AGING THEORY: CAUSE 3: TELOMERE SHORTENING
TELOMERES AND OUR GENETIC CLOCK: WILL WE ENJOY LIFE AT 300:?
2022- Vitamin C (AREDs+Mito-C) preserves telomere length – The telomere length (TL) has increasingly been used as a biomarker of human aging because it has been shown to predict the chances of survival and longevity. Oxidative stress is presumed to be a major cause of telomere shortening, Our findings supported the idea of a possible correlation between the TL and biomarkers of oxidative stress in aging.
2014- I have read that the combination of green tea and blueberries, which provide EGCG and quercetin, help maintain longer telomeres. EGCG and quercetin can also be obtained twice a day by taking Mito-C, a supplement I developed.
Notes added March, 2011 – Telomere shortening is key control in declining human health. Nutrition investigator’s former student who is an expert in telomere research sent a commentary with a recent article in Nature (17 Feb 2011 pg 359-65) showing how telomere shortening is responsible for chronic disease in humans. Many factors have been shown in recent years to influence the length of telomeres. With the Nobel Prize this year going to discoveries related to telomeres, I investigated what helped maintain telomere length. A key site from Science is here. And a recent Science article (Dec. 2010) showing lengthening mouse telomeres caused them to grown 80% younger!
In the 2009 AGE meeting, it was explained that people who take vitamin C and E supplements and multivitamins are likely to have longer telomeres. One can take Mito-C and AREDs to get the vitamin C and E required for this.
Other bad habits – Cigarette smokers, obese and sedentary individuals, and those with unhealthy habits in general often exhibit not only increases in the systemic burden of oxidative stress and inflammation but also shortened telomeres. One discovery connected with this year’s Nobel Prize is the women who live with chronic stress, like a parent with Alzheimer’s or a child with a serious disability, are likely to have shortened telomeres.
Simply search for telomeres to find many more recent reports of how to maintain your telomere length.
Notes added Oct, 2009 – Telomere sequence is TTAGGG. Telomeres are longer in indivduals getting vitamin C and E in the diet, and in people taking multivitamins. See editorial in AJCN . Leukocyte telomere length: the telomere tale continues, Abraham Aviv, Vol. 89, No. 6, 1721-1722, June 2009.
From Science 18 Sept 2009, vol. 235, pg 1475 “Local Connections Matter”, reports on how telomeres work via telomeric RNA, called TERRA. It binds to factors called Shelterins, that shelter the DNA from damage and allow it to replicate. When telomeres get short from aging, this protection of DNA diminishes leading to cancer, and the ability of DNA to replicate stops so cells can no longer divide and replace other failing cells.
Original essay: Is it really possible that the human lifespan could be extended indefinitely? The above quotation, from the Journal of the American Medical Association, indicates that our futures are very uncertain. On September 19-23, 2003, at Queen’s College in Cambridge, England, there is a conference, “Strategies for Engineered Negligible Senscence: Reasons to View Genuine Control of Aging as Forseeable”. One keynote speaker is Dr. Bruce Ames, who designed the product Juvenon.
When research into aging was in its infancy, Dr. Leonard Hayflick observed that human cells grown in tissue culture would only divide a certain number of times, a phenomonon nicknamed “the Hayflick limit”. After that fixed maximum, the cells became senescent, that is they lost the ability to divide further, and eventually died. Further studies showed that this limit applied to cells from a variety of animals. Particularly striking was that it did not matter the length of time the cells were maintained between cell divisions, all that mattered was how many times they divided. For human cells, after about 70 cell divisions, the cells stopped dividing. For chicken cells, the Hayflick Limit was about 56. For each animal, there was a specific number of cell divisions possible before senescence occurred. The only exception to the rule was cancer cells. They go on dividing as long as there is sufficient medium, that is nutrition, and space. These cancer cells appear to be “immortal”, that is they have an infinite capacity to go on dividing. Hayflick’s research was the first clear indication that there was a “biological clock” in our cells which determines the maximum life span, a clock which is broken in cancer cells.
The wear and tear process of aging, caused primarily by free radical damage which is discussed in the next chapter, causes us to get age-associated diseases like cancer, which end most lives before they succumb simply to old age. But there are genetic programs which control the limit of human longevity to around 120 years. Around 1986, the genetic basis of the Hayflick limit was confirmed in part by Dr.Howard Cooke in Edinburgh, who found that telomeres were shorter in differentiated cells like skin and muscle than germ cells. We now understand that this limit is imposed by small repeating sequences of DNA on the ends of our chromosomes known as telomeres. A short sequence of the GCAT bases which repeats over and over at the end of each chromosome, usually a repeat of the pattern TTAGGG, this telomere cap helps to protect the genetic information from being damaged, and probably regulates the way that information is expressed. Every cell in your body started as a fertilized egg with a long set of telomeres. Every time one of those cells divides, a short stretch of the chromosome ends, the telomeres, do not replicate and thus get shorter. Eventually, the telomeres become so short that the genetic information in the chromosomes is no longer protected properly, and the cell loses its ability to divide. At this point, you are destined to die.
The enzyme which is capable of restoring telomeres to their original length is known as telomerase. It is produced under two conditions. First, a newly fertilized egg produces telomerase, so that each newly fertilized egg starts out with a complete set of telomeres, capable of dividing 70 times as it develops into a new generation. Second, cancer cells produce telomerase, which explains why cancer cells can multiply indefinitely.
Astounding progress has been made since the discovery of telomeres. Outstanding medical scientists, like Michael Fossel, M.D., Ph.D., in his book, “Reversing Human Aging” (Quill, New York, 1996), suggest that within a decade or so we will be able to restore our telomeres to a length that maintains our youthful physiology. If this becomes possible, it is likely that we can literally grow young again, restoring our physiological age perhaps back to our twenties. For those who find this prospect exciting, which about half the people I have spoken with do, there is all the more reason to try to maintain excellent health and prevent irreversible damage to our bodies.
2004 Note: AGE meeting: Hayflick Limit is becoming controversial, because telomerase is now being found in non-cancerous cells, e.g. stem cells. Thus potential for regeneration without cancer exists, but how to do this remains unclear. Senescent cells are harmful to aging tissue, and senescence is telomere-driven, according to Prof. Faragher from the Univ. of Brighton.
INTERESTING REFERENCES
For information on extending human lifespan, click here.
Banks, DA, and Fossel, M., “Telomeres, cancer, and aging”, JAMA 278: 1345-48 (1997)
“Population projections of the aging global society and its fiscal and social impact have depended on assumptions regarding the human life span. Until now, the assumption that the maximum human life span is fixed has been justified…We may soon be able to extend the maximum human life span and postpone or prevent the onset of diseases associated with aging…An appropriate uncertainty regarding the human life span undermines any attempt to accurately predict health costs in the next century.”
Eun-Soo Han and Morgen Hickey
Microarray Evaluation of Dietary Restriction
J. Nutr. 2005 135: 1343-1346.
A comparison of altered genes by DR in mice, rats, pigs, monkeys, yeast, and flies showed no common gene altered by DR among different species. It seems that individual genes altered in the expression by DR were constrained within species.
