{"id":258,"date":"2014-06-26T21:13:24","date_gmt":"2014-06-26T21:13:24","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=258"},"modified":"2014-06-27T03:04:33","modified_gmt":"2014-06-27T03:04:33","slug":"v-n-anisimov-russian-optomist-on-longevity","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2014\/06\/26\/v-n-anisimov-russian-optomist-on-longevity\/","title":{"rendered":"V.N. Anisimov: Russian Optimist on Longevity"},"content":{"rendered":"

Last March, I wrote a column entitled Reality Check<\/a>, featuring the work of Stephen Spindler. \u00a0Spindler is a veteran researcher at UCRiverside, and perhaps the world\u2019s foremost expert in the design and execution of longevity studies in mice. \u00a0But Steve is a glass-half-empty kind of guy. \u00a0And ever since I wrote that column, I\u2019ve been thinking that I need to write about Spindler\u2019s opposite number in Russia: \u00a0Vladimir Anisimov<\/a> is a veteran gerontologist at the Petrov Institute in St Petersburg, who has also been testing longevity potions on mice through a long career. \u00a0Anisimov is a glass-half-full kind of guy. \u00a0His best contribution to anti-aging medicine may be epithalamin,<\/strong> a treatment that has been hiding in plain sight for over thirty years.<\/em><\/p>\n

An innovator with a deep knowledge of biochemistry, Anisimov has published theoretical as well as practical science. \u00a0His lab has tested biochemical ideas about aging, as well as doing many studies on genetics and longevity in rodents and flies. \u00a0He has reported and summarized results of other Russian labs in English-language journals.<\/p>\n

Some of Anisimov\u2019s findings are well-known to me, and therefore to followers of this blog and of my Aging Advice<\/a> web site. \u00a0Metformin reduces mortality and slashes cancer risk in people who take it as a medication for diabetes. \u00a0Metformin increases life span of ordinary non-diabetic mice. \u00a0Anisimov thinks it will do the same<\/a> for non-diabetic humans, and I agree it\u2019s a good bet. \u00a0Melatonin, the hormone that regulates our daily cycle, is also found to prolong life span in mice. \u00a0\u00a0Melatonin in the blood is very sensitive to light exposure, and melatonin disappears with the dawn\u2019s early light \u00a0\u00a0Anisimov found that sleeping in total darkness is better for longevity than exposure to light during the night. \u00a0Here are two reviews by Anisimov of mostly Russian work on life extension with melatonin [2003<\/a>, 2006<\/a>].<\/p>\n

(Unrelated to melatonin and to Anisimov: A recent study<\/a> also suggests sleeping in the cold helps preserve insulin sensitivity.)<\/p>\n

Another of Anisimov\u2019s lines of research is less well-known to me, and I report here my first impressions. \u00a0He has worked with \u201cshort peptides\u201d, strings of less than 10 amino acids, that can act as signals or switches that control body chemistry globally. \u00a0Short peptides are small enough to pass easily through the skin or through the blood-brain barrier. \u00a0Unlike full-size proteins, short peptides tend to resist dismemberment<\/a> by stomach enzymes. \u00a0Carnosine and carnitine are familiar examples of di-peptides, consisting of 2 amino acids.<\/p>\n

Here\u2019s the theory: \u00a0We know that gene expression is quite different in old and young people. \u00a0In the literature, you find various interpretations and explanations why this might be true. \u00a0But my interpretation is clear and simple: \u00a0The body times its life cycle using gene expression. \u00a0When we\u2019re young, we express genes that make us grow. \u00a0When we\u2019re middle-aged, we express genes that keep us healthy. \u00a0When we\u2019re old, we express genes that destroy us.<\/p>\n

\u201cGene expression\u201d is the translation of DNA into proteins. \u00a0Proteins are the signals and the workhorses of body chemistry. \u00a0The translation is well understood since Francis Crick discovered the Genetic Code in the 1960s. \u00a0But the language for determining which gene gets expressed when is apparently much more complicated, and it is just beginning to be decoded in the 21st Century. \u00a0This is the science of epigenetics.<\/p>\n

Among the signals that can locate a particular stretch of DNA, and turn it ON or OFF are short stretches of RNA called pi-RNAs, methyl transferases and histone de-acetylases. \u00a0(I\u2019m sorry to throw biochem jargon at you, but I\u2019m excited to have just barely begun to educate myself about the fundamentals of epigenetics<\/a> with a Coursera course this spring.) \u00a0But the point is that these short peptides that Anisimov has been studying for 20 years work also as gene promoters and repressors – epigenetic signals that are more specific than the methyl transferases and less specific than pi-RNAs. \u00a0Apparently they can affect whole categories of genes [ref<\/a>].<\/p>\n

Here\u2019s a paper<\/a> in which Anisimov summarizes 35 years\u2019 experience with animal experiments, and some tantalizing human results as well. \u00a0(One of the differences in Russian bio-medicine, for better and for worse, is that regulations about experiments on humans are more relaxed than in the US.) \u00a0\u00a0Here\u2019s a table summarizing results in mice and rats. \u00a0(As usual, life extension in flies is more dramatic, but less indicative of human benefits.) \u00a0As you can see, this is a science that goes back to the 1970s, when the top two preparations were purified from epithalamus and thymus glands.<\/p>\n

\"Anisimov-table-of-short-peptides\"<\/a><\/p>\n

The thymus<\/a> is a gland in the upper chest that trains the immune cells in our blood to attack invading cells, but to lay off our own body\u2019s cells. \u00a0As we get older, the thymus shrinks<\/a>, and I believe this to be a basic cause of aging immune function, auto-immune disease, and increased susceptibility to infection. \u00a0Thymalin<\/a> was found to stimulate thymus re-growth and to rejuvenate immune function.<\/p>\n

Epithalamin<\/a> is also called epitalon or epithalon, and was discovered in extacts from a region of the brain called the epithalamus. \u00a0This region contains the pineal gland, or \u201cthird eye\u201d, which controls wake\/sleep cycles and is the body\u2019s source of melatonin. \u00a0Like thymalin, epithalamin is a string of four amino acids. \u00a0Thymalin generated excitement in the 1980s, until epithalamin stole its thunder. \u00a0Not only did it extend life more consistently, but its effect on thymic growth<\/a> was found to be superior to thymalin.<\/p>\n

In the table, epithalamin has been the best-studied short peptide, and it has the best record for life extension in rodents. \u00a0In a separate table, the same paper shows that epithalamin and thymalin suppress cancer in rodents. \u00a0There is also evidence of large reductions in mortality when epithalamin was given to older human subjects:<\/p>\n

\"Anisimov-short-peptides-human-mortality\"<\/a><\/p>\n

In addition, it has recenty been reported (2003<\/a>, 2004<\/a>) that epithalamin is a telomerase activator<\/a>. \u00a0Skeptics (Spindler in particular) point out that caloric restriction is such a strong influence on life span that many treatments will appear to show benefit only because they affect appetite. \u00a0Some of the studies<\/a> do measure food intake, and find that epithalamin is able to increase lifespan without decreasing food consumption.<\/p>\n

(Epitalon is available commercially<\/a>, but not from most supplement sources. \u00a0Recommended dosage is usually less than 10mg, but experience with different dosages is very limited.)<\/p>\n

 <\/p>\n

Reference: a crash course in mid-brain anatomy<\/strong><\/p>\n

Here\u2019s a picture of the human brain, courtesy of Wikipedia. \u00a0The mid-brain is the endocrine function, where computations made with neurons are translated into prescriptions for internal secretion.<\/p>\n

\"Mid-brain\"<\/a><\/p>\n

The epithalamus is shown in cherry. \u00a0It includes the pineal gland, the so-called \u201cthird eye\u201d which is responsible for the body\u2019s light-sensitive clock, and where melatonin comes from. \u00a0The hypothalamus is shown in lime. \u00a0It includes various \u201cnuclei\u201d, notably the suprachiasmatic nucleus, which is the closest thing science has found to a developmental clock. \u00a0The pituitary is also part of the hypothalamus, and secretes hormones involved in the life cycle and the menstrual cycle: HGH, LH, FSH, TSH and sex hormones.<\/p>\n

Conclusions<\/strong><\/p>\n

All of this looks so promising that I wonder why there hasn\u2019t been more follow-up, and why American researchers haven\u2019t built on the Russian results. \u00a0Russian science tends to be more adventurous than American science. \u00a0That doesn\u2019t mean they make more mistakes. \u00a0The problem with American science is that it is too rigidly institutionalized and controlled within an establishment. \u00a0It is usually not possible to get funding to ask a question to which you do not already know the answer. \u00a0So the mistakes of American science are more likely to be under the header \u201cconfirmation bias\u201d, while Russian science is more likely to be offering results that may not pan out. \u00a0This seems to be a well-established field, with positive results that have been affirmed over decades in different labs with flies, rodents, and humans. \u00a0My web search identified no dangers or reports of toxicity. \u00a0I\u2019d say it\u2019s high time the American and European gerontology communities picked up this thread. \u00a0In the mean time, please comment if you have any experience with epitalon or other short peptides.<\/p>\n","protected":false},"excerpt":{"rendered":"

Last March, I wrote a column entitled Reality Check, featuring the work of Stephen Spindler. \u00a0Spindler is a veteran researcher at UCRiverside, and perhaps the world\u2019s foremost expert in the design and execution of longevity studies in mice. \u00a0But Steve is a glass-half-empty kind of guy. \u00a0And ever since I wrote that column, I\u2019ve been … 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-258","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nV.N. 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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":"V.N. 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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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