The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 11 No. 1 • January 2008

Nutrients That Inhibit Age-Associated Reduction in Telomere Length

The ends of chromosomes are capped by structures called telomeres. With each cell division, telomeres become shorter due to the loss of the most distal part of the lagging strand, which cannot be replicated.1 It was realized in the early 1990s that the reduction in telomere length with each cell division could act as a biological clock that could measure how many times a cell had divided and could eventually cause replicative senescence (the Hayflick limit), in which cells were alive but could no longer divide.

However, “cells in a senescent culture display a broad distribution of replicative histories: some cells become permanently arrested after very few cell divisions, whereas others might go through many more divisions than indicated by the Hayflick limit of the population as a whole.”1 It has been discovered that there are many mild stressors that can accelerate telomere shortening and reduce replicative lifespan independently of how many times the cell has divided. Such stressors include mild chronic oxidative stress, chronic hyperoxia (high levels of oxygen), treatment with homocysteine, tert-butylhydroperoxide, or hydrogen peroxide, or acute treatment with a variety of DNA-damaging agents that cause damage short of long-lasting growth arrest.1 The authors of this paper conclude that “rates of cellular ageing and telomere-shortening in bulk culture depend on the balance between oxidative stress and antioxidative defense.” Hence, “The rate of telomere shortening per cell division is not an innate constant. Rather, it changes from cell to cell, possibly from one division cycle to the next, as a function of (external) oxidative stress and (internal) antioxidant defense.”

Another paper2 reported similar findings in a study of human and sheep fibroblast cell cultures exposed to a wide range of oxidant (peroxide) stress conditions. They found a continuous exponential correlation between cellular oxidative stress levels and telomere shortening rates, independent of donor age, species, and cell strain.

Longer Leukocyte Telomere Lengths with Higher Serum Vitamin D Concentrations in Women

We have written often of the various old and new health benefits of vitamin D, including reducing the risks of a number of different cancers. Decreased vitamin D has been associated with increased risks of developing autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and type 1 diabetes, and administration of vitamin D has been shown to attenuate the activity of these diseases.3

Now, excitingly, a paper reports that higher vitamin D serum levels in women are associated with longer leukocyte (a type of white blood cell) telomere length in women.3 (Although we know of no mechanism whereby men would have a different response, nevertheless a similar study needs to be done in men to be certain, as there are sometimes surprising biological differences between the genders.)

The new paper reports that shorter leukocyte telomeres are found in individuals with chronic inflammation, because the inflammatory response results in an increased turnover (replication) of leukocytes. Vascular diseases and autoimmune diseases, as well as cigarette smoking and obesity, have also been associated with shorter leukocyte telomeres. They report that a recent randomized case-control analysis revealed that shortened leukocyte telomeres were an independent risk factor for coronary heart disease (CHD), not surprisingly, as inflammation is a risk factor for CHD and could also be the cause of the shorter telomeres.

In this study,3 the LTL (leukocyte telomere length) in the lowest tertile of 25-hydroxyvitamin D was 6.97; in the middle tertile, LTL was 7.02; and in the highest tertile of 25-hydroxyvitamin D, LTL was 7.08. The authors also report, “Vitamin D supplement information was available on a subset of the study population (n = 700). Vitamin D supplement users had longer LTLs, despite adjustment for age, season of vitamin D measurement, menopausal status, use of hormone replacement therapy, and physical activity, than did nonusers. Mean adjusted LTL in subjects who did not use vitamin D supplements was 6.95 kb, whereas that of current users of vitamin D supplements was 7.06 kb; however, this difference was not statistically significant . . .” at <0.06. (<0.05 would be significant, so this result just barely fails to reach significance.) It is also useful to consider that most vitamin D users receive their vitamin D as part of a one-per-day-type multivitamin supplement, where the typical dose would be 400 IU of vitamin D. This is way too low. On a summer day, 15 minutes’ exposure of the body to the sun would result in the skin’s manufacture of about 18,000 IU of vitamin D. We take our own vitamin D formulation, SunPower Vitamin D™, 2000 IU/capsule, one capsule four times a day.

Carnosine Reduces Telomere Shortening

Carnosine is a dipeptide (alanine-histidine) that has interesting antisenescence effects, having been shown to increase the lifespan (both in terms of population doublings and in chronological terms) of human diploid fibroblasts grown in culture containing 20-mM carnosine.4 Carnosine is also a powerful antiglycating agent, protecting proteins from becoming chemically bound to sugars circulating in the bloodstream. Carnosine is one of the ingredients in our new Durk & Sandy’s AGEless™, a formulation that inhibits the formation of advanced glycation endproducts (AGEs). Increased amounts of AGEs are associated with aging,5 cancer,6 and cardiovascular disease.7 Shorter telomere lengths has been associated with heart disease.8

A recent paper7 reports that human fetal lung fibroblasts grown in culture containing 20-mM carnosine “exhibited a slower telomere shortening rate and extended lifespan in population doublings. When kept in a long-term nonproliferating state, they accumulated much less damages in the telomeric DNA when cultured in the presence of carnosine.” We recommend taking 1 gram of carnosine a day in three or (preferably) four divided doses. This is the amount contained in the recommended dosage of Durk & Sandy’s AGEless.

Telomere Shortening Repressed by Phosphorylated Alpha-Tocopherol

Phosphorylated alpha-tocopherol (alpha-tocopheryl phosphate) is a water-soluble form of vitamin E that is more bioavailable than the fat-soluble alpha-tocopherol. A recent study9 reports that the cellular lifespan of neonatal human brain microvascular endotheliocytes, estimated from population doublings, was 2.4-fold longer when continuously exposed to 150-μM alpha-tocopheryl phosphate. Ascorbate 2-phosphate at the same concentration increased cellular lifespan 1.3-fold. Telomeric lengths were markedly shortened at a rate of 291 base pairs per population doubling for the control cells, while telomeric lengths were maintained at 165 base pairs per population doubling in cells cultured with alpha-tocopheryl phosphate. The telomeric lengths in cells cultured only in ascorbate 2-phosphate had a slight reduction in the telomere shortening rate, down to 227 base pairs per population doubling, as compared to the controls.


  1. von Zglinicki. Oxidative stress shortens telomeres. Trends Biochem Sci 27(7):339-44 (2002).
  2. Richter and von Zglinicki. A continuous correlation between oxidative stress and telomere shortening in fibroblasts. Exp Gerontol 42:1039-42 (2007).
  3. Richards et al. Higher serum vitamin D concentrations are associated with longer leukocyte length in women. Am J Clin Nutr 86:1420-5 (2007).
  4. McFarland and Holliday. Retardation of the senescence of cultured human diploid fibroblasts by carnosine. Exp Cell Res 212:167-75 (1994).
  5. Snow et al. Advanced glycation end-product accumulation and associated protein modification in type II skeletal muscle with aging. J Gerontol A Biol Sci Med Sci 62A(11):1204-10 (2007).
  6. Tesarova et al. Carbonyl and oxidative stress in patients with breast cancer—is there a relation to the stage of the disease? Neoplasma 54:219-24 (2007). “In conclusion, breast cancer patients had an early increase of AGEs (marker of the carbonyl stress) followed by further increase of AGEs and elevation of AOPP (marker of oxidative stress) in patients with progressive disease.”
  7. Zhang et al. Glycated proteins stimulate reactive oxygen species production in cardiac myocytes. Circulation 113:1235-43 (2006).
  8. Starr et al. Association between telomere length and heart disease in a narrow age cohort of older people. Exp Gerontol 42:571-3 (2007). The authors note that the findings in this study “. . . adds to the growing body of evidence for an association between telomere shortening and ischemic heart disease. Telomere shortening in peripheral blood leukocytes is a promising index of ischemic disease risk in older people . . .”
  9. Tanaka et al. Age-dependent telomere shortening is repressed by phosphorylated alpha-tocopherol together with cellular longevity and intracellular oxidative-stress reduction in human brain microvascular endotheliocytes. J Cell Biochem 102:689-703 (2007).

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