{"id":602,"date":"2017-08-23T13:28:40","date_gmt":"2017-08-23T13:28:40","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=602"},"modified":"2017-09-12T17:16:54","modified_gmt":"2017-09-12T17:16:54","slug":"new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/08\/23\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\/","title":{"rendered":"New Evidence that Long Telomeres cause Cancer, and Why I Think It\u2019s Wrong"},"content":{"rendered":"<p><i>Since <\/i><a href=\"http:\/\/www.sciencedirect.com\/science\/article\/pii\/S0140673603123847\"><i>2003<\/i><\/a><i>, I\u2019ve been saying that long telomeres are a path to long life. \u00a0The opposing view says that nature allows our telomeres to shorten to protect us against cancer. \u00a0Up until this spring, there has been little evidentiary support for the cancer theory. \u00a0Now, a <\/i><a href=\"http:\/\/jamanetwork.com\/journals\/jamaoncology\/article-abstract\/2604820\"><i>major new study<\/i><\/a><i> uses genetics to argue that longer telomeres increase risk of cancer as much as five-fold. \u00a0The study contains many statistical checks, but I\u2019m going out on a limb to say I think the experts have made a conceptual error.<\/i><\/p>\n<p><i>Up until now, epidemiological studies in humans and lab studies in animals have shown consistently that shorter telomeres increase risks for all the diseases of old age. \u00a0People\u2019s telomere length tends to decline with age, but among people of the same age, those with shorter telomeres tend to die sooner.<\/i><\/p>\n<p><i>The new study finds a very different conclusion: that shorter telomere length leads to much lower risk of cancer, while longer telomere length leads to slightly lower risk of heart disease. \u00a0Put these two together, and you predict pretty much the same life expectancy for people with long telomeres and short telomeres.<\/i><\/p>\n<p><i>The new studies are based on genetics and account for telomere length only indirectly. \u00a0Nevertheless, it is claimed, they are more reliable than the old studies (based on direct observation) because they are able to eliminate a statistical anomaly that <\/i>(<i>they claim<\/i>)<i> is super-important. \u00a0<\/i><\/p>\n<p><i>I believe the new study is actually <\/i><b><i>less<\/i><\/b><i> reliable, and that we should believe the more direct studies like the ones I have reported here <\/i><a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/04\/29\/large-new-survey-tracks-telomere-length-and-mortality\/\"><i>in the past<\/i><\/a><i>. \u00a0My reasons are that<\/i><\/p>\n<ul>\n<li style=\"font-weight: 400\"><i>The previous studies are straightforward, direct correlations. \u00a0Methodology in the new study relies on very small differences in telomere length, tiny differences that are lost in the noise and very difficult to detect.<\/i><\/li>\n<li style=\"font-weight: 400\"><i>The new studies require very large implicit extrapolation that is not necessary in the old studies. \u00a0The 50 to 1 extrapolation is very speculative, and it magnifies the noise along with the signal.<\/i><\/li>\n<li style=\"font-weight: 400\"><i>It is likely what these new studies are seeing are actually direct effects of genetics on cancer risk. \u00a0Even very small (direct) effects of genotype on cancer would appear in their methodology as though they were huge (indirect) effects of telomere length. \u00a0This is what I believe is happening, and why I don\u2019t trust their results.<\/i><\/li>\n<\/ul>\n<p><i>I may be wrong about this. \u00a0I\u2019m questioning seasoned experts in the field based on my general knowledge of statistics.<\/i><\/p>\n<hr \/>\n<p>Two years ago, <a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/04\/29\/large-new-survey-tracks-telomere-length-and-mortality\/\">I reported<\/a> on a <a href=\"http:\/\/jnci.oxfordjournals.org\/content\/107\/6\/djv074.short\">Danish study<\/a> linking short telomeres to higher mortality, especially heart disease (CV). \u00a0I took this as clear proof that telomere length was not just a marker of aging but a cause. \u00a0The implication is that you can live longer by adopting lifestyles and taking supplements that extend your telomeres.<\/p>\n<p>The core of my argument, based on the the Danish study, was this:<\/p>\n<ul>\n<li style=\"font-weight: 400\">Impact of telomere length on mortality, raw data: \u00a0\u00a0<b>3.38<\/b> (meaning that the 10% of people with the shortest telomeres were dying at a rate 3.38 as high as the 10% with the longest telomeres)<\/li>\n<li style=\"font-weight: 400\">Same calculation, corrected for age: \u00a0<b>1.54<\/b><\/li>\n<li style=\"font-weight: 400\">Same calculation, corrected for age and all other hazard variables: \u00a0<b>1.40<\/b><\/li>\n<\/ul>\n<p>Conclusion: This demonstrates that age is the biggest factor in mortality, and telomere length is second, with a strong effect, independent of age. \u00a0All the health variables together have only minor effect compared to age and telomere length.<img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-large\" src=\"http:\/\/learn.genetics.utah.edu\/content\/basics\/telomeres\/images\/telomeres_big.jpg\" width=\"704\" height=\"855\" \/><\/p>\n<p>The Danish study did a multivariate analysis, also called ANOVA. \u00a0This is a statistical technique designed to separate out the factors that contribute to an outcome (in this case, mortality) and assign percentages of causality. \u00a0What their analysis revealed was that the strongest cause of increased mortality is age itself, and that telomere length comes second. \u00a0Everything else, from smoking to depression to a history of infections, is much less important than age and telomere length. \u00a0I interpret this to say that short telomeres are probably a direct cause of increased disease risk.<\/p>\n<p>A popular theory is that the association of short telomeres with higher mortality is only incidental. \u00a0Stresses, infections, smoking, etc. cause both shorter telomeres and higher mortality. \u00a0But these are separate pathways. \u00a0It is not the shorter telomeres that are causing higher mortality, but short telomeres happen to be associated with higher mortality because both are caused by various stressors in a person\u2019s past. \u00a0If this is true, you can\u2019t improve your odds of living longer just by extending your telomeres.<\/p>\n<p>But I believe that the Danish study disproves this theory. \u00a0If the stressor theory were correct, then the Danish analysis would have found that the relationship between stressors and mortality was stronger than the relationship between telomere length and mortality. \u00a0In fact, they found the opposite.<\/p>\n<p>&nbsp;<\/p>\n<p><b>The New Genetic Study<\/b><\/p>\n<p>The result reported by the <a href=\"http:\/\/jamanetwork.com\/journals\/jamaoncology\/article-abstract\/2604820\">new study<\/a> is that longer telomeres creates a very much higher risk of several common cancers. \u00a0On the other hand, longer LTL (=leucocyte telomere length) protects against heart disease. \u00a0The protective effect for heart disease is much smaller, but many more people die of heart disease than of these particular cancers. \u00a0The result is a wash. \u00a0Longer LTL is neither a net benefit to health nor is it a net risk. \u00a0People with longer and shorter LTLs have similar overall mortality risk, about the same life expectancy.<\/p>\n<p>&nbsp;<\/p>\n<table bgcolor=\"FFBB00\">\n<tbody>\n<tr>\n<td><strong>Disease<\/strong><\/td>\n<td><strong>Odds Ratio<\/strong><\/td>\n<\/tr>\n<tr>\n<td>Glioma<\/td>\n<td>5.27<\/td>\n<\/tr>\n<tr>\n<td>Ovarian cancer<\/td>\n<td>4.35<\/td>\n<\/tr>\n<tr>\n<td>Lung cancer<\/td>\n<td>3.19<\/td>\n<\/tr>\n<tr>\n<td>Neuroblastoma<\/td>\n<td>2.98<\/td>\n<\/tr>\n<tr>\n<td>Bladder<\/td>\n<td>2.19<\/td>\n<\/tr>\n<tr>\n<td>melanoma<\/td>\n<td>1.87<\/td>\n<\/tr>\n<tr>\n<td>Testicular<\/td>\n<td>1.76<\/td>\n<\/tr>\n<tr>\n<td>Kidney<\/td>\n<td>1.55<\/td>\n<\/tr>\n<tr>\n<td>Endometrial<\/td>\n<td>1.31<\/td>\n<\/tr>\n<tr>\n<td>Basal cell skin<\/td>\n<td>1.22<\/td>\n<\/tr>\n<tr>\n<td>Breast Cancer<\/td>\n<td>1.06<\/td>\n<\/tr>\n<tr>\n<td>Heart disease<\/td>\n<td>0.78<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p><i>\u201cOdds ratio\u201d refers to a person\u2019s probability of contracting the corresponding disease. \u00a0For example, the first line means that people whose telomere length is one standard deviation <\/i>(<i>1 sigma<\/i>)<i> longer than average have a risk of glioma 5 times greater than people who have average telomere length.<\/i><\/p>\n<p>This result gains credibility because it is exactly what the theory would predict. \u00a0Nature has optimized LTL by compromising between two risks. \u00a0If the average LTL for our species were longer, then we\u2019d get more cancer. \u00a0If it were shorter, we\u2019d get more heart disease. \u00a0The reason there is so much variation among the population, people with much longer and much shorter telomere length, is that it doesn\u2019t matter very much.<\/p>\n<p>So here is agreement between experiment and theory, a tidy situation that scientists like to see. \u00a0What is more, there is a widely-held belief that the methodology of the new study is more reliable than studies in the past that are more direct and simpler. \u00a0Nevertheless, I\u2019m about to offer my opinion that the previous studies were right, the theory is wrong, and, in fact the design of the new study is seriously flawed.<\/p>\n<p>This was the latest and far the largest in a series of GWAS studies going back four years [<a href=\"https:\/\/www.nature.com\/articles\/ng.2528\">ref<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/26138067\">ref<\/a>, <a href=\"http:\/\/www.sciencedirect.com\/science\/article\/pii\/S0735109717375113\">ref<\/a>]. \u00a0<b>GWAS <\/b>stands for Genome-Wide Association Study. \u00a0The idea is to work around life experience variables that might create a correlation without a causal connection. \u00a0In the present case, the target is to detect any causal relationship between leucocyte telomere length (LTL) and various diseases, while filtering out associations between LTL and disease risk that might be incidental, as described above. \u00a0The researchers looked for small genetic differences (called SNPs) that are linked to telomere length. \u00a0These vary from one individual to the next, and they persist through a lifetime. \u00a0The next step is to compare numbers of people with a particular SNP variant among those who have the disease and those who don\u2019t have the disease. \u00a0Are people who have the SNP associated with longer telomeres more or less likely to develop the disease? \u00a0From the answer to this question, they infer a causal relationship, not between SNP and the disease but between telomere length and the disease.<\/p>\n<p>Observational studies look for a direct relationship between LTL and disease. \u00a0GWAS studies look for an indirect relationship between SNP and LTL, SNP and disease. \u00a0The indirect study is widely considered to be a more reliable indicator of causal connection than the direct study. \u00a0Why?<\/p>\n<blockquote><p>\u201cMendelian randomization studies are less susceptible to confounding in comparison to observational studies&#8230;Given the random distribution of genotypes in the general population with respect to lifestyle and other environmental factors, as well as the fixed nature of germline genotypes, these results should be less susceptible to confounding and reverse causation than those generated by observational studies.\u201d<\/p><\/blockquote>\n<p>The reasoning is that people have their genomes for their entire lives, independent of how they live, what they do, what they are exposed to. \u00a0By working with the genome, the statisticians can be sure to eliminate the standard objection that (for example):<\/p>\n<ul>\n<li style=\"font-weight: 400\">Stress directly decreases LTL<\/li>\n<li style=\"font-weight: 400\">Stress directly increases risk of disease<\/li>\n<li style=\"font-weight: 400\">Therefore, short LTL will appear to be linked with disease, even though short LTL doesn\u2019t <b>cause<\/b> disease.<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<p><b>Problems with GWAS studies<\/b><\/p>\n<p>But the GWAS methodology also introduces new problems of its own. \u00a0The main problem is that the statistical sensitivity of the study is seriously reduced. \u00a0This is because the relationship between SNP and LTL is very weak. \u00a0All sixteen SNPs together constitute a very small factor among many larger ones that create difference in LTL between one person and the next.<\/p>\n<blockquote><p>\u201cThe selected SNPs correspond to 10 independent genomic regions that collectively account for 2% to 3% of the variance in leukocyte telomere length\u201d<\/p><\/blockquote>\n<p>And of course, very few people have all 16 SNPs going in the same direction. \u00a0The study is forced to work with people who have, for example 10 positive SNPs out of 16 compared to others who may have 5 positive SNPs out of 16.<\/p>\n<p>Their LTL is really quite close together. \u00a0To compensate for this, the statisticians divide by a small number to extrapolate outwards. \u00a0For example, the difference between typical people in the study is about 1\/20 sigma*. \u00a0And the difference between risk of glioma (brain cancer) for these people is only about 0.08** . \u00a0But the difference is reported as \u201cwhat <b>would have been<\/b> the risk of brain cancer if the difference had been not 1\/20th but one full sigma. \u00a0They extrapolate exponentially, so the conclusion comes out quite startling: They claim that people with 1 sigma of extra LTL have 5 times greater chance of getting brain cancer.<\/p>\n<table bgcolor=\"#CCEEAA\">\n<tbody>\n<tr>\n<td><b>What they find: <\/b>people with 0.05 sigma extra LTL have 1.08 times the risk of getting brain cancer.<\/p>\n<p><b>What they report: <\/b>people with 1 sigma extra LTL would have (by extrapolation) 5 times the risk of getting brain cancer.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>They conclude that there is a large effect of telomere length on cancer, but they do this by the following reasoning:<\/p>\n<ul>\n<li style=\"font-weight: 400\">There is a small effect of these genetic variations on telomere length.<\/li>\n<li style=\"font-weight: 400\">There is a small effect of these genetic variations on cancer risk.<\/li>\n<li style=\"font-weight: 400\">Dividing the small by the small, they conclude: if the mechanism for these genetic variations affecting cancer is mediated by their effect on telomere length, then the effect of telomere length on cancer must be quite large.<\/li>\n<\/ul>\n<p>I\u2019m sorry to belabor this, but it\u2019s important, and it\u2019s hidden in the methodology. \u00a0People who do these studies know that an odds ratio (OR) of 1.08 means nothing. \u00a0The state of the art in epidemiology is rarely able to attach meaning to odds ratio that is close to 1. \u00a0It is lost in the nosie. \u00a0But an OR of 5 is something easy to see. \u00a0It stands out from the noise and is easy to detect.<\/p>\n<p>The description of the methodology in this study hides the fact that they are working with ORs less than 1.08 and extrapolating exponentially outward to make the ORs look very large and significant.<\/p>\n<p>&nbsp;<\/p>\n<p><b>What I think is really going on<\/b><\/p>\n<p>The study finds a large and consistent result that demands some explanation. \u00a0I\u2019m claiming that the explanation they offer (in terms of telomere length) is wrong. \u00a0So why do I think they get the results that they did?<\/p>\n<p>A few of the sixteen SNPs that are considered in the study correspond to slight variations on the form of the telomerase molecule. \u00a0I\u2019m guessing that these mutated forms of telomerase cause an increased risk of cancer. \u00a0The increased risk doesn\u2019t have to be large. \u00a0As in my example above, the increased risk for brain cancer would have to be just 8%, and the increased risk for lung cancer (more important because it is more common) only 6%. \u00a0Because of the extrapolation by an exponent of 20 that is implicit in their methodology, these small effects would be reported as though they were odds ratios of 5 (for brain cancer) and 3 (for lung cancer).<\/p>\n<p>Another possibility is that one or more of the SNPs happen to be more common in a segment of the population that is prone to cancer, for whatever reason. \u00a0It may be that a particular SNP is more common in an ethnic group that has high smoking rates, or that is prone to melanoma because of lighter skin, or has a diet and lifestyle that leads to a slightly greater risk of cancer. \u00a0For example, it is known that people of African extraction have SNPs associated with longer telomere length, and they also have higher risks for many cancers, including lung and [<a href=\"https:\/\/academic.oup.com\/hmg\/article-abstract\/25\/11\/2324\/2445992\">ref<\/a>]. \u00a0(Africans have lower risk of glioma, so the correlation goes in the wrong direction for this particular example.) \u00a0At the risk of beating a dead horse, I emphasize again that even a small increased risk would be magnified by the extrapolation that is implicit in the methodology of the GWAS, and appear very large and scary when misinterpreted as an effect of telomere length.<\/p>\n<p>GWAS is also referred to as \u201cMendelian randomization studies\u201d because they depend very much on the assumption that different SNPs are randomly distributed in the population. \u00a0Of course, this assumption is not literally satisfied. \u00a0How significant is the deviation from random distribution? \u00a0I will be investigating this question, and I\u2019ll let you know what I find.<\/p>\n<p>&nbsp;<\/p>\n<p><b>The Bottom Line<\/b><\/p>\n<p>There is a sharp conflict between the new GWAS results [<a href=\"http:\/\/jamanetwork.com\/journals\/jamaoncology\/article-abstract\/2604820\">Haycock, 2017<\/a>] and the observational results [<a href=\"http:\/\/jnci.oxfordjournals.org\/content\/107\/6\/djv074.short\">Rode, 2015<\/a>] reported two years ago. \u00a0They can\u2019t both be right. \u00a0If the GWAS results are as Haycock claims, there would have been glaring increases in cancer risk that Rode could not have missed. \u00a0If Rode is correct, then the methodology of Haycock must be flawed.<\/p>\n<p>The reasoning in GWAS studies depends on a huge extrapolation. \u00a0I am saying it is more likely that the effect of genetic variations on cancer risk is direct, not (as per Haycock\u2019s assumption) mediated by telomere length. \u00a0It could be that a very small direct effect of one of these SNPs is reported as though it were a large indirect effect, working via telomere length.<\/p>\n<p>For now, I\u2019m sticking with my previous counsel: Lengthening telomeres is a viable strategy for improving health and longevity. \u00a0If you take supplements that promote telomerase, you are not adding to your cancer risk. \u00a0Because of the large net benefit, lengthening of telomeres should be a major target for medical research.<\/p>\n<p>But as I said at the outset, I am criticizing the new study from the outside, and it is quite possible that I have misunderstood the methodology. \u00a0I have sided with the direct observational studies and I have been skeptical of the GWAS studies, but it may be that the consensus in the field is correct, and that GWAS studies really are more reliable indicators of causality.<\/p>\n<p>I intend to get to the bottom of this, and will report my findings in future columns.<\/p>\n<p>__________<\/p>\n<p>* Sigma is a standard deviation of telomere length in the population at large. If you know what that means, that\u2019s great; if you don\u2019t it doesn\u2019t matter to the logic of what I\u2019m saying.<\/p>\n<p>** Disease risk is typically reported as an odds ratio. \u00a0In this case, 0.08 would mean that, in their raw data, people in the study with the longer LTLs had a risk of 1.08 times as great as people with shorter LTLs. \u00a0You get to 1.08 not by adding 1 but by raising e to the power 0.08.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Since 2003, I\u2019ve been saying that long telomeres are a path to long life. \u00a0The opposing view says that nature allows our telomeres to shorten to protect us against cancer. \u00a0Up until this spring, there has been little evidentiary support for the cancer theory. \u00a0Now, a major new study uses genetics to argue that longer &#8230; <a title=\"New Evidence that Long Telomeres cause Cancer, and Why I Think It\u2019s Wrong\" class=\"read-more\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/08\/23\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\/\" aria-label=\"Read more about New Evidence that Long Telomeres cause Cancer, and Why I Think It\u2019s Wrong\">Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":603,"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-602","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 v27.7 (Yoast SEO v27.7) - https:\/\/yoast.com\/product\/yoast-seo-premium-wordpress\/ -->\n<title>New Evidence that Long Telomeres cause Cancer, and Why I Think It\u2019s Wrong - 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\/2017\/08\/23\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"New Evidence that Long Telomeres cause Cancer, and Why I Think It\u2019s Wrong\" \/>\n<meta property=\"og:description\" content=\"Since 2003, I\u2019ve been saying that long telomeres are a path to long life. \u00a0The opposing view says that nature allows our telomeres to shorten to protect us against cancer. \u00a0Up until this spring, there has been little evidentiary support for the cancer theory. \u00a0Now, a major new study uses genetics to argue that longer ... Read more\" \/>\n<meta property=\"og:url\" content=\"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/08\/23\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\/\" \/>\n<meta property=\"og:site_name\" content=\"Josh Mitteldorf\" \/>\n<meta property=\"article:published_time\" content=\"2017-08-23T13:28:40+00:00\" \/>\n<meta property=\"article:modified_time\" content=\"2017-09-12T17:16:54+00:00\" \/>\n<meta property=\"og:image\" content=\"https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2017\/08\/telomeres.jpg\" \/>\n\t<meta property=\"og:image:width\" content=\"704\" \/>\n\t<meta property=\"og:image:height\" content=\"855\" \/>\n\t<meta property=\"og:image:type\" content=\"image\/jpeg\" \/>\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=\"13 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"Article\",\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2017\\\/08\\\/23\\\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\\\/#article\",\"isPartOf\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2017\\\/08\\\/23\\\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\\\/\"},\"author\":{\"name\":\"Josh Mitteldorf\",\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/#\\\/schema\\\/person\\\/214c5d1dad9f15c48f03128d5cfccdb1\"},\"headline\":\"New Evidence that Long Telomeres cause Cancer, and Why I Think It\u2019s Wrong\",\"datePublished\":\"2017-08-23T13:28:40+00:00\",\"dateModified\":\"2017-09-12T17:16:54+00:00\",\"mainEntityOfPage\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2017\\\/08\\\/23\\\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\\\/\"},\"wordCount\":2659,\"commentCount\":301,\"publisher\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/#organization\"},\"image\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2017\\\/08\\\/23\\\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\\\/#primaryimage\"},\"thumbnailUrl\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/wp-content\\\/uploads\\\/sites\\\/2\\\/2017\\\/08\\\/telomeres.jpg\",\"inLanguage\":\"en-US\",\"potentialAction\":[{\"@type\":\"CommentAction\",\"name\":\"Comment\",\"target\":[\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2017\\\/08\\\/23\\\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\\\/#respond\"]}],\"copyrightYear\":\"2017\",\"copyrightHolder\":{\"@id\":\"https:\\\/\\\/scienceblog.com\\\/#organization\"}},{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2017\\\/08\\\/23\\\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\\\/\",\"url\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/2017\\\/08\\\/23\\\/new-evidence-that-long-telomeres-cause-cancer-and-why-i-think-its-wrong\\\/\",\"name\":\"New Evidence that Long Telomeres cause Cancer, and Why I Think It\u2019s Wrong - 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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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