{"id":547,"date":"2016-12-12T03:44:40","date_gmt":"2016-12-12T03:44:40","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=547"},"modified":"2016-12-13T18:38:01","modified_gmt":"2016-12-13T18:38:01","slug":"telomeres-too-much-of-a-good-thing","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2016\/12\/12\/telomeres-too-much-of-a-good-thing\/","title":{"rendered":"Telomeres—too much of a good thing?"},"content":{"rendered":"

One of the major themes in aging science of the last 15 years has been that there is natural variation in telomere length, and individuals with longer telomeres have lower disease risk and longer life expectancy than those with shorter telomeres. \u00a0A <\/i>paper last week<\/i><\/a> in <\/i>Nature Structural and Molecular Biology found that stem cell telomeres are actively maintained at a target length, not just by elongation (with telomerase or ALT) when they get too short but by active trimming when they get \u201ctoo long\u201d. \u00a0We know what \u201ctoo short\u201d means:<\/i> short telomeres lead to cellular senescence. \u00a0Cells with short telomeres are not just falling down on the job; they are toxic. \u00a0But what does it mean for telomeres to be \u201ctoo long\u201d?<\/i><\/p>\n

\n

The headline in MedicalXpress<\/a> says \u201cScientists find that for stem cells to be healthy, telomere length has to be just right\u201d. \u00a0The story underneath includes the claim that \u201creally long telomeres caused telomeric fragility, which can lead to initiation of cancer\u201d. \u00a0But now that I\u2019ve read the research article<\/a> on which it is based and some of the references in that article, I see that the part about cancer was tacked onto a (new and interesting) research finding. \u00a0I\u2019m convinced that the meme \u201clong telomeres lead to cancer\u201d has been resounding in an academic echo chamber for 25 years; that it never has had an experimental foundation, and its theoretical foundation is just wrong.<\/p>\n

What is new and interesting is this: \u00a0researchers at Salk Institute have discovered a mechanism for trimming telomeres. \u00a0In our previous understanding, telomeres lose length every time a chromosome is copied (every time a new cell is created). \u00a0Telomeres are partially rebuilt by the enzyme telomerase, or by a less direct mechanism called ALT. \u00a0Telomeres are fully rebuilt only when new life is created, in a germ cell or a fertilized egg. \u00a0In the previous understanding, shortening of telomeres is passive, while lengthening is active. \u00a0The new study documents an active mechanism for shortening telomeres.<\/p>\n

Part of each telomere is unpaired, a single strand of DNA extending past the end of the chromosome, and folded back over the main (double-stranded) part. \u00a0Single-stranded DNA normally means a problem, and the cell nucleus has multiple means to repair or degrade it. \u00a0To protect the telomere from being attacked (to prevent fixing of what ain\u2019t broke) the telomere is chaperoned by various protective proteins, most famously shelterin<\/a>.<\/p>\n

We have known that stem cells can express telomerase to counteract telomere shortening, though (in humans) there is not enough to keep telomeres from shortening progressively through a lifetime. \u00a0The new finding is that when a stem cell detects that telomeres are \u201ctoo long\u201d, there is a way to trim them back. \u00a0A strand of DNA is manufactured that is complementary to the telomere\u2019s repeated sequence TTAGGG. \u00a0The complementary strand (that would be AATCCC, repeated) \u00a0has an affinity for the telomere repeats, and it finds and binds to a segment of telomere, then circles, \u201cbites its tail\u201d, and breaks off a ringlet of double-stranded telomere-stuff (called a T-circle), effectively shortening the telomere.<\/p>\n

\"\"<\/p>\n

What\u2019s wrong with extra-long telomeres?<\/b><\/p>\n

The obvious question: why is the cell doing this? \u00a0What is the danger of telomeres that are too long? \u00a0One natural place to look is in the telomere position effect<\/a> (TPE). \u00a0Telomeres fold back over the chromosome in such a way as to silence genes near the ends. \u00a0We might expect that the right genes must be silenced at the right times, and that silencing too many genes with an extra-long telomere would cause problems. \u00a0My own best guess is that this is the right answer.<\/p>\n

Another hypothesis is that extra-long telomeres are inherently unstable and unmanageable. \u00a0But the present studies were done with human cell cultures, where telomeres are ~10,000 BP in length; mice commonly have telomeres ten times that long<\/a> without causing problems.<\/p>\n

The conventional hypothesis is that telomeres are trimmed to prevent cancer, and that is the spin put on the findings by the authors of the paper in their press release<\/a>. \u00a0\u201cWe were surprised to find that forcing cells to generate really long telomeres caused telomeric fragility, which can lead to initiation of cancer.\u201d \u00a0In the paper itself, they were more circumspect about this explanation, as is academically appropriate. \u00a0These people are masters at what they do (Since spending time at NIBS<\/a> in Beijing, I have an expanded awe for the experimental virtuosi who are able to infer reliable data about the inner workings of cells.) \u00a0But they are not theorists and they trust the community of biological theorists to supply the theoretical framework for interpreting their result.<\/p>\n

In this case, the trust is misplaced. \u00a0The idea that telomeres are kept short to prevent cancer was originally proposed by (Nobel laureate) Carol Greider (1990<\/a>), and has been promoted most explicitly by Judith Campisi (1999<\/a>) before she became convinced by experimental data that the situation is more complicated, that short telomeres are more likely to cause than to prevent cancer (2013<\/a>). \u00a0Through strength in numbers the cancer\/telomere hypothesis has achieved \u201cecho chamber\u201d status–many researchers cite each other\u2019s secondary statements on the subject, until tracing the empirical support for the hypothesis becomes unnecessary. \u00a0It is common knowledge.<\/p>\n

One of the authorities cited in the original paper is this article<\/a> which is actually about deletion of a gene for a shelterin-related protein that binds to telomeres. \u00a0When this gene is deleted, telomeres become unstable and cancer rates rise. \u00a0But the article is not about telomeres that are \u201ctoo long\u201d. \u00a0Another authority for the hypothesis that is cited in the original paper is this book chapter<\/a>. \u00a0The chapter is not about cancer, but it does peripherally cite this study from NCI<\/a>, which finds that cancer is associated with short telomeres, but not long telomeres.<\/p>\n

Contrary evidence: health benefits from extra-long telomeres<\/b><\/p>\n

Just last spring, Maria Blasco\u2019s group at the Spanish National Cancer Research Centre gave us this study<\/a>, in which stem cells with hyper-long telomeres (up to 300,000 BP) were introduced into mice (in which telomeres normally are already 10 times as long as humans\u2019). \u00a0\u201cMice with hyper-long telomeres…accumulate fewer cells with short telomeres and less DNA damage with age, and express lower levels of p53\u2026.We further show that wound-healing rates in the skin are increased in chimaeric mice.\u201d \u00a0No life span data is reported, but cancer risk was lower in the mice with hyper-long telomeres.<\/p>\n

This study<\/a> from another research group at the same institution linked the extraordinary healing and regeneration capacity of very young mice to their extra-long telomeres.<\/p>\n

In this study<\/a> from UCSF, published just this fall, heart patients whose telomeres were lengthening over the four-year span of the study had 1\/3\u00a0the mortality rate of matched patients whose telomeres were shortening over the same time span.<\/p>\n

Are short telomeres a symptom or a cause of age-related disease?<\/b><\/p>\n

This is a controversial question only because the causal hypothesis is in direct opposition to standard evolutionary theory. \u00a0So much the worse for standard evolutionary theory.<\/p>\n

One causal mechanism which is incontrovertible is that cells become senescent when their telomeres shorten beyond a critical length. \u00a0Senescent cells are not just non-functional, they are toxic<\/a>. \u00a0Removing senescent cells from the body has been shown to lengthen life span in mice<\/a>, and senolytic<\/a> agents are being developed<\/a> for human use. \u00a0Many of us in the life extension movement regard senolytics as the #1 most promising strategy<\/a> for major life extension in the near term.<\/p>\n

The question of causality can be answered definitively by intervening to make telomeres longer or shorter \u201cby hand\u201d. \u00a0If short telomeres are a mere marker of past stress, then this should make little difference in the trajectory of aging; but if short telomeres are a cause of aging, then we expect that lengthening telomeres should lengthen life expectancy and lower the (age-adjusted) risk of disease. \u00a0In fact, this experimental model has been realized several times in mouse studies, two of which are referenced just a few paragraphs above [#1<\/a>, #2<\/a>]. \u00a0The most dramatic success<\/a> was in dePinho\u2019s Harvard lab, but there are also impressive results<\/a> from Blasco\u2019s group in Madrid.<\/p>\n

If lengthening telomeres is an effective life extension strategy for mice, it should be all the more so for humans, who have shorter telomeres, longer life spans, and less telomerase than mice.<\/p>\n

In the face of this evidence, there are still some influential researchers and advocates in the anti-aging community who opine that \u201cOn the whole telomere length looks a lot like a marker of aging rather than the cause of problems: the groups that primarily seek to engineer longer telomeres in search of a way to slow aging are probably putting the cart before the horse.\u201d [quoted today at FightAging.org<\/a>] \u00a0Meanwhile, Michael Fossel<\/a> has initiated a clinical trial of telomerase gene therapy to treat dementia. \u00a0Cancer scares from the echo chamber are\u00a0spooking the venture capital that would be so welcome for startups that are seeking to bring telomerase therapy to the public.<\/p>\n","protected":false},"excerpt":{"rendered":"

One of the major themes in aging science of the last 15 years has been that there is natural variation in telomere length, and individuals with longer telomeres have lower disease risk and longer life expectancy than those with shorter telomeres. \u00a0A paper last week in Nature Structural and Molecular Biology found that stem cell … 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_newsletter_access":"","_jetpack_dont_email_post_to_subs":true,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":"","jetpack_post_was_ever_published":false},"categories":[1],"tags":[],"class_list":["post-547","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nTelomeres—too much of a good thing? - 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\/2016\/12\/12\/telomeres-too-much-of-a-good-thing\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Telomeres—too much of a good thing?\" \/>\n<meta property=\"og:description\" content=\"One of the major themes in aging science of the last 15 years has been that there is natural variation in telomere length, and individuals with longer telomeres have lower disease risk and longer life expectancy than those with shorter telomeres. \u00a0A paper last week in Nature Structural and Molecular Biology found that stem cell ... 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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":"Telomeres—too much of a good thing? - 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\/2016\/12\/12\/telomeres-too-much-of-a-good-thing\/","og_locale":"en_US","og_type":"article","og_title":"Telomeres—too much of a good thing?","og_description":"One of the major themes in aging science of the last 15 years has been that there is natural variation in telomere length, and individuals with longer telomeres have lower disease risk and longer life expectancy than those with shorter telomeres. \u00a0A paper last week in Nature Structural and Molecular Biology found that stem cell ... 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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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