks of the “machines” which carry out this step in the process. Not only is the production of energy reduced by such deficiency, but oxygen is also insufficiently converted to water. As a result the mitochondria empty free radicals into the surrounding cell where they can cause mutations, cancer, and weakness.

More Energy
Why does Ames believe that it is necessary to take more vitamins than recommended? This is as a result of the third and last point in his thought process. It regards the consequence of the uncountable mutations which by the aforementioned methods unavoidably arise during ones life. These mutations cause the cells to produce less effective enzymes that bind less effectively to the vitamins which they need to aid their function. Ames maintains that this poor binding can be overcome simply by increasing the amount of vitamins. This makes the enzymes work again.

A particular problem in this regard is the weakening of the mitochondria which occurs with age. Without energy, nothing functions within the cell and the degeneration of the mitochondria is central to what we call aging. But Ames emphasizes that it is possible to make old rats faster by giving them supplements of the two vitamin-like substances lipoic acid and carnitine.

Both substances are important intermediates for energy production in the mitochondria. With age they bind poorly to the enzymes which cause the mitochondria to function poorly. But this poor binding can also be overcome with supplements. As well as making the rats faster it was possible to measure that their mitochondria once again functioned normally. Clinically such treatment has been able to result in improvement in people with mild Alzheimer’s.

The unique thing about Ames is that his arguments are based on biochemistry. This means that he refers to elementary chemical reactions which are demonstrable in the organism. Many others base their views of more or less uncertain clinical trails, sometimes without knowledge of the biochemistry behind them. It might not be coincidental that The Nobel Prise in medicine typically is given to a biochemist.

By: Vitality Council

References:
1. Bruce N Ames. Increasing longevity by tuning up metabolism. EMBO reports 2005;6:S20- S23.
2. Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: Partial reversal by feeding acetyl-L-carnitine and/or R-a-lipoic acid. J. Liu et al. Proc Natl Acad Sci USA.2002;99:2356-61.
3. B N Ames et al. High-dose vitamins stimulate variant enzymes with decreased coenzyme-binding affinity (increased Km): Relevance to genetic diseases and polymorphisms. Am J Clin Nutr 2002;75:616-58.