An end to the old weakling

July 14, 2006

The deficiency of an important antioxidant enzyme seems to be the most important reason that the elderly develop weak muscles. This paves the way for interesting perspectives.

The most striking sign of aging is that muscle strength is reduced and movement becomes slower. Even the most persistent exerciser cannot avoid it. The weakening of the muscles is the most important reason that old people become frail.

Why does this happen? We know that with age more and more signs of oxidation by free radicals can be found in muscles and other tissue. But is this why the muscles weaken?

A group of 12 researchers from both Texas and Stanford University in U.S.A. have undertaken an unusual and very detailed study which indicates that this is precisely the reason. According to them, the age related muscle weakness is due to strain from free oxygen radicals. This can shine light on possible ways to slow this process and maintain mobility longer.

Aging mice are a reliable model for age related muscle weakness in humans. But the American study was just possible because they had a special genetically manipulated mouse which lacked the ability to produce SOD (superoxide dismutase), a very important anti-oxidative enzyme.

In order to understand this it is necessary to know that free radicals are broken down in a chain reaction. SOD is necessary in the first step. In this step “active oxygen” (superoxide anions) is converted to less dangerous hydrogen peroxide. Without SOD this occurs very slowly, but with SOD this occurs at breakneck speed. In the next step hydrogen peroxide, which is also dangerous, is converted to harmless water. This occurs with the help of a selenium rich enzyme. This is one of the best known reasons that selenium, which we get too little of, is necessary for life.

Vital SOD
Back to SOD. It is also necessary to know that there are many forms of SOD. One of them is found in the mitochondria, which are the small power plants of the cells where cell metabolism occurs. If a mouse lacks SOD here, it dies after no more than three weeks. The power plants are destroyed by the free radicals which they produce. Another form of SOD is found outside the mitochondria, but still inside the cells. If the mice lack this type they can survive, but their lifespan is shortened by about 30%.

The researchers worked with mice which lacked the latter SOD form. They saw that the mice already started to develop weakened muscles while young. When the mice were 29 months old, they lacked half of their muscle mass in their hindquarters, whereas normal mice of the same age retain all of their youthful muscle. The so called fast type II muscle fibres were the most affected. The mice were left with slower type I fibres. Heart muscle remained undamaged.

The strength and speed of the muscles were not the only things affected. The mice also became less curious and less willing to engage in exhausting exercises like running in a mouse wheel. When they become old, they shook slightly in their weakened muscles.

It is hard to contest that this damage was caused by oxygen radicals. SOD has no other function other than being an antioxidant. As always it can be added that more research is necessary. This was only a study on mice. But if the results can be transferred to humans it can be argued that it is beneficial to increase the body’s production of SOD. SOD production is decreased with age.

Because SOD is an enzyme, which is to say a protein, it cannot be eaten without being destroyed in the stomach unless given as a special preparation. In combination with other antioxidants and possibly vitamin D (but that’s another story) the effect is supposedly more pronounced. This is not certain, but it is interesting.

By: Vitality Council

1. Muller, Florian L et al. Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy. Free Radical Biology & Medicine 2006;40:1993-2004
2. Jackson Malcolm J. Lack of CuZnSOD activity: A pointer to the mechanisms underlying age-related loss of muscle function, a commentary on “Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy”. Free Radical Biology & Medicine 2006;40:1900-01

Perhaps Prostate Cancer may be a Rarity in the Future

April 1, 2005

Every forth man lives with a highly increased risk of getting cancer of the prostate, the next most frequent cause to cancer deaths in men. It does not have to be like that. Exactly these exposed men could easily decrease their risk to a tenth.

Researchers from Harvard University in Boston have published a landmark study. It strongly suggests that most cases of cancer in the prostate are due to lack of balance in the body’s defense against free oxygen radicals. And most importantly: This balance can be restored with antioxidants – especially with selenium, but also vitamin E and the red dye of the tomatoes, lycopene. Prostate cancer can thus become a rare disease.

The imbalance occurs especially in men who get too little selenium and who, for hereditary reasons, have a particularly effective antioxidant enzyme (manganese-containing SOD) in their mitochondria. The mitochondria are the cells’ internal energy factories, which are worn down by free oxygen radicals with age. This wear and tear, parenthetically noted, is believed to be a very significant cause of aging and age-related diseases.

One would therefore think that it was an advantage to have a particularly effective antioxidant enzyme in one’s mitochondria. But very often it is not. The SOD enzyme transforms free oxygen radicals into the less risky hydrogen peroxide, but this creates a new problem: the hydrogen peroxide must also be removed, since it also causes harmful oxygenation. The removal requires an enzyme (glutathione peroxidase), the quantity of which depends on the supply of selenium.

The more free oxygen radicals (e.g. from smoking) that need to be neutralized and the more efficient the SOD enzyme is, the more harmful hydrogen peroxide accumulates and the greater the need for selenium.

Balance in things
The Harvard study is part of a study of approx. 15,000 American doctors who have been followed since 1982. Around 1990, 275 of them had developed serious prostate cancer, and it was those who were primarily found interesting.

By: Vitality Council

1. Haojie Li et al. : Manganese superoxide dismutase polymorphism, prediagnostic antioxidant status, and risk of clinical significant prostate cancer. Cancer Res. 2005;65:2498-2504.
2. Woodson et al. Manganese superoxide dismutase (MnSOD) polymorphism, α-tocopherol supplementation and prostate cancer risk in the α-Tocopherol, β-Carotene Cancer Prevention Study. Cancer Causes Control 2003;14:513-8
3. Niels Hertz. Selen – et livsvigtigt spormineral. Forlaget Ny Videnskab 2002.;jsessionid=2sf53q49osdn1.victoria