{"id":551,"date":"2016-12-31T23:18:15","date_gmt":"2016-12-31T23:18:15","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=551"},"modified":"2017-01-01T11:56:12","modified_gmt":"2017-01-01T11:56:12","slug":"epigenetics-and-the-direction-of-anti-aging-science","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2016\/12\/31\/epigenetics-and-the-direction-of-anti-aging-science\/","title":{"rendered":"Epigenetics and the Direction of Anti-Aging Science"},"content":{"rendered":"

Dear Readers –<\/p>\n

It\u2019s been a deeply gratifying year for me. \u00a0Twenty years ago, I first started writing that aging is something the body does to itself, a body function, rather than deterioration or loss of function. \u00a0Journals would not even send my submission out for peer review. \u00a0Journal of Theoretical Biology sent me the considered opinion of their anonymous reviewer, \u201cJTB shouldn\u2019t touch this topic with a ten-foot pole.\u201d \u00a0The conflict with prevailling evolutionary theory was just too deep.<\/p>\n

But in the interim, the evidence has continued to pile up, and many medical researchers have taken the message to heart in a practical way, setting aside the evolutionary question and just pursuing approaches that seem to work. \u00a0The most promising developments in anti-aging medicine involve changing the signaling environment rather than trying to \u201cfix what goes wrong\u201d with the body.<\/p>\n

My popular book<\/a> exploring the evolutionary origins of aging (and implications for medical science) came out in June, and an academic version<\/a> of the same content came out in October. \u00a0Gandhi taught me,<\/p>\n

\u201cFirst they ignore you…
\nthen they laugh at you…
\nthen they fight you…
\nthen you win.\u201d<\/p><\/blockquote>\n

The paradigm of programmed aging passed this year from stage 2 to stage 3, with prominent articles arguing against the possibility of programmed aging [Kirkwood<\/a>, de Grey<\/a>, Vijg & Kennedy<\/a>]. \u00a0Current Aging Sciences devoted a full issue<\/a> to the question. \u00a0I welcome the discussion. \u00a0This is a debate that colleagues and I have sought to initiate for many years. \u00a0There are powerful theoretical arguments on one side, and diverse empirical observations on the other. \u00a0The scientific community will eventually opt for empiricism, but not until theory digs in its heels and fights to the death. \u00a0A basic principle of evolution is at stake, and many theorists will rise to defend the basis of their life work; but a re-evaluation of basic evolutionary theory is long overdue.<\/p>\n

The idea that fitness consists in reproducing as fast as possible is no longer tenable. \u00a0For plants, this may be approximately true. \u00a0But animal populations cannot afford to reproduce at a pace faster than the base of their food chain can support. \u00a0Animals that exploit their food supply unsustainably will starve their own children, and there is no evolutionary future in that. \u00a0This is a principle that links together entire ecologies, and the foundation of evolutionary theory will have to be rewritten to take it into account.<\/p>\n

 <\/p>\n

The Programmed Aging Paradigm: Is it a Cause for Optimism in the Quest for Extended Human Life?<\/b><\/p>\n

For many years, I put forward the argument that programmed aging means there are genes that serve no other purpose than to hasten our death, and that medical research should be targeting the products of those genes. \u00a0(Once a pathway has been identified, pharmaceutical science knows well how to block it with engineered drugs, like beta blockers and MAO inhibitors and serotonin re-uptake inhibitors.)<\/p>\n

But in recent years, epigenetics has eclipsed genetics as the major theme in molecular biology. \u00a0Everything that happens in the body is determined by which genes are expressed where and when. \u00a0The vast majority of our DNA is devoted not to coding of proteins but to promoter and repressor regions that control gene expression with exquisite subtlety.<\/p>\n

There has been a growing recognition of aging as an epigenetic program. \u00a0As we get older, genes that protect us are dialed down, and genes for inflammation and apoptosis are dialed up so high that healthy tissue is being destroyed. \u00a0Many epigenetic scientists have discovered this, and they find it natural to see aging as a programmed phenomenon. \u00a0(Most have never been to graduate courses in evolutionary science, where they would have been indoctrinated into the perspective of the selfish gene.)<\/p>\n

At first blush, it seems that an epigenetic program is just as amenable to pharmaceutical intervention as a genetic program. \u00a0A few years ago, I wrote about transcription factors as the key to aging. \u00a0Transcription factors bind to DNA and turn whole suites of genes on and off in a coordinated way. \u00a0If we can restore a youthful transcription environment in an older animal or human, the body knows how to repair damage and re-create a younger self. \u00a0The model I had in mind was based on a small number of powerful transcription factors controlling expression of a much larger number of genes, controlling a yet larger population of metabolites.<\/p>\n

\"\"
I no longer believe in this model.<\/figcaption><\/figure>\n

This summer, I had a chance to work in a worm genetics lab<\/a> and consult closely with people who know the experimental details. \u00a0I learned that there is no clear line between functional proteins and transcription factors, that many proteins have multiple functions, and that metabolites feed back to control gene expression. \u00a0Instead of a pyramid, I should think of a web of causes and effects.<\/p>\n

<\/p>\n

The entire system is primed for homeostasis, meaning that it responds to any intervention, seeking to move the system back toward its previous state. \u00a0Of course, it is this capacity for recovery that makes life robust; but it also means that there is no \u201ccommand central\u201d which can be tweaked to move the whole system at once toward a desired state.<\/p>\n

I still believe that there are one or more aging clocks<\/a> that inform the body of an age-appropriate metabolic state, and synchronize the aging of different systems. \u00a0Telomere length<\/a> is one such clock. \u00a0If we can reset an aging clock, the body will repair and clean itself up. \u00a0If we can reset several clocks, the body may be able to restore itself to a younger state. \u00a0But I recognize the possibility that the clock is diffused through the detailed epigenetic status of a trillion cells, and may be beyond the reach of foreseeable technology.<\/p>\n

A few years ago, Steve Horvath<\/a>\u00a0of UCLA gave us the most explicit picture of an aging clock. \u00a0He found it in one particular epigenetic marker: the pattern of DNA methylation. \u00a0The Horvath clock is distributed over 353 sites. \u00a0This is a clock that can be read for any given cell, but can it be changed or adjusted in each of the body\u2019s trillions of cells? \u00a0The prospect is daunting, and we do not yet know how to go about it. \u00a02016 saw the first use of CRISPR technology<\/a>\u00a0for therapy in a living human. \u00a0CRISPR could, in principle, be used to alter gene expression, one gene at a time. \u00a0To re-regulate the expression of 353 genes in one treatment would probably require new concepts and new discoveries.<\/p>\n

Short of resetting the aging clock, there are several technologies just over the horizon that should offer substantial life extension benefit. \u00a0I believe the best prospects are senolytics<\/a> (ridding the body of senescent cells), telomerase activators (rejuvenating old stem cells), and adjusting blood levels of key hormones and cytokines<\/a> that increase or decrease with age.<\/p>\n

 <\/p>\n

The Bottom Line<\/b><\/p>\n

Programmed aging is the right model to keep in mind as we search for interventions that slow the aging process and lessen the incidence of heart disease, cancer and Alzheimer\u2019s all at once. \u00a0Prospects are good for real breakthroughs, perhaps as soon as 2017, but I am no longer as optimistic as I was just a few years ago that complete rejuvenation is on the horizon.<\/p>\n

Wishing you health and vitality for the coming year,<\/p>\n

\"\"<\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

– Josh Mitteldorf<\/p>\n","protected":false},"excerpt":{"rendered":"

Dear Readers – It\u2019s been a deeply gratifying year for me. \u00a0Twenty years ago, I first started writing that aging is something the body does to itself, a body function, rather than deterioration or loss of function. \u00a0Journals would not even send my submission out for peer review. \u00a0Journal of Theoretical Biology sent me the … 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":true,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-551","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nEpigenetics and the Direction of Anti-Aging Science - 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\/31\/epigenetics-and-the-direction-of-anti-aging-science\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Epigenetics and the Direction of Anti-Aging Science\" \/>\n<meta property=\"og:description\" content=\"Dear Readers – It\u2019s been a deeply gratifying year for me. \u00a0Twenty years ago, I first started writing that aging is something the body does to itself, a body function, rather than deterioration or loss of function. \u00a0Journals would not even send my submission out for peer review. \u00a0Journal of Theoretical Biology sent me the ... 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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":"Epigenetics and the Direction of Anti-Aging Science - 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\/31\/epigenetics-and-the-direction-of-anti-aging-science\/","og_locale":"en_US","og_type":"article","og_title":"Epigenetics and the Direction of Anti-Aging Science","og_description":"Dear Readers – It\u2019s been a deeply gratifying year for me. \u00a0Twenty years ago, I first started writing that aging is something the body does to itself, a body function, rather than deterioration or loss of function. \u00a0Journals would not even send my submission out for peer review. \u00a0Journal of Theoretical Biology sent me the ... 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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\/"}]}},"jetpack_featured_media_url":"","jetpack_shortlink":"https:\/\/wp.me\/pgtN8h-8T","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/551","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/users\/65"}],"replies":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/comments?post=551"}],"version-history":[{"count":0,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/551\/revisions"}],"wp:attachment":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/media?parent=551"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/categories?post=551"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/tags?post=551"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}