Can Antioxidants Prolong Life and Prevent Memory Loss?
Of Telomeres and Dementia
By Ed Winfield

Today it may be possible to affect directly the length of your telomeres, the tail-end strands of your chromosomes. These snippets of DNA have been discovered to harbor important genetic material. As we have learned in the past few years, each time a cell undergoes division, a portion of its chromosomes' telomeres is lost.1 And when the loss of this genetic material reaches a predetermined point, a program is initiated that causes the cell to destroy itself, ending its life through suicide.

New research indicates that the length of our telomeres may be related to our memory or cognitive function and that the shorter our telomeres when we are still young, the more likely it is that we will suffer dementia and the probable loss of memory long before we reach old age.2 As fortune would have it, the researchers found that the length of our telomeres is also related to the general state of our antioxidant defense system, which can be significantly bolstered through the wise use of antioxidant supplements. If our antioxidant system is enhanced, according to the researchers, we are likely to retard the age-related degeneration of telomeres. Thus not only memory, but life itself, may be prolonged.

At the Protestant Geriatric Center of Berlin, Dr. Thomas von Zglinicki and colleagues found a significant association between telomere length and vascular dementia, a type of brain damage caused by blood vessel disease. Of 186 subjects in the study - 149 of whom were 55-98 years old - the researchers found that 41 had probable or possible vascular dementia. It was found that the telomere lengths in the leukocytes (white blood cells) of these 41 subjects were shorter than those in age-matched control subjects, in cognitively competent subjects, and in subjects with Alzheimer's disease. By contrast, those subjects in the study with the longest telomeres were 100 times less likely to have vascular dementia than those with the shortest telomeres. Because telomeres generally get shorter with age, this finding is provocative.

Is there some way that telomere length can be maintained? Dr. von Zglinicki and colleagues argue that telomere length is a marker for a person's ability to withstand oxidative stress. It is a reflection of the damage to cells and their DNA caused by aging and associated stresses.

When the investigators examined the rate of telomere shortening, they found that it correlated neatly with the state of the cells' ability to resist oxidative damage. If a cell was more vulnerable to oxidative damage, telomeres shortened more rapidly. On the other hand, cells that had significant defenses and thus resisted this type of damage had a slower rate of telomere shortening.

After Alzheimer's disease, vascular dementia is the second leading cause of memory decline throughout the developed world. So these findings are quite important, and they suggest, thinks Dr. von Zglinicki, that long-term use of antioxidants might be helpful in inhibiting telomeric shortening. In light of his discovery, it seems plausible that life extension may be more dependent on comprehensive antioxidant protection than most researchers to date have been willing to believe.

Dr. von Zglinicki does not believe that any one antioxidant is the answer, but rather that a well-balanced, concerted front of antioxidants is required. He suggests that it would be valuable to monitor the cumulative effect of a long-term antioxidant program by measuring telomere length and correlating that to general health status.

In Japan at the Hiroshima Prefectural University School of BioSciences, research was conducted to determine whether a more oxidation-resistant ascorbate compound could inhibit telomere shortening.3 Using ascorbate-2-O-phosphate (Asc2P) on human vascular endothelial cells, the researchers succeeded in retarding age-dependent telomere shortening to 52-62% of the norm. Cellular lifespan was extended, and cell enlargement - an indication of cellular senescence - was prevented.

The experiment established that a 3.9-fold increase in intracellular ascorbate levels from the addition of Asc2P could significantly reduce telomere shortening, whether through diminishing oxidative damage or some more circuitous route. The researchers concluded that age-dependent telomere shortening can be decelerated by suppressing intracellular oxidative stress as well as by increasing telomerase activity (telomerase is an enzyme that protects telomeres).

Durk Pearson and Sandy Shaw have been using Asc2P in skin-care lotion since about 1992 because this form of vitamin C is known to increase vitamin C levels within cells more effectively than ordinary vitamin C, as well as being more stable in aqueous solution exposed to air. To that, the ability to slow the age-dependent telomere shortening in at least some cultured cells and increase their lifespan has been added.

It would appear that telomeres provide a key to switch human cells between mortality and immortality - between having a limited number of cell divisions to having a potentially unlimited replication capability. When the telomere-shortening "switch" is turned off, the number of cell divisions remaining is increased, and ultimately replicative senescence (aging) is defeated (see Figure 1). This age-related inability to continue cell division is caused, at least in part, by oxidative damage and is therefore a vindication of the free radical theory of aging.4

Figure 1. The telomeric theory of the "aging clock" holds that the length of the telomere determines both the age of the cell and the number of cell divisions that remain before the cell dies. Until recently, there was thought to be only one way that telomeric length could be preserved, i.e., through the action of the enzyme telomerase. Now, however, based significantly on the work of Dr. Thomas von Zglinicki, antioxidants are believed to provide another mechanism that can preserve telomeric length.

Aside from the effect of oxidative damage to telomeres, oxygen free radicals target mitochondria - the intracellular sources of energy production - and the resulting mitochondrial malfunction has long been suggested as the intracellular basis of aging.5 Adding more fuel to the fire, there is abundant evidence that free radical reactions lead to the formation of lipofuscin - a type of cellular refuse - which accumulates in cells and impedes their normal function.

It has long been thought that the loss of our cells' ability to replace themselves through division - i.e., the loss of replicative potential - is the principal determining factor of the maximum lifespan in different species, including our own.1 That may very well be true.

There is at least one agent native to our bodies that can, under certain circumstances, slow the loss of replicative potential: telomerase. This enzyme blocks the shortening process of telomeres, yet at present we do not know how this capacity might be usefully employed. Nevertheless, it is fascinating - and pregnant with significance - to have learned that oxidative stress may very well exercise a stong influence over telomere shortening, independent of telomerase activity. And reducing oxidative damage to a significant degree is something we can definitely accomplish through the use of supplemental antioxidants.

The moral of this tail (pun intended) is to keep it long and take lots of antioxidants, especially a well-designed multivitamin/multimineral/multiantioxidant formulation.


  1. Saretzki G, von Zglinicki T. Replicative senescence as a model of aging: the role of oxidative stress and telomere shortening - an overview. Z Gerontol Geriatr 1999 Apr;32(2):69-75.
  2. von Zglinicki T, Serra V, Lorenz M, Saretzki G, Lenzen-Grossimlighaus R, Gessner R, Risch A, Steinhagen-Thiessen E. Short telomeres in patients with vascular dementia: an indicator of low antioxidative capacity and a possible risk factor? Lab Invest 2000 Nov;80(11):1739-47.
  3. Furumoto K, Inoue E, Nagao N, Hiyama E, Miwa N. Age-dependent telomere shortening is slowed down by enrichment of intracellular vitamin C via suppression of oxidative stress. Life Sci 1998;63(11):935-48.
  4. von Zglinicki T, Saretzki G, Docke W, Lotze C. Mild hyperoxia shortens telomeres and inhibits proliferation of fibroblasts: a model for senescence? Exp Cell Res 1995 Sep;220(1):186-93.
  5. von Zglinicki T, Brunk UT. Intracellular interactions under oxidative stress and aging: a hypothesis. Gerontol 1993 Jul-Aug;26(4):215-20.

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