Carnosine: the new anti-aging
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Alzheimer's Donation
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Marios Kyriazis MD
Although carnosine (also known as L-carnosine) has been known for about a century, its antiaging properties have only been extensively studied during the past few years. A recent literature review revealed over 780 published studies on carnosine, mainly by Russian and Japanese researchers. However, more widespread interest in this natural nontoxic product has only recently been increased, fuelled by dramatic Australian and British discoveries about its antiaging actions (1). to order
Carnosine (B-alanyl-L-histidine) is a naturally-occurring di-peptide (a combination of two amino acids), found in muscle, brain and other innervated animal and human tissues. It is formed by a process involving the enzyme carnosine-synthetase which bonds the amino acids alinine and histidine. This process occurs mainly in muscles and brain. It is kept in equilibrium by the carnisinases which are enzymes specifically aimed at inactivating carnosine in the tissues or in the blood.
There are several other related dipeptides such as carcinine, anserrine, homocarnosine and ophidine, all of which are naturally-occurring. These are believed to be buffering agents, helping to maintain the homeostatic equilibrium (2).
High concentrations of carnosine are present in long-lived cells (such as in neuronal tissues). The concentration of carnosine in muscles correlates with maximum lifespan, a fact that makes it a promising bio-marker of aging. It is high in actively contracting muscles and low in cases of muscular disease such as Duchennes's muscular dystrophy. Its concentration in mammalian muscles possibly decreases with age, a fact which strengthens the case for supplementation.
In cases of cataract in animals, carnosine concentration in the lens was found to be low. The lower the concentration of carnosine, the higher the severity of cataract. Rabbits fed on a high cholesterol diet, were found to be well protected against atherosclerosis and cataract if given carnosine supplements. In another experiment, dogs were also found to be protected against cataract if given carnosine supplements (2).
Amyloid Protection
In experiments, treatment with carnosine was found to reduce or completely prevent cell damage caused by beta amyloid (9), the substance found in the brain of Alzheimer's disease patients. Beta amyloid can interact with certain RAGE receptors causing damage to the nerves and arteries of the brain. Carnosine blocks and inactivates beta amyloid, so it protects neural tissues against diseases such as dementia.
There have been some concerns regarding carnosine's ability to form lipofuscin (the age pigment commonly found in the aging brain and in other tissues). Lipofuscin is merely a sign that other deleterious reactions have already taken place. For example; free radicals and toxic aldehydes may react with valuable proteins as described above, and cause damage, leaving lipofuscin as a left-over product. (Ed.-it may be advisable to take a lipofuscin supplement such as DMAE or acetyl-L-carnitine while on a carnosine program). One way to save the protein molecule is to use carnosine instead. Carnosine actively and swiftly binds to aldehydes before these are able to cause any damage. The end-result of this reaction may also be inactive lipofuscin compounds.
In this case, lipofuscin is formed not by wasting valuable protein material but by using sacrificial carnosine, leaving the proteins free to function properly. Lipofuscin, however formed, is thought to be generally inactive to normally everyday situations. High amounts of free radicals and toxin in the organism are best inactivated by using supplementary carnosine than tissue protein. Of course, it would be best to reduce the exposure to too many free radicals in the first place. This can be achieved for example, by avoiding pollution, cigarette smoking, sedentary life, and unsuitable nutrition.
.
Alzheimer's Donation
Donate Online Now
.
Marios Kyriazis MD
Although carnosine (also known as L-carnosine) has been known for about a century, its antiaging properties have only been extensively studied during the past few years. A recent literature review revealed over 780 published studies on carnosine, mainly by Russian and Japanese researchers. However, more widespread interest in this natural nontoxic product has only recently been increased, fuelled by dramatic Australian and British discoveries about its antiaging actions (1). to order
Carnosine (B-alanyl-L-histidine) is a naturally-occurring di-peptide (a combination of two amino acids), found in muscle, brain and other innervated animal and human tissues. It is formed by a process involving the enzyme carnosine-synthetase which bonds the amino acids alinine and histidine. This process occurs mainly in muscles and brain. It is kept in equilibrium by the carnisinases which are enzymes specifically aimed at inactivating carnosine in the tissues or in the blood.
There are several other related dipeptides such as carcinine, anserrine, homocarnosine and ophidine, all of which are naturally-occurring. These are believed to be buffering agents, helping to maintain the homeostatic equilibrium (2).
High concentrations of carnosine are present in long-lived cells (such as in neuronal tissues). The concentration of carnosine in muscles correlates with maximum lifespan, a fact that makes it a promising bio-marker of aging. It is high in actively contracting muscles and low in cases of muscular disease such as Duchennes's muscular dystrophy. Its concentration in mammalian muscles possibly decreases with age, a fact which strengthens the case for supplementation.
In cases of cataract in animals, carnosine concentration in the lens was found to be low. The lower the concentration of carnosine, the higher the severity of cataract. Rabbits fed on a high cholesterol diet, were found to be well protected against atherosclerosis and cataract if given carnosine supplements. In another experiment, dogs were also found to be protected against cataract if given carnosine supplements (2).
Amyloid Protection
In experiments, treatment with carnosine was found to reduce or completely prevent cell damage caused by beta amyloid (9), the substance found in the brain of Alzheimer's disease patients. Beta amyloid can interact with certain RAGE receptors causing damage to the nerves and arteries of the brain. Carnosine blocks and inactivates beta amyloid, so it protects neural tissues against diseases such as dementia.
There have been some concerns regarding carnosine's ability to form lipofuscin (the age pigment commonly found in the aging brain and in other tissues). Lipofuscin is merely a sign that other deleterious reactions have already taken place. For example; free radicals and toxic aldehydes may react with valuable proteins as described above, and cause damage, leaving lipofuscin as a left-over product. (Ed.-it may be advisable to take a lipofuscin supplement such as DMAE or acetyl-L-carnitine while on a carnosine program). One way to save the protein molecule is to use carnosine instead. Carnosine actively and swiftly binds to aldehydes before these are able to cause any damage. The end-result of this reaction may also be inactive lipofuscin compounds.
In this case, lipofuscin is formed not by wasting valuable protein material but by using sacrificial carnosine, leaving the proteins free to function properly. Lipofuscin, however formed, is thought to be generally inactive to normally everyday situations. High amounts of free radicals and toxin in the organism are best inactivated by using supplementary carnosine than tissue protein. Of course, it would be best to reduce the exposure to too many free radicals in the first place. This can be achieved for example, by avoiding pollution, cigarette smoking, sedentary life, and unsuitable nutrition.
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