{"id":199,"date":"2014-01-25T17:12:02","date_gmt":"2014-01-25T17:12:02","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=199"},"modified":"2014-05-16T20:10:50","modified_gmt":"2014-05-16T20:10:50","slug":"the-most-promising-medical-technology-on-the-horizon-today","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2014\/01\/25\/the-most-promising-medical-technology-on-the-horizon-today\/","title":{"rendered":"The most promising medical technology on the horizon today"},"content":{"rendered":"

T<\/strong>elomere biology has the potential to extend human life span, to dramatically lower rates of the great remaining killer diseases: heart disease, stroke, and Alzheimer\u2019s. \u00a0All three diseases increase exponentially with age, and their toll will be slashed as we we learn how to address the body\u2019s aging clocks<\/a>.<\/em><\/p>\n

You would think that the 2009 Nobel Prize<\/a> might have done more to raise the profile of research in telomere biology, but the field remains a specialized backwater of medical research, and few biologists (fewer doctors) take it seriously as a panacea for the diseases of old age. \u00a0If the National Institute of Health has money to put into heart disease and cancer and Alzheimer\u2019s and Parkinson\u2019s diseases, there is no better place to invest than in telomere biology. \u00a0Research on these diseases commands multi-billion dollar budgets<\/a>, because they are considered \u201cmedicine\u201d, funded by NIH, while telomere biology is considered \u201cscience\u201d and is funded by NSF. \u00a0The total NSF budget for all cell biology is only $123 million<\/a>, and the portion devoted to telomere biology is a few million. The private sector is doing a little better – there are several companies selling herbs that stimulate our own bodies to liberate telomerase. \u00a0But this is short-sighted venture capital, and what we need is focused research with a ten-year vision.<\/p>\n

There is good reason<\/a> to think that telomere length is a primary aging clock in the human body. \u00a0The body knows perfectly well how to lengthen telomeres, but chooses not to. \u00a0All we have to do is to signal the body to activate the telomerase genes that are already present in every cell. \u00a0\u00a0Of course, there is no guarantee that this will work, but compared to the sluggish rate of progress on individual diseases, it\u2019s a pretty good bet, and the target is rather simple. \u00a0IMHO, it\u2019s worth a crash research effort.<\/p>\n

Three objections raised against telomerase research<\/strong><\/p>\n

1. \u00a0\u201cAging is inevitable because Physics tell us that nothing can last forever.\u201d<\/strong> \u00a0This statement refers to the Second Law of Thermodynamics, which says that closed systems, evolving in isolation, must become more disordered over time. \u00a0But living systems are open, taking in free energy in the form of food or sunlight, dumping their entropy out into the environment. \u00a0There is no reason that such systems cannot maintain themselves indefinitely. \u00a0Indeed, growth and maturation would not be possible if this law of physics applied to open thermodynamic systems. Since the 19th Century when the laws of thermodynamics were formulated, it has been understood that aging cannot be explained from physics, and therefore commands an explanation from evolution.<\/p>\n

2. \u201cEvolution has been working to maximize animal life spans in order to increase fitness. \u00a0It is unlikely that any simple adjustment to physiology that humans can discover will do better than evolution has done over millions of years.\u201d<\/strong> \u00a0In fact, evolution has not worked to maximize life span, but only to make it sufficient to assure time for reproduction. \u00a0Aging is a form of programmed death, on a flexible but finite schedule. \u00a0It is fixed in our genes. \u00a0There are mechanisms of aging that have been programmed into living things since the first eukaryotic<\/a> cells. \u00a0Telomere attrition has been used to time the life cycle and form a basis for programmed death for at least a billion years. \u00a0Many species of protozoans do not express telomerase during mitosis (but only during conjugation<\/a>), so their telomeres shorten with each reproduction, leading to a limit of a few hundred reproductions per cell line. \u00a0This mechanism is the precursor to telomeric aging that exists to the present day in humans and many other higher animals.<\/p>\n

3. \u00a0\u201cExpressing telomerase will increase the risk of cancer.\u201d<\/strong> There is a great deal of theoretical concern in this direction, which I think is entirely misguided. \u00a0It is true that cancer cells express telomerase. \u00a0It is not true that expressing telomerase causes a cell to become cancerous. \u00a0This relationship is clearly explained by two seasoned experts (Shay and Wright 2011<\/a>)<\/p>\n

In early studies, the only way of increasing telomerase activity in lab animals was to add extra genes for telomerase. \u00a0Technology in the early 2000s did not permit a gene to be added at a targeted location, but only inserted randomly into a chromosome. \u00a0Tampering with the structure of DNA in this way is known to increase cancer<\/a> risk no matter what gene is added or subtracted. \u00a0In three of these early studies, cancer rates in mice were increased [1<\/a>, 2<\/a>, 3<\/a>].<\/p>\n

There are no lab studies to my knowledge in which activating the native telomerase has increased the risk of cancer. \u00a0The modern view<\/a> is that \u201cwhile telomerase does not drive the oncogenic process, it is permissive and required for the sustain growth of most advanced cancers.\u201d \u00a0Recent perspectives from both Harvard lab of de Pinho<\/a> and the Spanish lab of Blasco<\/a> focus on the potential for telomerase to decrease cancer risk, and these were the very people who produced the three studies suggesting caution a decade earlier.<\/p>\n

And there are many studies showing that (a) telomerase expression does not increase cancer risk in lab animals, and (b) short telomeres are a very strong cancer risk. \u00a0I believe that telomerase activators will greatly reduce the cancer rate, first by eliminating cells that are pro-inflammatory and potentially carcinogenic because their telomeres have become short, and second by rejuvenating the immune system, which is our primary defense against cancer. \u00a0I published an article on this subject<\/a> last year.<\/p>\n

Why we might expect big life expectancy gains from extending telomeres<\/strong><\/p>\n

This is the affirmative question, then: what makes me think that telomere extension will have such a powerful effect on diverse aspects of aging biology?<\/p>\n

A) \u00a0 \u00a0Telomere attrition is an ancient mechanism of aging.<\/strong><\/p>\n

Protists were the first eukaryotic cells, and they appeared on earth a billion years ago (they were a leap up in complexity from bacteria, which had been around 3 billion years before). \u00a0In protists, DNA is linear and hence there are telomeres and a need for telomerase. \u00a0Since protists reproduce by simple cell division, you would not expect that the cells would \u201cage\u201d or even that the concept of aging could have any meaning for their life cycle. \u00a0But a protist cell lineage can age, and indeed some do. \u00a0This is the oldest known mechanism of aging, and it is implemented through withholding telomerase.<\/p>\n

Paramecia are an example. \u00a0When paramecia reproduce, their cells simply fission, the DNA replicates, and no telomerase is expressed. \u00a0Hence, telomeres get shorter with each cell division. Paramecia can conjugate, which is a primitive form of sexual gene exchange. \u00a0Two paramecium cells merge, mingle their DNA, and then separate. \u00a0It is only in the conjugation process that telomerase is expressed. \u00a0Therefore, any cell lineage that does not conjugate will die out after a few hundred generations. \u00a0This prevents cell colonies from becoming too homogeneous. \u00a0Thus aging is a billion years old, and some of the genetic mechanisms of aging have been conserved and passed on through all the transformations of multicellular life (William R Clark has written two accessible books [1<\/a>, 2<\/a>] on this topic.)<\/p>\n

B) \u00a0 \u00a0Telomeres shorten with age in humans.<\/strong><\/p>\n

This has been known for twenty years<\/a>.<\/p>\n

C) \u00a0 \u00a0People with shorter telomeres have a much higher risk of mortality.<\/strong><\/p>\n

This was established by Richard Cawthon (2003<\/a>) in a paper which took the field by surprise. \u00a0Researchers before then had assumed on erroneous theoretical grounds that telomere attrition, which was known to occur, could not have anything to do with human aging. \u00a0After all, if aging were as simple as telomere attrition, then the body could solve the problem merely by expressing telomerase. \u00a0This would enhance individual fitness. \u00a0Why would not evolution have found such a simple expedient? \u00a0(The answer, of course, is that natural selection favors aging, for the sake of the demographic stability \u2013 an evolutionary force not recognized by most evolutionary biologists.) \u00a0In Cawthon\u2019s study, the top \u00bc of 60-year-olds in terms of telomere length had half the overall mortality risk as the bottom \u00bc. \u00a0Cawthon had access to a unique database of 20-year-old blood samples, and to my knowledge his study has not been replicated or refuted these 11 years.<\/p>\n

\u00a0<\/strong><\/p>\n

D) \u00a0\u00a0\u00a0\u00a0People with short telomeres have a higher risk of diseases, especially CVD, after adjusting for age. \u00a0<\/strong>The association with cardiovascular disease has been consistent, not just in Cawthon\u2019s original<\/a> study, but also several other studies [Ref<\/a> Ref<\/a> Ref<\/a>]. \u00a0There are also associations with dementia [Ref<\/a>, Ref<\/a>] and with diabetes [Ref<\/a>, Ref<\/a>].<\/p>\n

E) \u00a0 \u00a0Animals with short telomeres also have a higher risk of mortality, after adjusting for age.<\/strong><\/p>\n

This has been established in several bird species [Ref<\/a> Ref<\/a> Ref<\/a>], and in baboons<\/a>. \u00a0In 2003, it was already known<\/a> that long-lived species tend to lose telomere length more slowly, and short-lived species lose telomeres more rapidly.<\/p>\n

F) \u00a0 \u00a0In limited studies with mice, telomerase enhancers have led to rejuvenation.<\/strong> \u00a0(Mice are expected to be a much less effective target for this strategy than humans, because to all appearances, aging in humans relies on telomere attrition much more so than in mice.)<\/p>\n

The first experiment of this type was done in 2008. \u00a0In the Spanish lab of Maria Blasco, Tomas-Loba<\/a> engineered mice that were both cancer-resistant and contained an extra telomerase gene, expressed in some tissues where, even in mice, it would not normally be found. \u00a0Cancer-free mice with the extra telomerase lived 18% longer than cancer-free mice with only the normal gene for telomerase.<\/p>\n

But soon it was discovered that all the experimental precautions around cancer may not have been necessary. \u00a0The same lab Bernardes de Jesus (2011)<\/a> reported that they could increase health span in mice with the commercial product called TA-65 (widely rumored to be cycloastragenol) with no increase in the incidence of cancer. \u00a0Cycloastragenol is a weak telomerase activator compared to man-made chemicals discovered at Sierra Sciences, and even compared to some other herbal extracts. \u00a0Nevertheless, the Blasco lab was able to show that the shortest telomeres in the mice were elongated, and that markers of health including insulin sensitivity were improved by short-term treatment with TA-65.<\/p>\n

Blasco\u2019s lab then worked with a more potent (though more dangerous) method of telomerase induction: infection with a retrovirus engineered to introduce telomerase into the nuclear DNA of the infected cell. \u00a0\u201cTreatment of 1- and 2-year old mice with an adeno associated virus (AAV) of wide tropism expressing mouse TERT had remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging.\u201d (Bernardes \u00a0de Jesus, Vera et al. 2012) \u00a0The mice lived 13% longer when AAV treatment began at age 2 years, and 24% longer when treatment began at 1 year. \u00a0There was no increase in cancer incidence.<\/p>\n

The most dramatic example of rejuvenation<\/a> is from the Harvard laboratory of Robert de Pinho. \u00a0Normally, mice (unlike people) express telomerase freely through their lifetimes. \u00a0These scientists engineered a mouse without the normal (always on) gene for telomerase, but instead had a telomerase gene that could be turned on and off at will by use of a chemical signal that the experimenters could feed to the mice. \u00a0As these mice grew older, they developed multiple, severe symptoms of degeneration in the testes, spleen, intestine, nervous system and elsewhere. \u00a0All these symptoms were not just halted but reversed when telomerase was turned on late in the animals\u2019 lives. The effect on the nervous system is particularly interesting because nerve cells last a lifetime and do not depend on continual regeneration from stem cells, the way blood and intestinal and skin cells do. \u00a0Nevertheless, these mice with telomerase turned off suffered sensory deficiencies and impaired learning that was reversed when the experimenters administered the chemical signal to turn telomerase back on.<\/p>\n

A Stanford\/Geron research group<\/a> worked with \u201cskin\u201d grown from human cells in a lab setting. \u00a0They found they were able to restore youthful elasticity, softness and texture to the cultured \u201cskin\u201d by infecting the cells with an engineered retrovirus that inserted the gene for telomerase.<\/p>\n

G) \u00a0 \u00a0 In addition to its function in lengthening telomeres, telomerase also acts as a kind of growth hormone.<\/strong><\/p>\n

This fact was suspected as early as the 1990s, and confirmed definitively in a Stanford experiment [Ref<\/a>, Ref<\/a>, Ref<\/a>, Ref<\/a>]. \u00a0In this experiment, mice were engineered with \u201cdenatured\u201d telomerase that lacked the RNA template for creating telomeres. \u00a0Still, the telomerase was shown to induce hair growth. \u00a0Telomerase has been shown to activate affect a hormonal signaling pathway<\/a> called Wnt. Other functions for telomerase are reviewed by Cong and Shay (2008<\/a>).<\/p>\n

H) \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0In one human case, huge doses of herbal telomerase activators has led to rejuvenation.<\/strong><\/p>\n

I am recently in touch with a physicist from Kansas who has been taking super-high doses of telomerase-activating herbs and supplements for six years and claims to look and feel younger, with improved athletic performance. \u00a0He may be an interesting case study. \u00a0Jim Green<\/a>\u00a0has commented on this blog site.<\/p>\n

\u00a0The Bottom Line<\/strong><\/p>\n

In my opinion, telomerase activation is a field that offers the most potential for human life extension in the next few years. \u00a0This research is languishing for lack of funds, and for lack of attention.<\/p>\n","protected":false},"excerpt":{"rendered":"

Telomere biology has the potential to extend human life span, to dramatically lower rates of the great remaining killer diseases: heart disease, stroke, and Alzheimer\u2019s. \u00a0All three diseases increase exponentially with age, and their toll will be slashed as we we learn how to address the body\u2019s aging clocks. You would think that the 2009 … Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"jetpack_post_was_ever_published":false,"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-199","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nThe most promising medical technology on the horizon today - Josh Mitteldorf<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2014\/01\/25\/the-most-promising-medical-technology-on-the-horizon-today\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"The most promising medical technology on the horizon today\" \/>\n<meta property=\"og:description\" content=\"Telomere biology has the potential to extend human life span, to dramatically lower rates of the great remaining killer diseases: heart disease, stroke, and Alzheimer\u2019s. \u00a0All three diseases increase exponentially with age, and their toll will be slashed as we we learn how to address the body\u2019s aging clocks. 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\\\/\\\/mathforum.org\\\/~josh\",\"sameAs\":[\"http:\\\/\\\/AgingAdvice.org\"],\"url\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/author\\\/joshmitteldorf\\\/\"}]}<\/script>\n<!-- \/ Yoast SEO Premium plugin. -->","yoast_head_json":{"title":"The most promising medical technology on the horizon today - Josh Mitteldorf","robots":{"index":"index","follow":"follow","max-snippet":"max-snippet:-1","max-image-preview":"max-image-preview:large","max-video-preview":"max-video-preview:-1"},"canonical":"https:\/\/scienceblog.com\/joshmitteldorf\/2014\/01\/25\/the-most-promising-medical-technology-on-the-horizon-today\/","og_locale":"en_US","og_type":"article","og_title":"The most promising medical technology on the horizon today","og_description":"Telomere biology has the potential to extend human life span, to dramatically lower rates of the great remaining killer diseases: heart disease, stroke, and Alzheimer\u2019s. \u00a0All three diseases increase exponentially with age, and their toll will be slashed as we we learn how to address the body\u2019s aging clocks. 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. 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