Mounting research suggests that carnosine has anti-aging potential due to its unique abilities to protect and extends the functional life of the body’s key building blocks, i.e., cells, proteins, DNA and lipids. Carnosine may be fairly called an agent of longlivety. When that agent is safe, naturally present in the body and in food, and has demonstrated prolongation of life span in animals and cultured human cells, it is fundamental to any life extension program.

How does carnosine prolong life span? We do not yet know the full answer, but carnosine’s properties may point up key mechanisms of tissue and cell aging, as well as the anti-aging measures that counteract them.

Do carnosine’s rejuvenating effects on cells extend to the entire organism? Similar anti-senescence effects have now been demonstrated in mice. A Russian study tested the effect of carnosine on life span and indicators of senescence in senescence-accelerated mice. Half the mice were given carnosine in their drinking water starting at two months of age. Carnosine extended the life span of the treated mice by 20% on average, compared to the mice not fed carnosine.

Carnosine did not alter the 15 month maximum life span of the senescence-accelerated mice strain, but it did significantly raise the number of mice surviving to old age. The mice given carnosine were about twice as likely to reach the ”ripe old age” of 12 months as untreated mice. It also improved indicators of senescence measured at the ”old age” of ten months.

Carnosine distinctly improved the appearance of the aged mice, whose coat fullness and colour remained much closer to that of young animals. Significantly more carnosine-treated mice had glossy coats (44% vs. 5%), while significantly fewer had skin ulcers (14% vs. 36%). However, carnosine did not affect the loss or texture of hair. Carnosine significantly reduced the rates of spinal lordokyphosis (spinal curvature) and periopthalmic lesions, but did not affect corneal opacities.

The sharpest contrast between the treated and untreated mice was seen in their behaviour. Only 9% of the untreated mice displayed normal behavioural reactivity, compared to 58% of the carnosine treated mice.

The researchers also measured biochemical indicators associated with brain aging. Brain membranes of the carnosine treated mice had significantly lower levels of MDA (malondialdehyde), a highly toxic product of membrane lipid oxidation. MAO-B (monoamine oxidase B) activity was 44% lower in the carnosine-treated mice, indicating maintenance of dopamine metabolism. Glutamate binding to its cellular receptors nearly doubled in the carnosine treated group. Since glutamate is the main excitatory neurotransmitter, this may explain the more normal behavioural reactivity of the carnosine-fed mice.

This study showed that carnosine significantly improved most measures of appearance, physiological health, behaviour, and brain biochemistry—as well as extended life span—in senescence-accelerated mice. The researchers therefore conclude that ”carnosine-treated animals can be characterized as more resistant to the development of features of aging” (Boldyrev AA et al., 1999).

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