{"id":892,"date":"2019-10-29T17:01:18","date_gmt":"2019-10-29T17:01:18","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=892"},"modified":"2019-10-29T17:01:18","modified_gmt":"2019-10-29T17:01:18","slug":"telomeres-the-longer-the-better","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2019\/10\/29\/telomeres-the-longer-the-better\/","title":{"rendered":"Telomeres: The Longer the Better"},"content":{"rendered":"<p><i>Mice have much longer telomeres than we do, long enough that telomeres never get critically short in a mouse lifetime. Yet, when designer mice were engineered to have even longer telomeres (hyper-long by any standard, longer than we can account for the use of them), these mice lived longer and were healthier in every way than mice with normal-long telomeres. Lab mice usually die of cancer, and these with the longer telomeres were protected from cancer, along with every other ailment that was looked at.<\/i><\/p>\n<hr \/>\n<p>First, I ask your indulgence if I harp on the obvious: this result is not consistent with the prevailing theory of telomeres. In most vertebrates, telomerase is rationed so that telomeres are allowed gradually to shorten over a lifetime, and this is explained by most evolutionary biologists and geroscientists as an anti-cancer program. According to theory, in each species, telomere length has been optimized by natural selection as a compromise between longer telomeres (allowing stem cells to last longer without senescing) and shorter telomeres (which provide a firewall against cancer, a drop-dead signal when unchecked cell growth might be life-threatening). In contrast, experiments have frequently shown that longer telomeres lead to a <b><i>lower<\/i><\/b> cancer rate. Blasco\u2019s new result is a clear case. We can\u2019t explain telomere dynamics as a cancer prevention program.<\/p>\n<p>(For background on what telomeres are and how they function, I refer you to my <a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2012\/11\/01\/telomerase-as-a-fountain-of-youth\/\">early blogs<\/a> on the subject.)<\/p>\n<p>But beyond this, there remain many mysteries. This study highlights the truth that we don\u2019t understand the mechanisms. How exactly are hyper-long telomeres working on a biochemical level? What can a hyper-long telomere do that an extra-long (regular mouse) telomere can\u2019t do?<\/p>\n<p>Known mechanisms include:<\/p>\n<ul>\n<li style=\"font-weight: 400\">Senescent cells. Much of the literature has focused on the importance not of <b><i>average TL<\/i><\/b> but on the <b><i>shortest<\/i><\/b> because a few cells run out of telomere and become senescent, and they poison the rest of the body. This is called <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC4166495\/\">SASP<\/a>, for Senescent-Associated Secretory Phenotype.<\/li>\n<li style=\"font-weight: 400\">Telomerase as an enzyme. Telomerase is best known for its ability to elongate telomeres, but there is evidence that it has <a href=\"https:\/\/www.nature.com\/articles\/cr200874\">other effects as well<\/a>.<\/li>\n<li style=\"font-weight: 400\">TPE &#8211; the <a href=\"http:\/\/genesdev.cshlp.org\/content\/28\/22\/2464.short\">telomoere position effect<\/a>.\u00a0 This is the only one that fits. Long telomeres wrap back around the end of the DNA, actually masking expression of the genes closet to the end of the chromosome.\u00a0 The Blasco study raises the possibility that we\u2019re better off when the genes near the ends of the telomeres are silenced.<\/li>\n<\/ul>\n<p>In my story, genes that have legitimate uses are turned against the body in old age. But there are no pure \u201caging genes\u201d because it\u2019s hard for such genes to evolve uphill (against individual selection). Has Blasco discovered an exception? Are these genes near the end of the chromosometrue \u201caging genes\u201d? Or is it an example of evolved pleiotropy [<a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2018\/05\/14\/3-stories-of-sex-and-death-in-evolution\/\">my blog<\/a>; <a href=\"https:\/\/www.biorxiv.org\/content\/10.1101\/321588v1\">BioRxiv preprint<\/a>].<\/p>\n<figure id=\"attachment_893\" aria-describedby=\"caption-attachment-893\" style=\"width: 574px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"size-large wp-image-893\" src=\"https:\/\/scienceblog.com\/wp-content\/uploads\/sites\/2\/2019\/10\/blasco-2019-1024x354.png\" alt=\"\" width=\"584\" height=\"202\" srcset=\"https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2019\/10\/blasco-2019-1024x354.png 1024w, https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2019\/10\/blasco-2019-300x104.png 300w, https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2019\/10\/blasco-2019-768x266.png 768w, https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2019\/10\/blasco-2019-500x173.png 500w, https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2019\/10\/blasco-2019.png 1290w\" sizes=\"auto, (max-width: 584px) 100vw, 584px\" \/><figcaption id=\"caption-attachment-893\" class=\"wp-caption-text\">From Munos-Lorente, 2019, https:\/\/www.nature.com\/articles\/s41467-019-12664-x\/<\/figcaption><\/figure>\n<p><b>Context<\/b><\/p>\n<p>Maria Blasco\u2019s Madrid telomere lab has been at the forefront of this field for more than a decade. The new experiment is right on the bleeding edge of biotech and genetic manipulation, where the Blasco lab has staked out territory.<\/p>\n<p>I learned that you can\u2019t make mouse egg cells with long telomeres because the body\u2019s process of making the egg standardizes the telomere length as it wipes clean the epigenetic markers and rewrites a starting imprint. How to get around this? Blasco grew eggs just until the third cell division (8 cells), then injected embryonic stem cells that had been grown saturated with telomerase to give them the hyper-long telomeres. Yes, this tiny embryo, just 8 cells in size, was micro-injected by hand with many stem cells, cloned to be genetically identical, so they would not fight immunologically with the cells already in the embryo. The injected cells were marked with a gene for green fluorescent protein (GFP) so descendants of the long-telomere stem cells could be identified later. The <a href=\"https:\/\/www.nature.com\/articles\/s41467-019-12664-x\">article<\/a> doesn\u2019t indicate exactly how, but the original 8 cells were induced to bow out, so that 100% of the cells in the mice that grew from these embryos had the GFP marker, and presumably, they all had the hyper-long telomeres as well. Thus, the lab made \u201cdesigner\u201d mice out of cells, every one of which had telomeres that (AFAWK) were longer than nature has any use for.<\/p>\n<p>The stated inspiration for the experiment was to determine whether the hyper-long telomeres led to any detrimental effects. What they found was that hyper-long telomeres were <b><i>beneficial <\/i><\/b>in every way. The effect seems to be related to caloric restriction, since the mice are noticeably leaner and their insulin sensitivity remains high at advanced ages when mice usually become insulin resistant. Perhaps independent of these changes, the hyper-long mice had less DNA damage with age and more efficient mitochondrial metabolism.<\/p>\n<p>Telomeres are full of surprises, and this may signal a new telomere mechanism, probably epigenetic, that is undescribed previously. But if it is to be described with known biochemistry, the only candidate is TPE, the <a href=\"https:\/\/science.sciencemag.org\/content\/292\/5524\/2075\">telomere position effect<\/a>. Long telomeres fold back on the end of the chromosome, masking some genes that are located near the end. It is already known that unmasking those genes when telomeres become short has pro-aging effects. But the new result involves telomeres that are (presumably) longer than anything that is found in nature or in the mouse evolutionary history. It follows that the hyper-long telomeres are folding back so as to mask genes that just happen to be near (but not to near) the chromosome end. In this picture, these genes just happen to be pro-obesity, or insulin-blocking. The effect is not evolved, but just a chance occurrence. I don\u2019t like such explanations from chance, so I\u2019d bet on a new telomere mechanism that is yet to be characterized.<\/p>\n<p>&nbsp;<\/p>\n<p><b>Related study from the Blasco Lab<\/b><\/p>\n<p><a href=\"https:\/\/www.pnas.org\/content\/pnas\/116\/30\/15122.full.pdf\">Another study<\/a> (last summer) from the Blasco lab looked across species for relationships between telomere dynamics and species life span. This follows on the work of <a href=\"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1111\/j.1474-9726.2006.00262.x\">Seluanov and Gorbunova<\/a> a few years ago. The previous work concluded that telomere length is most closely related to the body mass but not lifespan across rodent species. The authors tried to relate this to <a href=\"https:\/\/en.wikipedia.org\/wiki\/Peto%27s_paradox\">Peto\u2019s Paradox<\/a>, which is the observation that large, long-lived animals ought to have much higher cancer rates than observed, assuming that cancer results from a random transformation event in a single cell. In the new work, Blasco finds the closest correlation between lifespan and the rate of telomere loss.<\/p>\n<blockquote><p>We observed that mean telomere length at birth does not correlate with species life span since many short-lived species had very long telomeres, and longlived species had very short telomeres.<\/p><\/blockquote>\n<p>In short-lived species, telomere erosion happens much more rapidly: 7,000 base pairs per year are lost in mice, compared with less than 100 in humans.<\/p>\n<p>In the old story [<a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/telomerase-as-a-fountain-of-youth\/\">as I have reported it<\/a>], telomeres shorten over a lifetime because stem cells lose a little telomere length with each cell replication. But this huge difference in telomere attrition rates can\u2019t be accounted for in this way. Stem cells in mice don\u2019t replicate 100 times faster than in humans. So something else is going on. Probably, there is partial expression of telomerase in a way that is programmed under control of natural selection. Telomere shortening with age has evolved in a way that contributes to aging via TPE. But (probably, by my account) telomere shortening is <b><i>not<\/i><\/b> the principal means of programmed aging, because the correlation between telomere length and age is <a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/04\/29\/large-new-survey-tracks-telomere-length-and-mortality\/\">too weak<\/a>. <a href=\"https:\/\/www.google.com\/books\/edition\/The_Telomerase_Revolution\/oceECgAAQBAJ\"><span style=\"font-weight: 400\">Mike Fossel<\/span><\/a><span style=\"font-weight: 400\"> continues to promote the idea that <strong><em>relative<\/em><\/strong> but not absolute telomere length is a good indicator, and indeed a driver of aging. That sounds like it accords in the abstract with the new results, but details remain elusive.<\/span><\/p>\n<p><b>The Bottom Line<\/b><\/p>\n<p>It\u2019s clear that telomere shortening plays a role in aging, though not a dominant role. It\u2019s clear that telomere shortening is completely under the body\u2019s control, therefore an evolved adaptation. Beyond this, the subject seems complicated, and there is good evidence that there are mechanisms involved beyond what we know about.<\/p>\n<p>At a given age, telomere length in humans does not correlate with health risks. On this basis, I have argued that various methylation clocks are far better measures of biological age, and perhaps the <a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2019\/03\/05\/dnam-grimage-the-newest-methylation-clock\/\">GrimAge clock<\/a> is best.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Mice have much longer telomeres than we do, long enough that telomeres never get critically short in a mouse lifetime. Yet, when designer mice were engineered to have even longer telomeres (hyper-long by any standard, longer than we can account for the use of them), these mice lived longer and were healthier in every way &#8230; <a title=\"Telomeres: The Longer the Better\" class=\"read-more\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2019\/10\/29\/telomeres-the-longer-the-better\/\" aria-label=\"Read more about Telomeres: The Longer the Better\">Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":893,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_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":"","jetpack_post_was_ever_published":false},"categories":[1],"tags":[],"class_list":["post-892","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-uncategorized"],"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v27.6 (Yoast SEO v27.6) - https:\/\/yoast.com\/product\/yoast-seo-premium-wordpress\/ -->\n<title>Telomeres: The Longer the Better - 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\/2019\/10\/29\/telomeres-the-longer-the-better\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Telomeres: The Longer the Better\" \/>\n<meta property=\"og:description\" content=\"Mice have much longer telomeres than we do, long enough that telomeres never get critically short in a mouse lifetime. Yet, when designer mice were engineered to have even longer telomeres (hyper-long by any standard, longer than we can account for the use of them), these mice lived longer and were healthier in every way ... Read more\" \/>\n<meta property=\"og:url\" content=\"https:\/\/scienceblog.com\/joshmitteldorf\/2019\/10\/29\/telomeres-the-longer-the-better\/\" \/>\n<meta property=\"og:site_name\" content=\"Josh Mitteldorf\" \/>\n<meta property=\"article:published_time\" content=\"2019-10-29T17:01:18+00:00\" \/>\n<meta property=\"og:image\" content=\"https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2019\/10\/blasco-2019.png\" \/>\n\t<meta property=\"og:image:width\" content=\"1290\" \/>\n\t<meta property=\"og:image:height\" content=\"446\" \/>\n\t<meta property=\"og:image:type\" content=\"image\/png\" \/>\n<meta name=\"author\" content=\"Josh Mitteldorf\" \/>\n<meta name=\"twitter:card\" content=\"summary_large_image\" \/>\n<meta name=\"twitter:label1\" content=\"Written by\" \/>\n\t<meta name=\"twitter:data1\" content=\"Josh Mitteldorf\" \/>\n\t<meta name=\"twitter:label2\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data2\" content=\"7 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"Article\",\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2019\\\/10\\\/29\\\/telomeres-the-longer-the-better\\\/#article\",\"isPartOf\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2019\\\/10\\\/29\\\/telomeres-the-longer-the-better\\\/\"},\"author\":{\"name\":\"Josh Mitteldorf\",\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/#\\\/schema\\\/person\\\/214c5d1dad9f15c48f03128d5cfccdb1\"},\"headline\":\"Telomeres: The Longer the Better\",\"datePublished\":\"2019-10-29T17:01:18+00:00\",\"mainEntityOfPage\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2019\\\/10\\\/29\\\/telomeres-the-longer-the-better\\\/\"},\"wordCount\":1412,\"commentCount\":68,\"publisher\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/#organization\"},\"image\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2019\\\/10\\\/29\\\/telomeres-the-longer-the-better\\\/#primaryimage\"},\"thumbnailUrl\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/wp-content\\\/uploads\\\/sites\\\/2\\\/2019\\\/10\\\/blasco-2019.png\",\"inLanguage\":\"en-US\",\"potentialAction\":[{\"@type\":\"CommentAction\",\"name\":\"Comment\",\"target\":[\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2019\\\/10\\\/29\\\/telomeres-the-longer-the-better\\\/#respond\"]}],\"copyrightYear\":\"2019\",\"copyrightHolder\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/#organization\"}},{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2019\\\/10\\\/29\\\/telomeres-the-longer-the-better\\\/\",\"url\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2019\\\/10\\\/29\\\/telomeres-the-longer-the-better\\\/\",\"name\":\"Telomeres: The Longer the Better - 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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: The Longer the Better - 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\/2019\/10\/29\/telomeres-the-longer-the-better\/","og_locale":"en_US","og_type":"article","og_title":"Telomeres: The Longer the Better","og_description":"Mice have much longer telomeres than we do, long enough that telomeres never get critically short in a mouse lifetime. Yet, when designer mice were engineered to have even longer telomeres (hyper-long by any standard, longer than we can account for the use of them), these mice lived longer and were healthier in every way ... 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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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