Carnosine

Carnosine: New Gun Against Aging
Michael Colgan

The answers to aging will not be found in ever more esoteric drugs or hormones, but rather in understanding basic chemical processes in the human body. Previously, I have explained how the chemical s-adenosylmethionine, formed from the amino acid methionine and ATP, is critical for all methylation reactions. I also showed its normal function is inhibited by the increase in homocysteine now endemic in Western Society. Without normal s-adenosylmethionine function - a basic chemical process that holds your body together, all the vitamins, minerals, hormones, exercise and other fountains of youth will fail utterly to inhibit aging.1

Many other chemicals, such as vitamin C and vitamin E, have certain specific actions, in their case antioxidant actions, which combat aging. But s-adenosylmethionine has general action which benefits virtually all bodily functions. Discovering these general basic chemical effects and how to use them is the new frontier for longevity.

Another basic chemical is carnosine (not carnitine). Carnosine is a dipeptide, composed of beta-alanine and l-histidine which occurs naturally throughout your body, especially in the brain, the muscles and the lenses of your eyes. More obscure in function than s-adenosylmethionine, for 50 years researchers have searched for carnosine's main function. We know it is involved in many processes, such as buffering of acidity in muscles, transport of minerals, and anti-oxidation.2 But until now a major role for carnosine, especially its role in preventing aging, went undiscovered.

A Death Rattle For Hayflick

The pivotal studies began in the 1990s. They involved the addition of carnosine to cell cultures of human fibroblasts. Thirty years ago Leonard Hayflick showed that human cells in culture can divide only a set number of times before they die, a phenomenon widely accepted as the Hayflick Limit, which seemed strong evidence of an inbuilt clock of human aging. But Hayflick and others did not realize that their culture medium, used to feed the cells, was lacking some nutrients, or contained them in the wrong proportions for optimal lifespan.

One such nutrient is carnosine. Robin Holliday of the CSIRO Division of Molecular Science in Sydney, Australia, and other researchers, first reported in 1994 that addition of specific amounts of carnosine to human cell cultures, dramatically prolonged the ability of cells to continue to divide beyond the Hayflick Limit.3 Lifespan of cultures was increased by as much as 50%.

This finding prompted a flurry of new studies on carnosine, because no one had any idea how this simple basic chemical could cause such a large and reliable anti-aging effect. Carnosine's known antioxidant and acid buffering functions were certainly insufficient. It was boosting the cultures by a much more powerful mechanism.

Teams of molecular biologists at Kings College, London and CSIRO, Sydney now seem to be getting to the nub of it. To see where the science is going, we have to dip into another cause of aging - glycation. Despite all the rah-rah books and articles that try to pin aging down to a single cause, such as a biological clock, or free radicals, or accumulating toxins, regular readers will understand that their bodies degenerate under multiple influences. One major influence first proposed by Bjorksten in 1968, is the formation of cross-links that bind proteins together into stiff pathological clumps. We know now that this cross-linking is caused primarily by what are called reactive aldehydes.

These nasty little buggers come from multiple sources. To mention a few, there are reducing sugars such as ketose and aldose, and end-products of free radical damage, such as malondialdehyde (MDA), which results from oxidation damage to fats in your cell membranes and elsewhere. Unchecked, these toxins accumulate irreversibly over many years, gradually changing into what are called advanced glycosylation end-products (AGEs). (I wonder what genius idled his brain coining that one)? Up to now scientists have been at a loss to combat glycosylation directly. Carnosine may be just the winning ticket.

Carnosine Inhibits Glycosylation

From 1993-1998, Hipkiss and colleagues at Kings College, London have conducted a series of studies showing that carnosine prevents protein cross-linking, neutralizes reactive aldehydes, and acts in human cells as a natural anti-glycation agent.4,5 They have also shown that carnosine can protect cells from the otherwise certain damage caused by AGEs.5

That's not all. You may recall from some of my earlier articles, or from other reading, how one way that your brain degenerates with aging is by accumulation of what are called amyloid peptides in the hippocampus. When this accumulation reaches a certain level, the result is called Alzheimer's or premature senility. Oxidative damage by free radicals and glycation damage are both involved.6

Hipkiss and colleagues have now shown that carnosine can protect cultured cells against amyloid peptides.5 The implications for aging brains are tremendous. Carnosine is a virtually non-toxic normal basic component of your body. It's cheap too, or should I say still is cheap, until this research becomes generally public and greed sets in.

Reactive aldehydes, including reducing sugars, are also known to be critical causes of progression of numerous degenerative diseases, including diabetes, arthritis, and atherosclerosis. And if carnosine proves to prevent the progression of senility in vivo, we might get not only longer life but also saner life. As a mandatory supplement for our politicians, carnosine just might help them think beyond their bellies their peckers, and their bank accounts.

Carnosine Protects Your Eyes

Recent research shows that carnosine helps to prevent cataract formation in the eye.7,8 It can be administered topically to eye in the form of N-acetyl-L-carnosine. This form moves easily into the water-soluble and lipid containing parts of your eye. Once in the eye it helps to prevent DNA breakdown caused by UV radiation and enhances DNA repair.9

In two separate recent studies the researchers applied a one percent solution of N-acetyl-carnosine to the affected eyes of cataract patients twice a day.10 Only patients with mild cataracts were part of these studies. A matched control group received placebo drops and another small matched group received no drops at all. The first study lasted six months, the second 24 months. 90% of eyes treated with N-acetyl-carnosine showed improvements in visual acuity ranging from 7% to 100%. Glare sensitivity improved from 27% to 100% in 88.9% of cases. Examination of eyes revealed fewer areas of lens opacity. No worsening of vision was found in any of the subjects.

Adding carnosine as part of your anti-aging regime is a good idea.

References:

Colgan M. Protect Your Prostate. Vancouver, B.C. Apple Publishing, 1999.
Quinn PR, et al. Carnosine: its properties, functions and potential therapeutic applications. Mol Aspects Med, 1992;13:379-444.
McFarland GA, Holliday R. Retardation of the senescence of cultured human fibroblasts by carnosine. Exp Cell Res, 1994;212:167-175.
Hipkiss AR, et al. Non-enzymatic glycosylation of the dipeptide carnosine: a potential anti-protein cross-linking agent. FEBS Lett, 1995;371:81-85.
Hipkiss AR, et al. Pluripotent protective effects of carnosine, a naturally occurring dipeptide. Ann NY Acad Sci, 1998;854:37-53.
Smith MA, et al. Oxidative damage in Alzheimer's disease. Nature, 1996;382:120-121.
Quinn PJ, et al. Carnosine: its properties, functions and potential therapeutic applications. Mol Aspects Med, 1992;13(5):379-444.
Specht S, et al. Continuing damage to rat retinal DNA during darkness following light exposure. Photochem Photobiol, 2000;71(5):559-566.
Lou MF. Thiol regulation in the lens. J Ocul Pharmacol Ther, 2000;16(2):137-148.
Rabizhayev M, et al. Efficacy of N-acetylcarnosine in the treatment of cataracts. Drugs Research & Development, 2002;3(2):87-103.