Tag: elderly

An end to the old weakling

Claus Hancke

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

References:
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

Deficiency in B-vitamin Causes Dementia

Claus Hancke

April 18, 2005

According to one American study, folic acid weakens the memory of the elderly. According to another study, the opposite happens. Nearly all studies, however, indirectly indicate that folic acid prevents both arteriosclerosis and dementia.

It is a well-known fact that the B-vitamin folic acid prevents congenital neural tube defects. However, it can also lower the blood’s content of homocysteine; a biproduct in human metabolism that promotes atherosclerosis, among other things. Having an increased level of homocysteine is just as dangerous as cholesterol: Up to 40% of all individuals with premature atherosclerosis have increased blood levels of homocysteine.

The fact that homocysteine also damages the brain is indicated by more than 20 different studies. It has been found with almost unerring certainty that demented old people have more homocysteine in their blood than others and that the ones who score highest on memory tests are the ones with the least homocysteine in their blood. This is a clear argument for taking folic acid.

However, completely unexpectedly, a fly in the ointment has now appeared. A study at Rush University in Chicago has shown that the exact opposite might be the case. If you are elderly and you get more than the typical 0.4mg. of folic acid a day, your memory will decline more rapidly.

A total of 3,718 trial subjects over 65 years of age were followed for five to six years after having reported their eating habits. They were then mentally tested three times during the course of the 5 – 6 years. The results were the same whether they got folic acid from their diet or from dietary supplements: In the people taking folic acid, memory declined more rapidly than in the others.

Are these results the result of a coincidence? Anyhow, it does make you wonder that the 20% who got the most folic acid (0.7 mg. a day) did far better on the mental tests than the rest. Granted, their memory deteriorated more rapidly, but they obviously had a better memory to begin with. Why was that so, if folic acid is actually harmful?

In addition to this, doctors from the UCLA in February 2005 published results stating the exact opposite. Among 499 well-functioning 70 – 79 year-olds, most folic acid was found in the blood of the ones who had the best memory. And equally importantly: Seven years later, they were in better posession of all their faculties.

No explanation
What is true, then? If the truth lies in the Chicago study, it might be based on the co-operation between vitamin B12 and folic acid. Both vitamins reduce blood levels of homocysteine and the major task of both of them is to produce small, chemical units – which only contain a single carbon atom – for building other molecules.

Folic acid delivers its units to vitamin B12 which are then further delivered to – homocysteine. In this way, homocysteine is neutralized and is transformed into a harmless amino acid and the blood level of homocysteine will drop.

Whether you lack vitamin B12, folic acid, or both, the transport of the single-carbon units will be complicated. In all three cases, the result will be a specific type of anaemia (pernicious anaemia) which is characterized by the red blood cells being abnormally large.

However, the symptoms in vitamin B12 deficiency and folic acid deficiency are not quite similar. In folic acid deficiency, neuritis – i.e. nerve damage – will not occur. In vitamin B12 deficiency, it will. The anaemia in vitamin B12 deficiency can be removed by taking folic acid, but the neuritis cannot. Vitamin B12 has an affect on nervous tissue that folic acid cannot imitate.

In up to 30% of all elderly people, vitamin B12 deficiency can be demonstrated. Imagine large amounts of folic acid enhancing the B12 deficiency in the nervous system by blocking the small amounts of vitamin B12 with single-carbon compounds. This could correlate to another finding in the Chicago study: Memory declined by 25% less in the ones with the largest consumption of vitamin B12.

The leader of the study, Martha Clare Morris, believes that folic acid might mask the very common vitamin B12 deficiency in the elderly. This is more or less the same thing. In both cases, the consequence should be that the elderly get more vitamin B12 and not less folic acid which can have a protective effect in other areas.

This is the message – that is if you do not choose to believe that the new finding is a coincidence and that the truth is the exact opposite – which is actually also quite likely!

For the time being, however, Morris’ conclusion is simple: “We don’t know yet what is going on,” she says.

Up to every third elderly person may have demonstrable signs of mild vitamin B12 deficiency. If the results of the Chicago study are truthful, elderly persons possibly should not reduce their folic acid intake but rather focus on getting enough vitamin B12.

By: Vitality Council

References:
1. Morris MC et al. Dietary folate and vitamin B12 and cognitive decline among community-dwelling older persons. Arch Neurol 2005;62:641-5
2. Austin RC et al. Role of hyperhomocysteinemia in endothelial dysfunction and atherthrombotic disease. Cell Death and Differentiation 2004;11:S56-S64
3. Morris MS. Homocysteine and Alzheimers disease. Lancet Neurol 2003;2:425-8
4. Kado DM et al. Homocysteine versus the vitamins folate, B6, and B12 as predictors of cognitive function and decline in older high-functioning adults: Mac Arthur Studies of Successfull Aging. Am J Med 2005;118:161-7
5. Garcia A et al. Homocysteine and cognitive function in elderly people. CMAJ, Oct. 12, 2004; 171 (8).

archneur.ama-assn.org
www.nature.com/cdd/index.html
www.thelancet.com
www.sciencedirect.com
www.cmaj.ca
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