Marks Daily Apple
Serving up health and fitness insights (daily, of course) with a side of irreverence.
30 May

The Tall Tail of Telomeres

For years now, it’s been said that telomeres – the tips of your chromosomes – are the key to cancer and aging. The shorter they are, the worse off you are – so the story goes. But what do we really know about them? Can the length of your telomeres help predict how long you’ll live? Could telomere research unlock a modern fountain of youth? Could humans one day live to be hundreds of years old?

Dr. Ron Rosedale of DrRosedale.com and The Rosedale Diet is here to answer some of these questions in this special guest post. In it he will introduce you to these little bits of genetic sequences, and provide his expert commentary on the state of telomere science. It will get somewhat technical in parts, but it’s well worth the read.

Now, Dr. Rosedale…

Summary – The Good, the Bad, and the Ugly

The Good: With considerably more research in the control of telomere length specific to different issues, it may be a new and powerful therapeutic tool to improve health.

The Bad: It is not likely a modality to extend maximal lifespan. It is far from the fountain of youth.

The Ugly: Without proper and exact knowledge of when and where to control telomere length, it will likely greatly increase one’s risk of cancer. In other words, it may very well increase healthspan as it reduces lifespan.

Introduction

Can the length of very simple, short genetic sequences at the tips of chromosomes called telomeres determine how healthy you are and how fast you will age? This has become a popular idea in paleo blogs and in the lay world of “anti-aging medicine”, especially now that telomere length (TL) can be relatively easily measured.

First, let’s examine very briefly the history of that idea. In 1961 Leonard Hayflick discovered that cells in a petri dish could only divide a limited number of times before cell division would cease permanently. This famously became known as the “Hayflick limit”. 10 years later Olovnikov, a Russian researcher, linked the tails of chromosomes to this cell division arrest. It was found that the enzymes that duplicate the DNA of chromosomes cannot continue this duplication all the way to the ends of linear chromosomes. If cells were to divide without telomeres, with each cell division they would lose a chunk of critical and functional DNA. The telomeres act as sacrificial lambs for DNA duplication. They are repeating nucleotide segments (TTAGGG) of relatively meaningless segments of chromosomes such that the loss of a small chunk of these when cells divide is genetically harmless… up to a point. If a cell divides too much, and its telomeres become too short, at best it can no longer divide. Worse, genetic harm befalls that cell. A process is initiated within the cell causing it to self-destruct (called apoptosis). Later, it was found that a natural enzyme that some cells manufacture called telomerase is capable of lengthening telomeres and potentially immortalizing that cell. The finding that telomeres shorten with increasing age has led to the theory that telomeres are at least a biomarker of aging, if not at least partially causative of the damage associated with aging (called senescence). It was, and still is in some circles, thought that increasing telomere length slows, if not reverses, aging. The telomere theory of aging was born. Should it continue to live, or die a peaceful apoptotic death as shortened telomeres themselves are apt to cause?

A full discourse on telomeres and the biology of aging would consume an excessive amount of all of our already telomere challenged lives. I will instead focus on telomeres as a potential biomarker and/or “anti-aging” therapy and the deeper meaning of this.

First, let’s get our terms straight. What is mean by “anti-aging”. The word itself is controversial. In the more scientific, biology of aging community where researchers are genetically manipulating specific (i.e. insulin) metabolic pathways and extending lifespan a hundred or more percent in some animals, that word has a negative connotation. To them, it conjures up images of modern day snake oil salesmen promising longevity treatments such as growth hormone therapy, that if anything, might likely shorten lifespan. To them, a slowing down of the typical aging process results in a lengthening of maximal lifespan as opposed to average lifespan. The two are quite different. The maximum human life span (that has been well-documented) is considered to be 122 years that Jean Calment, a French woman lived before dying in 1997. The average lifespan in the United States is roughly 78 years. If one greatly increased the health of the general population, one might increase average lifespan to be hypothetically 85 years. However, if no one still lived over 122 years, the maximal known human lifespan would continue to remain unchanged.

A treatment such as lengthening telomeres might well improve some, and possibly many, symptoms of aging and even the average or median lifespan, while leaving maximum lifespan unchanged…or perhaps even shortening it. It would not and should not then be considered an “anti-aging” treatment though possibly a good therapeutic modality.

On the other hand, biology of aging experts such as a friend of mine, Andrzej Bartke, past president of the American Aging Association, are able to extend the maximum lifespan in laboratory animals such as mice…a lot. He is the last recipient of one of the most prestigious and lucrative awards in aging research, the Methuselah Prize. He did this by genetically suppressing the growth hormone receptor in a strain of mouse such that it lived about twice as long as usual; the equivalent of a human living to be approximately 180 years old. In the published study that won the prize he states, “We propose that mechanisms linking GH [growth hormone] deficiency and GH resistance with delayed aging include reduced hepatic synthesis of insulin-­like growth factor 1 (IGF­-1), reduced secretion of insulin, increased hepatic sensitivity to insulin actions, reduced plasma glucose…An important role of IGF­1 and insulin in the control of mammalian longevity is consistent with the well­-documented actions of homologous signaling pathways in invertebrates.” (Life extension in the dwarf mouse; Curr Top Dev Biol. 2004;63). I mention this also, since a similarly hyped and very popular “anti-aging” treatment is growth hormone therapy, whereby growth hormone is regularly injected with supposed rejuvenating properties…exactly opposite to what was done to win the coveted Methuselah Prize… Caveat emptor.

Many so-called experts on health and longevity talk a lot about increasing telomere length as proof of efficacy of some sort of diet or other health modality. Let’s look at that statement. What do they mean by increasing their telomeres? They have about 15 trillion cells. Did they increase the telomere length of all chromosomes in all cells? Were they all measured? Was a representative sample measured? Is telomere length even indicative of health, or aging? Is it even a biomarker of aging, and if so, is that relevant?

One of several major problems with all this; less than 1% of a person’s cells have the enzyme telomerase and thus are even capable of increasing their chromosome’s telomere length. The other 99% are incapable of doing so. What about neurons, and heart cells that typically do not divide and where their telomeres do not shorten with age? The large majority of liver and kidney cells can’t lengthen telomeres, etc., etc. Perhaps the 1% that can are the most critical. They include white blood cells (WBCs) and many stem cells. We will examine that a bit more later.

Is it even good to increase telomere length? Maybe not. 90% of cancer cells do it. The fact that telomeres shorten may actually allow us to live longer, as it may reduce the risk of cancer. The good news is that the telomeres in almost all the cells other than WBCs and stem cells do not increase, for if they did, dying of cancer would be all but certain.

The chromosomes of nearly all multicellular life are linear; they have a beginning and an end. As such, for these cells, telomeres are essential to life. The exception are bacteria whose chromosomes are circular. They do not have a beginning or an end and thus telomeres are a moot point. Thus, there are no telomeric restrictions on bacterial reproduction. They continue to reproduce as often and as fast as they can; like cancer, that seems to be their singular goal. The purpose of linear chromosomes and telomeres is often thought to be secondary to our evolution from single celled bacteria to large, complex, multicellular individuals such that their now linear chromosomes with telomeres prevent cells from easily reverting back to their ancestral bacterial ways, i.e. the singular purpose of reproduction, that in multicellular life is cancer. It is a must to continually lengthen telomeres to lift the restriction on cell division if a cell hopes to stay a cancer cell.

Another major problem with the telomere theory of aging; if anything there is a negative correlation between telomere length and lifespan of different species. For instance, mice have much longer telomeres than humans but live a small fraction as long.

However, numerous studies have shown a correlation within a particular species between telomere length and length of life. This has therefore been used as strong evidence that length is a good biomarker of aging within a particular species and even that telomere attrition causes aging itself. Hopefully they mean the damage associated with aging. It is unlikely that you would not be a day older tomorrow.

A major mistake made so frequently in medicine, but rarely in other sciences, is the confusion and interchange between correlation and cause. An example is the consistent reference to cholesterol being a cause of heart disease, when in fact it is an association, and even a weak one at that. An entire industry and economy has been built over that “mistake”. I digress; that is a story for another day (or you can read on the web what I have already said about that long ago).

Getting wrinkles is far more correlated, and is therefore a far better biomarker for aging than telomere length, however undergoing a dermabrasion is not likely to extend lifespan. Once again, it is science 101 to not confuse correlation with cause. It could very well be, and in fact is likely, that reduced telomere length is a byproduct of the cell damage and turnover associated with aging, rather than a prime cause of it, though it likely does have some adverse repercussions especially to the immune system and possibly stem cells.

How about current laboratory testing for telomere length? It merely requires a tube of blood since one of the very few cell types that is easily accessible and where telomerase is present such that telomere length can increase are white blood cells. Is the test meaningful? Probably not very. The rate of telomere attrition, the rate of decrease in telomere length that may be more important than absolute length, will increase with increased cellular damage and turnover such as that caused by oxidation, free radical damage, glycation, and inflammation. In other words, all that a higher rate of telomere shortening of any kind might indicate is an increased rate of cellular damage, but it doesn’t tell you what is causing the damage. Glucose perhaps?

Many, including myself, believe that all shortening of WBC telomere length in particular reflects, is the state of inflammation. There are many other much simpler and less expensive, albeit less glamorous markers for this such as a C-reactive protein or even the sedimentation rate. Furthermore, both a healthy, though at the time less active immune system, and an overly stressed or suppressed immune system might, at least theoretically, lead to less telomere attrition due to less cellular proliferation.

Though the rate of white blood cell TL shortening has been shown to decrease and TL may even increase with certain changes in lifestyle such as exercise and diet (that might just reflect improved immune response), TL also has been shown to oscillate even if you don’t do anything; not change your diet, nor exercise, take antioxidants, or think positively about your TL.

However, the biggest problem in measuring TL in WBC’s is that there are many different telomeres of different lengths in many different kinds of cells with differing rates of attrition. An increase in white blood cell TL or reduced rate of shortening does not necessarily reflect a change in other telomeres, especially from other cell types. For instance, in cells that don’t divide, such as heart and nerve cells, TL is somewhat meaningless. Telomere length even varies depending on the kind of white blood cells.

Robust evidence also shows that it is not the length of telomeres, or even the rate of telomere reduction with age that matters, but rather that telomeres must get to a critically short length for adverse genetic repercussions to take place. Measuring WBC TL only measures average WBC telomere length and not the number of critically short telomeres.

For all of the above reasons, I feel that current measurement of WBC TL is not a very good biomarker of aging and is virtually meaningless as an important independent indicator of the rate of aging.

What about the other major cell type that produces telomerase and is capable of increasing telomere length? What about measuring stem cell TL? This is done, but currently only in research laboratories and generally only in animals. Not very many people would volunteer for heart biopsies, for instance. A jilted lover might volunteer their ex perhaps. However, stem cell TL is actually where the rubber meets the road. Stem cells are very important as is their preservation. They are certainly capable of regenerating many tissues, including those not producing telomerase. Unfortunately, WBC TL does not necessarily reflect stem cell TL, nor does it reflect telomere attrition, especially since there are so many different types of stem cells from so many different types of tissue with so many different rates of cellular turnover and damage. I discuss this more below when I show excerpts from some studies that are quite revealing.

Telomere length is correlated with rate of cellular replication, and cellular replication is increased with increasing mTOR, IGF-I and inflammation. Therefore, it very well could be that the correlation between telomere length and longevity is only just that, a correlation, and not a cause, and the underlying mechanism of aging has much more to do with levels of glucose, mTOR, IGF-I…and insulin and leptin. That is likely true. Indeed, telomere length, has been shown to be highly (negatively) correlated with leptin levels (see below).

As I was actually writing this article, one of the most significant studies to be published pertaining to telomeres in recent years came out of Maria Basco’s lab from Spain. I will discuss it more at length below. It shows just how important it is to orchestrate telomere length and telomerase. It must be turned on, or off, at a certain time and place for there to be any chance at significantly improved health without increasing cancer risk.

Conclusion

The telomere theory as a cause of aging was hotly debated over a decade ago in many biology of aging conferences where university researchers got together to discuss their latest findings. Now, this is barely discussed outside of pseudoscientific circles… Perhaps the latest Basco study will reinvigorate this debate.

I believe that lengthening telomeres, most specifically in stem cells, and then only temporarily to mitigate against increasing cancer risk, may offer potential to increase health span and delay the onset and even treat certain chronic diseases of aging. However, this is not the same or as powerful as increasing maximal lifespan and stretching out youth that research into genetic pathways of aging regulated by nutrient sensors (insulin, leptin, and mTOR) offer, as illustrated by the increase in maximal lifespan of many species by 200% and more when insulin, IGF-I, and mTOR are genetically suppressed.

One must accurately define health before directions to be healthy are given and just like health is not low cholesterol, health is not defined or synonymous with long telomeres.

Life is dependent on the coordination of its constituent parts. This is especially true pertaining to the length of telomeres of the various cells and organs to maintain health but prevent a high risk of cancer.

As I have said so frequently in the past, we are 15 trillion cells and 90 trillion bacteria that must work harmoniously as one for us to be healthy and remain alive. This requires an intricate orchestration of communication between the different parts. That includes the genes, telomeres, and telomerase. It is where, when, and how much they are played, like the keys of a piano playing an infinite variety of music from the same keys, that determine who we are, diabetic or not, and if we stay alive or die.

What we do want to do is slow down the reduction in the length of our telomeres in an organ and tissue-specific manner that can be orchestrated only through proper genetic expression. Leptin and insulin are among the most, if not the most powerful influences of this. And these in turn are controlled by what you eat.

Review of Telomere Literature

Need more convincing? Confused? Have insomnia? Quotes from various references with brief discussions will follow. (Paper titles are bolded and hyperlinked, quotes from the papers are in the quote boxes, and my comments follow each box).

Telomere biology in healthy aging and disease, Hisko Oeseburg, Eur J Physiol (2010) 459:259–268

In contrast to the similarity of the sequence, the telomere length is highly variable among species, within species, within an organism, and even between chromosomes.

Telomere length of a few different species;
Humans 5–15 kb [kilobase; 1000 base pairs]
Mice Up to 150 kb
Rats 20–100 kb
Birds 5–20 kb
Ants 9–13 kb

…mice strains with longer telomeres do not seem to have an increased lifespan compared to mice strains with shorter telomeres…in African Americans telomeres generally are longer than in White Americans.

Rosedale: …yet have shorter average lifespans. All of this well known data will tell you immediately that telomere length, per se, is not critical to biological aging.

Telomere length [is] highly variable between organs from one subject. This may be explained by variable telomere attrition rate.

Rosedale: One could postulate that rather than absolute telomere length, telomere attrition rate might be significant. However, this could and indeed likely is a reflection of the rate of cellular damage, death, and degree of cellular multiplication to replace that damage. In other words, telomere length would be secondary to aging rather than a cause of it. Measuring telomere attrition rate would, of course, necessitate the measurement of telomere length over time.

The major disadvantage of using leukocyte telomere length is that it is a measure of the activity state of the immune system and one might argue that leukocyte telomere length is rather a representation of increased inflammation than of aging.

Rosedale: The state of inflammation is quite variable over time. A strep throat, upset stomach, and a scraped knee could increase your general state of inflammation for weeks and this could reflect in variably lower WBC telomere length secondary to a healthy immune system.

Blood Cell Telomere Length Is a Dynamic Feature, Ulrika Svenson, PLoS ONE June 2011 Volume 6 Issue 6

Irrespective of the biological background, leukocyte telomeres appear to oscillate in length over time [months].

Rosedale: Therefore many measurements over time in a single individual would be necessary to know if a change in TL was due to normal oscillation or not.

Shortening telomeres are more secondary to aging and disease than a cause of it.

Telomere length and cardiovascular aging: The means to the ends?, Tim De Meyer, Aging Research Reviews, Vol 10, #2 April 2011, Pages 297–303

Conclusion: Shorter inherited telomeres do not appear to predispose to early atherosclerosis. Atherosclerosis related factors accelerate telomere attrition.

Rosedale: Shortening telomeres may have a huge evolutionary advantage, especially for larger animals…

Telomerase activity coevolves with body mass, not lifespan, Andrei Seluanov, Aging Cell. 2007 February ; 6(1): 45–52

Here we show that telomerase activity does not coevolve with lifespan but instead coevolves with body mass: larger rodents repress telomerase activity in somatic cells. These results suggest that large body mass presents a greater risk of cancer than long lifespan, and large animals evolve repression of telomerase activity to mitigate that risk.

Rosedale: What about the potential of increasing telomere length?…

Telomere length, stem cells and aging, Maria A Blasco, Volume 3 Number 10 October 2007 Nature Chemical Biology

The fact that the vast majority of human tumors seem to depend on telomerase reactivation to prevent critical telomere loss and to divide indefinitely suggests that telomerase inhibition could be an effective way to abolish tumor growth.
The fact that telomerase deficiency only results in loss of organismal viability when telomeres reach a critically short length is an important point when considering possible secondary effects of these therapies.
In particular, this predicts that putative anticancer therapies based on temporary telomerase inhibition will only trigger loss of viability in those cells with short telomeres that depend on telomerase activity. Presumably, these include tumor cells but not healthy tissues, which generally lack telomerase activity and have sufficiently long telomeres to maintain viability during the human lifetime, thus providing a window of opportunity for intervention.

Therapeutic agents that could be designed to [re-activate telomerase temporary] would preferentially target those cell types that normally divide to maintain organ homeostasis—such as stem cells, which, although telomerase-proficient, do not have sufficient telomerase activity to maintain telomere length over time.

Rosedale: As in all disease, especially having to do with genes, it is where, when, and how they are read that determines their contribution to health, disease, and even who you are.

Telomere Length of Circulating Leukocyte Subpopulations and Buccal Cells in Patients with Ischemic Heart Failure and Their Offspring, Wong LSM, PLoS ONE 6(8) August 18, 2011

For instance, it has been shown that vascular endothelial cells that endure more hemodynamic sheer stress have shorter telomeres than endothelial cells in low pressure arteries [secondary to a greater rate of turnover]

Rosedale: i.e. TL is a secondary byproduct of aging, not a primary cause of it.

To further dissect the association of ischemic heart disease with mean overall leukocyte TL we need to establish whether mean overall leukocyte TL is a reflection of TL in different cell types or whether it is more or less specific for leukocytes. Of particular interest in this regard are the CD34 positive (CD34+) cells as it is thought that these cells might be cardiovascular progenitor [stem] cells and play a role in cardiovascular repair…Furthermore, mean leukocyte telomere length has not been compared to non-circulating non-vascular cells and it is unknown whether leukocytes might merely be a reflection of overall TL of the whole body… One of the aims of this study was determining whether telomere length of CD34+ cells is different in IHF patients compared to healthy controls. We did not find a difference in TL between IHF patients and controls in CD34+ cells. These results clearly indicate that there is no significant difference in CD34+ cell TL between IHF patients and controls.

The major difference in telomere length between IHF patients and controls was observed in the overall leukocyte pool, not specifically in CD34+, MNCs or buccal cells as a source of non-blood derived cells.

The comparable TL of CD34+ cells in cases and controls strongly suggest that telomere shortening of CD34+ cells is not a major player in the pathophysiology of IHD…In the elderly, specific immune responses might be diminished, but many other functions are unchanged or even augmented compared to young persons.

Rosedale: This study is important for several reasons, the main one being to illustrate that even though WBC TL may correlate with a disease state such as ischemic heart failure (secondary to correlating with cellular damage and turnover), WBC TL did not correlate, at least in this study, with representative cells of the only major cell group that may have significant therapeutic potential, stem cells. One cannot extrapolate WBC telomere length to other tissues.

Telomerase, senescence and ageing., Shawi M, Autexier C., Mech Ageing Dev. 2008 Jan-Feb;129(1-2):3-10. Epub 2007 Dec 14

Paradoxically, the introduction of telomerase is proposed as a method to combat ageing via cell therapy and a possible method to regenerate tissue, while telomerase inhibition and telomere shortening is suggested as a possible therapy to defeat cancers..
Rosedale; In other words, telomerase must be turned on and turned off at the appropriate time and location, i.e. it must be orchestrated.

Rosedale: And again, one cannot extrapolate WBC telomere length to other tissues.

Measuring relative telomere length: Is tissue an issue?, Monica M. Gramatges and Alison A. Bertuch. AGING, November 2010, Vol 2 N 11

Although the number of subjects was small, strong correlations between blood, buccal cells, and fibroblasts were observed in the study population as a whole. When taken individually, however, only cells from subjects with DC demonstrated significant correlation. [dyskeratosis congenita (DC). DC is a rare genetic disorder stemming from a defect in telomere maintenance.]

Rosedale: Can TL predict centenarians? Not in the following study. Also, WBC TL was again not correlated with another representative tissue type.

Telomere length in fibroblasts and blood cells from healthy centenarians., Mondello C, Exp Cell Res. 1999 Apr 10;248(1):234-42.

In this paper we analyzed the mean length of the terminal restriction fragments (TRF) [frequently how TL is measured] in fibroblast strains from 4 healthy centenarians, that is, in cells aged in vivo, and from 11 individuals of different ages. No correlation between mean TRF length and donor age was found.

…chromosome analysis did not show the presence of telomeric associations in early passage centenarian fibroblasts. In blood cells from various individuals, the expected inverse correlation between mean TRF length and donor age was found. In particular, a substantial difference (about 2 kb) between telomere length in the two cell types was observed in the same centenarian.

No Association Between Telomere Length and Survival Among the Elderly and Oldest Old, Bischoff C, Epidemiology: March 2006 – Volume 17 – Issue 2 – pp 190-194

This longitudinal study of the elderly and oldest old does not support the hypothesis that telomere length is a predictor for remaining lifespan once age is controlled for.

Rosedale: We have lots of telomeres. We have at least 500 trillion of them and measuring a select few from one cell type is not necessarily going to tell you what the other telomeres are doing…

Ageing and telomeres: a study into organ and gender-specific telomere shortening, H. Cherif*, 1576±1583 Nucleic Acids Research, 2003, Vol. 31, No. 5

In humans, telomere length is relatively short, highly variable between tissues and individuals and, with regard to replicating somatic cells, inversely related to donor age

We show clearly in this study that the mean TRF length method is unable to detect small changes in telomere size or to visualise the length of individual short telomeres in a distribution of TRFs. There is increasing evidence suggesting that it is not average telomere length, but rather individual critically short telomeres that trigger cellular responses to the loss of telomere function

The latest study and the most promising to show health benefits in telomerase expressed mammals was published last week…

Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer, Bruno Bernardes de Jesus, Maria Blasco, EMBO Mol Med march 16, 2012 4, 1–14

Importantly, telomerase-treated mice did not develop more cancer than their control littermates, suggesting that the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms using AAV vectors telomerase treated mice, both at 1-year and at 2-year of age, had an increase in median lifespan of 24 and 13%, respectively.

Owing to its ability to confer with unlimited proliferative potential, over-expression of the telomerase reverse transcriptase (TERT) is a common feature of human cancers and can increase cancer incidence in the context of classical mouse TERT transgenesis.

A drawback of mTERT over-expression in transgenic mouse studies has been an increased cancer incidence, except for cancer-resistant backgrounds.

Telomerase expression late in life leads to overall telomere lengthening and decreased abundance of short telomeres in various tissues.

…telomerase activation can delay normal mouse aging in cancer resistant mice…

However, with the exception of mice genetically engineered to be cancer resistant, increased telomerase expression is associated with a higher susceptibility to develop cancer both in mice and humans…

Notably, in these studies increased TERT expression is forced since early embryo development through germ line modifications, which may favour the expansion of cancerous cells and the development of cancer later in life…Here, we show that increased TERT expression later in life (adult and old mice) by using a gene therapy strategy has rejuvenating effects without increasing cancer risk…the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms. Finally, re-introduction of mTERT in both 1- and 2-year old mice increased significantly its median lifespan (24 and 13%, respectively).

Rosedale: It generally takes at least several years for cancer to reveal itself. These mice only live 2 to 3 years. Therefore expressing telomerase when these mice only had one or less years to live likely did not give cancer cells enough time to manifest themselves. This would not be the case when using this sort of therapy in humans with more than 1 to 2 years to live. Note further that it is median lifespan that was modestly increased rather than maximal lifespan.] Also note that humans have much more body mass than mice, and therefore artificially activating telomerase in humans may have significantly greater negative consequences especially relative to cancer rate as compared to mice. See study above.

A commentary to the above article in the same journal:

Telomerase gene therapy: a novel approach to combat aging, Virginia Boccardi, Utz Herbig, EMBO Molecular Medicine 4, 1–3

…numerous studies using mouse models have demonstrated that critically short and dysfunctional telomeres indeed present a powerful barrier to cancer growth.

A question that has therefore intrigued researchers for many years is whether it is possible to slow aging and improve health span by re-activating telomerase in all of our cells. Constitutive expression of telomerase, unfortunately, is a characteristic of almost all cancer cells. It is therefore no surprise that transgenic animals over-expressing the catalytic subunit of mouse telomerase (mTERT), develop cancers earlier in life, thereby masking the potential beneficial lifespan extending properties of telomerase.

While these studies provide a proof-of-principle that telomerase gene therapy is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres [in mice], a clinical application in humans is likely still some time away. Low levels of integration of rAAV vectors into genomic DNA have been observed, raising the possibility that rare integration events of constitutively overexpressed TERT into genomes of long lived species might eventually promote cancer growth.

Furthermore, as with other gene therapeutic approaches, targeting the virus to specific cells in the body remains an obstacle. Also uncertain is specifically which cells should be targeted using a telomerase gene therapy.

Rosedale: Conclusions?

Association Between Telomere Length, Specific Causes of Death, and Years of Healthy Life in Health, Aging, and Body Composition, a Population-Based Cohort Study, Omer T. Njajou, J Gerontol A Biol Sci Med Sci 2009. Vol. 64A, No. 8, 860–864

In conclusion, we did not find any evidence of association between [WBC] TL [telomere length] and overall survival or between TL and specific causes of death. We also report for the first time that longer TL is associated with self-reported health status and greater YHL. Findings suggest that TL, although not a strong biomarker of survival in older individuals, may be an informative biomarker of healthy aging.

Is Telomere Length a Biomarker of Aging? A Review, Karen Anne Mather, J Gerontol A Biol Sci Med Sci. 2011 February; 66A(2):202–213

The observation that telomeres shorten with increasing age and are implicated in cellular aging has led to the proposal that telomere length is a biomarker of aging.

Currently, telomere length does not fully meet American Federation of Aging Research criteria that telomere length is (a) a better predictor of life span than chronological age (Criterion 1) and that (b) it monitors a basic process underlying normal aging at the pop-ulation level (Criterion 2).

Interestingly, an increase in intra-individual telomere length for a minority of participants at follow-up (ie, with increasing chronological age) has also been observed in three independent studies (27,39,78). However, this may not represent an increase in overall telomere length but rather could reflect the loss of cells with shorter telomeres.

Rosedale: It has been found that likely only cells with extremely short telomeres are so adversely affected that the process of apoptosis is initiated.

Could the significance of TL be secondary to leptin levels? TL is inversely correlated with leptin levels.

Obesity may accelerate the ageing process., Rowan Hooper, New Scientist 14 June 2005

But animal studies have failed to reveal any simple relationship between telomere length and lifespan… the youngest women had telomeres that were around 7500 base pairs long. Their length declined with age at an average rate of 27 base pairs per year.

When lifestyle factors were taken into account, however, dramatic differences emerged. The difference between being obese and being lean corresponds to 8.8 years of extra aging…

Smoking was the other big factor… Obesity accelerates the ageing process even more than smoking. Intriguingly, the link between high leptin concentrations and telomere shortening was even stronger than the link with obesity…The damage to telomeres is probably done by free radicals. Smoking causes oxidative stress ­ a source of free radicals ­as does obesity [and high leptin]

Free radicals can cause mutations in DNA, and there is some evidence that mutations in telomeres cause larger chunks than normal to be lost during cell division. In other words, it is a byproduct of aging that results in cellular turnover and molecular damage and therefore shortening of telomeres and not the other way around.

You want comments? We got comments:

Imagine you’re George Clooney. Take a moment to admire your grooming and wit. Okay, now imagine someone walks up to you and asks, “What’s your name?” You say, “I’m George Clooney.” Or maybe you say, “I’m the Clooninator!” You don’t say “I’m George of George Clooney Sells Movies Blog” and you certainly don’t say, “I’m Clooney Weight Loss Plan”. So while spam is technically meat, it ain’t anywhere near Primal. Please nickname yourself something your friends would call you.

  1. “Life is dependent on the coordination of its constituent parts.” Indeed. Messing with telomeres makes me nervous.

    Alison Golden - PaleoNonPaleo wrote on May 30th, 2012
  2. I really don’t think telomeres affect how long you live, because they don’t really have anything to do with your lifespan. As your chart stated above, mice and other small creatures have long telomeres but far shorter lifespans that most animals. So depending on the length of your telomeres, your not going to die right then and there if you have short telomeres. Also, what you do to your body affects your lifespan such as smoking, drinking, etc. That is what really matters.

    Michael wrote on May 30th, 2012
    • I agree to disagree.

      Telomerase is the key.

      I recommend any one interested in the topic of regenerative medicine, which includes but is not limited to, telomeres and induced pluripotent stem cells iPSC to follow the work of Dr. Michael West.

      Paleo Bon Rurgundy wrote on May 30th, 2012
      • Agreed as well, I’m just making the point to include that you cannot depend solely on telomeres for a longer lifespan.

        Michael wrote on May 30th, 2012
      • I agree with Mr. Burgundy here, in that I completely disagree.

        I can’t believe you said this:
        “The telomere theory as a cause of aging was hotly debated over a decade ago in many biology of aging conferences where university researchers got together to discuss their latest findings. Now, this is barely discussed outside of pseudoscientific circles… Perhaps the latest Basco study will reinvigorate this debate.”

        Not only is this a logical fallacy, but it’s also completely false. You even listed a study that was done on telomerase and aging that was done this year. Not only that, but I know of plenty more studies that have recently been done on this subject.

        I find it disturbing, how you try to frame this debate as already being settled using your fallacious argument by consensus.

        Matthew Caton wrote on May 31st, 2012
  3. And … now .. you know ….. the … rest .. of the…story.

    Alex wrote on May 30th, 2012
    • Real science almost always starts out with “Hmmm… that’s strange,” which is usually followed by “It’s a bit more complicated than we thought.”

      Which is the main reason I quit reading observational “studies” entirely. I haven’t found any instance of an observational “study” that didn’t come to the conclusion desired by the funding source.

      Howard wrote on May 30th, 2012
      • “Real science almost always starts out with “Hmmm… that’s strange,” which is usually followed by “It’s a bit more complicated than we thought.””

        That cracked me up because my dad is a chemist and I’ve probably heard him say those exact words five thousand times.

        Ellie wrote on May 30th, 2012
      • Well said.

        BillP wrote on May 30th, 2012
      • Real science almost always starts out with “Hmmm… that’s strange,” which is usually followed by “It’s a bit more complicated than we thought.”

        Loved that comment. Its amazing that no matter what we always think we know evrything and then a new discovery comes up that changes everything

        CMHFFEMT wrote on June 3rd, 2012
  4. I’m going to need to re-read this, but would it be accurate to say that oxidative stress reduces TL and leads to genetic mutations? That artifically lengthening TL then does not attack cause but symptom?

    And if that is so, would a person whose diet and lifestyle includes reduced oxidative stress benefit from something that would enhance TL, as astragalus has been studied to do? Bottom line, if you’re Primal, would it hurt or help to supplement with astragalus, or is the jury out on that?

    Finnegans Wake wrote on May 30th, 2012
  5. Very cool post but did it set a length record?

    Groktimus Primal wrote on May 30th, 2012
    • No kidding!

      Kimberly wrote on May 31st, 2012
  6. The reason I like primal/paleo so much is there is so much science behind it. So much stuff.

    Michael wrote on May 30th, 2012
  7. Is this right? It seems like “increase” and “decrease” might be backwards?

    The Ugly: Without proper and exact knowledge of when and where to control telomere length, it will likely greatly increase one’s risk of cancer. In other words, it may very well increase healthspan as it reduces lifespan.

    karen wrote on May 30th, 2012
    • I think what he’s saying is that if we try to manipulate telomere length, without full understanding, we could possibly slow aging but increase our cancer risk thus reducing our lifespan.

      Aaron wrote on May 30th, 2012
      • Or we accidentally start the zombie apocalypse. Whoops.

        CMW wrote on May 31st, 2012
  8. Worth the time reading, and I am certainly glad I waded through the whole post. The fact that Dr. Rosedale has actually critically studied several studies makes him an extremely rare example of an MD. Most of the MDs I have met get nearly all of what they “learn” after med school from pharmaceutical brochures and TV commercials.

    I am definitely grateful to Dr. Rosedale for providing this information. I now have a better background for evaluating the telomere literature.

    I wish that Dr. Rosedale could have been on the Low-Carb cruise so that I could have met him in person. Maybe next year.

    Howard wrote on May 30th, 2012
    • This is the second time I’ve read about the low carb cruise. I just googled it and am a bit sadden because that was an idea I submitted in MDA’s call to arms for ideas. Looks like that idea will not win. Back to my cubicle cage of agony.

      Paleo Bon Rurgundy wrote on May 30th, 2012
      • That’s because floating around in a carbon burning monument to conspicuous consumption is not paleo, not to mention the additional carbon combusted on the two way plane trip to the boat & back.

        conrack wrote on May 30th, 2012
        • Fossil fuels and burning carbon is totally paleo; it is also Archeozoic, Proterozoic and Mesozoic :)

          The majority of electricity the United States generates is from coal based plants.

          Computers weren’t around in the paleolithic either, yet we use them.

          Paleo Bon Rurgundy wrote on May 30th, 2012
  9. man, I tried to finish the whole article but I couldn’t. What I think he said was “Eat Food, Get Sleep, Have Fun, Love.”

    MikeD wrote on May 30th, 2012
    • Thanks for distilling that down for me. As I read the article and nodded off a few times, I was looking for the “so what do I do” part. I’m in remission from Non-hogkins Lymphoma of which I finished treatment for almost a year ago. It has been a process, first gave up gluten; then started juicing; then give up grains and refined sugar. I believe the cancer came from long term stress and trauma…years of sleep depravation and bad food…the perfect storm. Got a divorce and totally transformed my life. Only frustration…not losing much weight that I gained during chemo (steroids). Also doing crossfit. Any advice about that?

      Sandy Kingsley-Perkins wrote on May 30th, 2012
      • Keep working the plan. the insides take a while to repair. keep the food tight, the sleep long, release the crossfit and just have fun. love means happiness, friends and family too.

        2cents

        MikeD wrote on May 31st, 2012
      • Read Dr. Rosedale’s book. Despite adhering to paleo for over two years, I was only able to lose fat by eliminating sugar. For an already paleo-eater, that means dairy, fruit, and starchy veggies.

        Andrea wrote on June 1st, 2012
  10. The thought of people living hundreds of years is very frightening. If you think we have environmental problems now….

    Peter wrote on May 30th, 2012
    • If we cant figure out how to support our growing population, no need to fear… there is always the Black Plague to rescue us!

      MikeD wrote on May 30th, 2012
      • Well as some people say the governments of the world will kill us. I sorta of disagree because it could happen, but if Mother Nature wanted our population down, she would of already done so.

        Michael wrote on May 30th, 2012
    • Yeah, because they are known as vampires. Or Methusula. Wait a minute… by the beard of Zeus!

      Paleo Bon Rurgundy wrote on May 30th, 2012
  11. This subject is also covered in a book called Genome: Human History in 23 Chapters…or something like that. It’s a pretty good read. It’s an interesting topic to study and I enjoyed this post.

    Lisa wrote on May 30th, 2012
  12. http://www.youtube.com/watch?v=r2V7iSWMJHI&feature=BFa&list=PL53AA35449C7DD652#t=5m Smoking bad for telomeres, and a 120 food questionnaire

    Lance Strish wrote on May 30th, 2012
  13. This is how werewolves are made. True story.

    Matt Crandall wrote on May 30th, 2012
  14. What want to know is, If I am obese and I start eating healthier and lose the weight, do I get those 8.8 years worth of telemeres back at some point? Does this mean that even after 50 years of healthy living, I still don’t live as long or as healthfully as I would have had I never been obese in the first place?

    :-P wrote on May 30th, 2012
  15. Not sure I understand…. I thought the release of human growth hormone was good for you. ( think Dr. Mercola’s peak 8)…..

    janet wrote on May 30th, 2012
  16. I had never heard of this before, but thank you for a wonky article as a means of introducing me to something I ultimately don’t need to worry about.

    Sorry if that came off as sarcastic as it wasn’t my intention.

    zack wrote on May 30th, 2012
  17. Thanks so much for posting this. I am not going to debate the merits of lengthening lifespan for those who express concerns here – not the forum for it.

    But I would urge anyone really interested in extending lifespan to look into Aubry De Gray. The man is brilliant. I am in full support of his quest to add life to all of our lives.

    There are debates available where he discusses the pros and cons of extending human life spans very considerably, with those who disagree. I am convinced by his arguments. Yet I think we have time to plan for the changes.

    http://en.wikipedia.org/wiki/Aubrey_de_Grey

    Here’s to a very long, happy and healthy life to one and all!

    John Campbell wrote on May 30th, 2012
    • Yay! I was just about to link to Aubrey De Grey and SENS. You beat me to it. Here’s his TED talk:

      http://www.ted.com/talks/aubrey_de_grey_says_we_can_avoid_aging.html

      That beard! That brain! Love him!

      Patricia wrote on May 31st, 2012
      • I had seen this talk before and found it very interesting. I like to think that the possibilities are there but what it means for the use of natural resources is mind boggling without a fundamental change in how we use them. It deos no good to eliminate death from natural causes if you just die from starvation or pollution instead.

        CMHFFEMT wrote on June 3rd, 2012
  18. Also, I really appreciate the link to the cholesterol post. I am fascinated by it right now.

    zack wrote on May 30th, 2012
  19. Phenomenal insight into the raw science, and into how it is often oversimplified to produce a catchy story or product.

    Thanks Ron !

    Jordi Posthumus wrote on May 30th, 2012
  20. Great summary…but then again, I was at a presentation (by Dr. Bartke) that of the (very few) supplements that DID expend life in lab rats, TA-65 was one of them.
    I like the idea of developing ANY biomarkers of aging that can reinforce lifestyle habits that are difficult to institute unless people are motivated by “seeing the numbers.”
    Unfortunately, this type of information is driven by drug development (…just take a pill!), so it tends to not focus on all the lifestyle changes that can/should be made.

    I was privileged to be part of an experimental cohort that got their WBC telomere length measured (and compared to a sibling). I hope to repeat the test at a commercial lab to see if additional lifestyle strategies are having a measurable impact. Anecdotally, I’m pretty sure my new N=1 experiments ( stress reduction technology via emWav2) is helpful, while I’m not sure about the cold water immersion. I’m curious to re-measure and see if there will be any changes, as I’m not sure of any existing blood tests that would really give me a handle on this either.

    Perhaps because I already have the diet and exercise dialed in (focusing on keeping glucose/insulin low), by telomere base pair measurement seemed to be much “better” than my 6 year younger but highly stressed and poor eating habit sibling).

    Hope to see you posting more info here Dr. Ron – your work is always way ahead of the curve! Even in the highly motivated CRONie crowd, there is always a “suspension” of belief along the lines of “fruit is healthy” so I can eat as much as I want (regardless of its impact on blood glucose). SO easy to measure! Wish we could get THIS message out (instead of the cholesterol issue)…but as you know, billions $ of reasons NOT to. The Paleo movement is perhaps our best hope (once people understand that its focus is anti-inflammatory), vs. all the current misperceptions.

    deb b wrote on May 30th, 2012
  21. WOW…that was a lot of information. Very cool.

    “Not very many people would volunteer for heart biopsies, for instance. A jilted lover might volunteer their ex perhaps.”
    That made me giggle. :)

    Thank you, Dr. Rosedale!!

    Primal Pants wrote on May 30th, 2012
  22. Bottom line… Channge what you do ultimately have control over… diet, exercise, stress response, optomism & gratitude. All these factors are proven to both lengthen life and entend the enjoyment of it. What is currently beyond control isnt going to add years to your life or life to your years. I love to follow research, but I prefer to live on truth.

    kelly wrote on May 30th, 2012
  23. Great summary of theoretical contradictions. Thinking out loud: How about a careful study of proven centenarians lifestyles & diet – such as book “Blue Zones” – rather than petri dish / lab rat theories? Appears that IGF-1 and HGH may be necessary for a growing young person but not good for a mature person. Maybe high intensity interval exercise to stimulate IGF-1 and HGH is counter productive? Maybe slow steady physical stress-reducing practices such as gardening, Tai Chi, Yoga along with minimal calories are the answer? Keep up the study.

    JB wrote on May 30th, 2012
    • Thanks for that comment —that is what I was thinking as well. Writing about walking for health for over 25 years, it seemed to me that slow and steady held the key for long term health and longevity (though many factors can intercede) as well as reducing calories and avoiding processed foods like all the “whites.”
      . Obsessing over living longer or what one eats is probably less important than reducing stress and eating moderately with a focus on whole foods and getting moderate exercise every day.I am 62 and find it funny that when I visit a doctor they look surprised that the only med I am on is armour thyroid. Of course, I would be on Statins if I followed the advice of most doctors–who cater to the faulty cholesterol causes heart disease theory. Luckily, I escaped that debacle.

      Maggie wrote on August 19th, 2014
  24. what gets me is they show in the mice it extended their life…then say that mice have a short life and humans that live longer it might cause cancer….well, does that mean that all the test that they do on mice that have good outcomes that they tell us to take this or that to be healthier needs also to be questioned since we live longer..and those things could cause something too….

    mostly all you see in these test are that more studies need to be done..more money..

    melv wrote on May 30th, 2012
  25. I really, really don´t want to live longer than a “natural lifespan”. But I DO want to live well the time I have here. Gimthe 70-80 good years and I´ll be happy to make space for the next generations. :-)

    Elena wrote on May 30th, 2012
    • My throughs exactly.
      Don’t waste what you have been given.
      What a sad vision, an over populated world full of selfish cranky old farts and no children.

      Peter wrote on May 30th, 2012
      • Well-Said! Even longer, it’ll never be enough anyway.

        Joy Beer wrote on June 1st, 2012
    • One way people deal with mortality is to pretend they actually want it or that it benefits us.

      Al wrote on November 20th, 2012
  26. Excellent and well-written summary, Dr. Rosedale, very much appreciated.

    Your comments on the several biomarkers available for testing inflammation (as possible indicators of aging rates) raises the possibility of a controlled study comparing various diets, obviously including paleo/primal and low-fat, tracking inflammation across diets and at the same time, in the subjects (before adoption of the diet they are on, and after). Anything specifically like this been done?

    Great guest review, Mark, and great idea; how about doing it again (an expert commentator once every month or two)?

    BillP wrote on May 30th, 2012
  27. “One must accurately define health before directions to be healthy are given…”

    There is a lot of wisdom right there…

    Erin wrote on May 30th, 2012
  28. Fascinating. Well, this only confirms how important intermittent fasting is. I know its not specifically mentioned, but its a great way to improve insulin and leptin sensitivity, which is concluded to be very important.

    Graham wrote on May 30th, 2012
  29. Hmmm… I’m a little confused on the HGH statements!

    I thought the reason that we were practicing Sprints & Intermittent Fasting was that it *increased* our HGH by massive amounts.

    But yet, Dr. Rosedale sites evidence how GH *restriction* is what had the mice live longer!

    Is there a difference between HGH & IGF-1 (*insulin*-like GF)?

    Can someone help me out here?

    Joseph wrote on May 30th, 2012
    • On HGH and IGF-1 You might enjoy the book “The CR Way” – McGlothin & Averill – kinda contradictory to a lot of this site – but makes interesting supported observations from some top researchers.

      JB wrote on June 1st, 2012
  30. My telomeres were forced to extend to accommodate that motherload of info! In the best possible way. Love taking it further all the way to geektown. And discovering (very very late in the picture) the work of Dr. Ron Rosedale is an added plus.

    Catie wrote on May 30th, 2012
    • Haha, that was funny. :)

      CMW wrote on May 31st, 2012
  31. Thanks! great info!

    and also confused on HGH. as Joseph said:

    I thought the reason that we were practicing Sprints & Intermittent Fasting was that it *increased* our HGH by massive amounts.

    But yet, Dr. Rosedale sites evidence how GH *restriction* is what had the mice live longer!

    Anna K. wrote on May 30th, 2012
  32. Good guest post. I remember reading about telomeres a few years back and had pretty much the same conclusion: no solid evidence that having longer telomeres would extend your life, and artificially lengthening could risk cancer. I am also confused by the HGH mention.

    cnymicaa wrote on May 30th, 2012
  33. We could split the atom apart millions of times and we will find nothing conclusive.

    It is consciousness that influences our bodies, in ways we couldn’t imagine.

    The cause of aging is belief.
    Beliefs, thoughts, emotions = the state of our health.
    The food choices we make and the lifestyle choices are a direct response to the beliefs, thoughts, emotions.

    Even if this spirituality stuff is not accepted by mainstream science, it is as scientific as E=MC^2. :)

    Paul Alexander wrote on May 31st, 2012
  34. “When lifestyle factors were taken into account, however, dramatic differences emerged. The difference between being obese and being lean corresponds to 8.8 years of extra aging…

    “Smoking was the other big factor… Obesity accelerates the ageing process even more than smoking. Intriguingly, the link between high leptin concentrations and telomere shortening was even stronger than the link with obesity…”

    Blaming anything on obesity except weight-related joint damage and possibly some inflammation originating in the visceral fat is like blaming a runny nose for the fact that someone has just died of influenza.

    There’s a reason leptin is seen as a greater factor in aging than obesity is. It’s because OBESITY IS A SYMPTOM. In most cases it does not *cause* anything. The few things it *does* cause are roughly analogous to that aforementioned runny nose causing your upper lip to get chapped from all the wetness.

    So SOMETHING ELSE which happens to sometimes have obesity as a SYMPTOM is causing the extra aging. And you better bet you are going to find that “something else” in the slender as well as the fat. Those very selfsame slender people going around on maintenance drugs because they have “hereditary” high blood pressure or “hereditary” deranged cholesterol.

    I don’t know about anybody else here, but personally, I am after *dietary health.* I don’t care how much someone weighs, I care about how their whole body is working, and whether they’re getting enough of what their body needs in their diet each and every day. Fatness is a symptom of malnutrition (not “overnourishment” as so many argue–what an ugly, inaccurate word). I’m after eradicating malnutrition. It’d be nice if others would develop more of an interest in that as well. I’m beyond tired of the fat-bashing, whether disguised by scientific concern or not.

    Yes, it’s probable that *most* cases of obesity would resolve themselves in people who start eating right for their nutritional needs. But some people’s metabolisms are so broken by years of unwitting abuse (yes, unwitting–there are lots of ways to break a metabolism, only some of which are explained by mainstream medical culture) that they could eat perfectly and they still wouldn’t be normal BMI.

    And some of us are just going to have to learn to live with that. I know, I know, it’s tough.

    Dana wrote on May 31st, 2012
    • I think it’s a mistake to classify ‘obesity’ as either a cause or a symptom, a classic case of black-or-white, either-or thinking. In complex systems, there are conditions that can exhibit both behaviors, and seemingly morph from one to the other as the (multiple) feedback loops each gain or wane in strength and thus effect.
      But it’s best just to discard the terms ’cause’ and ‘effect’, and just try to understand the system dynamics. Even if we’re all on the same page as far as paleo or primal is concerned, the idea that one can reduce the issue of overweight to a simple axiom like ‘carbs drive insulin drives fat’ is very attractive but apparently an immense oversimplification.

      BillP wrote on May 31st, 2012
  35. I think it’s a shame that both sides of the argument were not presented. If you research the issue you will find many doctors with research that supports the telomere argument and also studies that show telomere lengthening sups do not grow cancer cells. I have been taking TA-65 for 8 months and it has taken at least 10 years off my face which is a great plus for me! My energy etc have also increased. I am a 40 year old female 5’2″ 114 lbs. I work out 6 days a week and eat only organic whole foods, and I follow a “warrior diet” way of eating, so I was already taking great care of myself but the TA-65 has made great improvements. Western docs will go to any length to prove supplements can’t replace their precious drugs. On any subject I would always read more then just one doctor’s opinion.

    Mice do not und any circumstance live as long as humans so a comparative study of mice to humans is a bit ridiculous. Rather than comparing telomere length in mice to that of humans doesn’t it make more sense to study how telomere length in the mice affected the life span of mice? Guess what that has been done and mice that were given telomere lengthening supps lived longer and were less likely to develop cancer then those without the supps.

    I love this site and think most of what is posted is dead on. In this case, I would have liked to have seen both opinions presented. Again, I have researched it a ton. I live in Seattle and have the privilege of being a patient at Dr. Jonathan Wright’s clinic. He is a true pioneer in the world of natural/alternative medicine. I feel great and love the shocked looks I get when I tell people my age!

    Addie wrote on May 31st, 2012
  36. Off the subject of today’s post but here is a great video any Primal Person or Libertarian will love.
    http://www.youtube.com/watch?feature=player_embedded&v=L5EixDJ25Lc

    Rick wrote on May 31st, 2012
  37. Medicine and science is always taking a reductionist approach: finding the ‘one thing’ that will provide the answer. Humans are as complex as the natural environment from whence we came. The thing I like about a paleo template is the eat well and move ethos. It’s not specific; it’s wholistic and recognizes what we eat and activity affects us intellectually, emotionally, and physically.

    Dr. Rosedale rocks, BTW . Thanks for taking the time to write this post.

    Leslie wrote on June 1st, 2012
  38. I have been on a Telomere support product (stronger than TA-65) for almost a year now so found this of interest. But I also found it misleading. I had heard of the May 2012 paper mentioned above (Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer) but was confused by the exerpts Dr Rosedale quoted. He does not make it clear that most are exerpts from assumptions made by much older research; this new research was looking at the validity of these old assumptions. The title of the paper indicates the result of the research found these assumptions are most likely incorrect. (I would never say definately disproves as there is always room for new research). Any quotes should be put into context by mentioning where they came from.

    Colin wrote on June 1st, 2012
    • Hi Colin- What are you taking that is stronger than TA-65? I have been taking TA-65 for several months and love the results but I would love to know what the other options are. I know a lot of experts say that cycloastragenol is the same as TA-65 and can be taken at much higher doses for a lower cost. Anyhow would love to know what your experience is and what you are taking?

      Addie wrote on June 2nd, 2012
      • Hi Addie,

        if you click on my name ‘Colin’ below, it will take you to my information site where you will find a lot of information on the product. If you fill in the ‘Find out more’ box I can chat to you directly. Cheers Col

        Colin wrote on June 5th, 2012
  39. Denckla had the answer the whole time…in the brain.

    james wrote on June 10th, 2012
  40. chummy wrote on February 19th, 2013

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