{"id":421,"date":"2015-09-04T17:31:15","date_gmt":"2015-09-04T17:31:15","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=421"},"modified":"2015-09-06T14:17:38","modified_gmt":"2015-09-06T14:17:38","slug":"hgh-and-igf-promise-and-danger","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/09\/04\/hgh-and-igf-promise-and-danger\/","title":{"rendered":"HGH and IGF–Promise and Danger"},"content":{"rendered":"

In the 1980s, Growth Hormone was explored by athletes to build muscles and by aging men to…build muscles. \u00a0GH made them feel younger, revived energy and sex drive and even cognitive performance. \u00a0Then the other shoe dropped: \u00a0Animals without the GH receptor lived longer, while animals with extra copies of the GH gene die early. \u00a0GH and IGF-1 are associated with higher rates of cancer, both in humans and in animals. \u00a0Now there are credible scientists seeking ways to separate the benefits of GH\/IGF from the tradeoffs. \u00a0A prominent NIH research group suggests we can activate IGF-1 in some tissues and not others. \u00a0In preliminary experiments on himself, Greg Fahy has regrown thymus tissue with GH and DHEA. \u00a0Rhonda Patrick recommends saunas and weightlifting. \u00a0Examine.com suggests supplementing with creatine as another option. \u00a0<\/span><\/i><\/p>\n

\n

HGH (human growth hormone) and IGF-1 (Insulin-like Growth Factor) are closely related steroid hormones which stimulate muscle and bone growth. \u00a0<\/span>GH is produced in the pituitary gland, deep in the brain, and it circulates through the blood to the liver, where it stimulates production of IGF-1. \u00a0In addition to the liver, there are local producers of IGF-1 in the body and the brain. \u00a0Most of the effects of GH are mediated through IGF-1. \u00a0<\/span>Here<\/span><\/a> is a good basic reference. \u00a0A few years ago, Journal of Gerontology devoted a <\/span>special issue<\/span><\/a> to IGF-1.<\/span><\/p>\n

\n

IGF-1 is part of an ancient signaling system that promotes growth and depresses life span across many species. \u00a0The system includes insulin, a protein structurally very similar to IGF-1 (hence the name). \u00a0Insulin is a mediator of life span regulation through food, exercise and the energy metabolism. \u00a0Some proteins carry instructions in the blood; they attach to receptors on the surface of a cell and tell the cell what to do. \u00a0Others get inside the cell and play a more direct role in the chemistry. \u00a0IGF-1 does both. \u00a0It has \u201cboth endocrine and autocrine functions\u201d.<\/span><\/p>\n

We have a lot more of both GH and IGF when we are growing children than later in life. \u00a0<\/span><\/p>\n

\"\"<\/p>\n

This discovery in the 1970s led medical researchers and others to the hope that HGH might be a kind of youth serum, and it was explored as a treatment for weakness, low energy, and depression in the elderly. \u00a0It worked. \u00a0IGF-1 combats the loss of muscle mass in old age, both by promoting new tissue growth and retarding apoptosis (cell suicide that protects against infection and cancer, but that can kill healthy cells as we get older). \u00a0IGF-1 promotes new nerve growth in the brain, and has been linked to better cognitive performance as well as subjective feelings of youth and wellbeing.<\/span><\/p>\n

But then it became clear that there are long-term risks associated with GH treatment, and GH treatment began to decline before it had really taken off. \u00a0<\/span>In the 1950s, long before genetic engineering, the Ames Dwarf Mouse* was as a mutant strain. \u00a0It lacks the gene for GH, and it lives 50% longer than other mice of the same species. \u00a0Other mice with GH or IGF deficiencies live longer, while mice with extra copies of these same genes have shorter life spans. \u00a0[<\/span>ref<\/span><\/a>, <\/span>ref<\/span><\/a>]. \u00a0But the results of lower IGF aren\u2019t all good, and they don\u2019t apply in all rodents [<\/span>ref<\/span><\/a>]. \u00a0In dwarf mice, low IGF leads to insulin resistance, diabetes symptoms and cardiovascular disease when the mice are fed a high-fat diet \u00a0[<\/span>ref<\/span><\/a>]. \u00a0<\/span>IGF-1 protects heart and arteries from deterioratation with age [<\/span>ref<\/span><\/a>].<\/span><\/p>\n

\u201cDespite the compelling data for enhanced life span in the presence of GH and IGF-1 defiiency in Ames dwarf and Snell dwarf mice, a review of the literature indicates that the effects of GH\/IGF-1 defiiency on life span in many other rodent models are, in many cases, inconsistent…Thus, despite the general consensus that the GH\/IGF-1 pathway is a conserved mechanism of aging, the data for increased life span in response to manipulation of this pathway in rodent models remain inconsistent and appear to be the result of studies in an important subset of animal models.\u201d [<\/em><\/span>ref<\/span><\/a>]<\/span><\/em><\/p><\/blockquote>\n

The story in people is even more complex. \u00a0Laron dwarfism is a genetic defect in the receptor for GH, which interrupts the connection GH \u2192 IGF-1. \u00a0Laron dwarfs have high GH, but low IGF-1. \u00a0(They are treatable with IGF-1.) \u00a0There is a region of Ecuador with a high frequency of Laron dwarfism [<\/span>NYTimes article<\/span><\/a>].<\/span><\/p>\n

\"\"
A 67-year-old man who has Laron-type dwarfism with his daughter, 5, and sons, 7 and 10.<\/figcaption><\/figure>\n

 <\/p>\n

People with Laron Dwarfism Syndrome have symptoms of premature aging<\/span>, including wrinkling and obesity. \u00a0But despite high insulin, they never develop diabetes symptoms. \u00a0What about life span? \u00a0There are contradictory claims of <\/span>longer<\/span><\/a> and <\/span>shorter<\/span><\/a> life span for Ecuador\u2019s dwarf population.<\/span><\/p>\n

Caloric Restriction provides another signpost. \u00a0Many hormone levels are affected by CR, and the direction in which they move is a suggestion about whether that hormone can be expected to be pro-longevity or the opposite. \u00a0Luigi Fontana of Washington Univ of St Louis has been conducting a long-term study of people on chronic (voluntary) CR. He found that circulating IGF-1 levels are\u00a0not different in this population. \u00a0Protein restriction is another classical life-extensio diet, and\u00a0Fontana found that protein restriction quickly causes IGF-1 levels to plummet [ref<\/a>].<\/p>\n

Are higher IGF-1 levels a risk factor for cancer in humans? \u00a0Maybe–but the association is weak and statistics are subject to different interpretations [<\/span>ref<\/span><\/a>].<\/span><\/p>\n

 <\/p>\n

Classical Example of Antagonistic Pleiotropy?<\/b><\/p>\n

The prevailing evolutionary theory of aging today is called \u201cAntagonistic Pleiotropy\u201d (AP). \u00a0The meaning is that there are genes that have multiple effects at different times in life, forcing evolution to accept costly tradeoffs (later) in exchange for peak fitness early in life. \u00a0IGF-1 is frequently cited as a prime example in support of the AP theory. \u00a0Evolution has selected IGF-1 in order to promote rapid growth, strength and development in youth, even though IGF-1 has long-term side effects that include cancer and higher all-cause mortality. \u00a0IGF-1 signaling is a pathway that is conserved over a long course of evolutionary history, helping to reconcile evolutionary theory with the existence of tightly-related genes that regulate aging across the biosphere—a relationship that took theoreticians quite by surprise when it was discovered in the 1990s. <\/span><\/p>\n

But a closer look at the biology of IGF-1 makes support for the AP theory more dubious. \u00a0The details of <\/span>where<\/i><\/b> and <\/span>when<\/i><\/b> IGF-1 is expressed don\u2019t fit the convenient story of AP. \u00a0There is a lot of IGF-1 early in life, but no sign of deleterious effects. \u00a0Later in life when the piper is to be paid, IGF-1 is expressed at very low levels. \u00a0It is not easy to relate high levels of IGF-1 in our teens to the cancer and heart risk in our 70\u2019s. \u00a0<\/span><\/p>\n

Also, <\/span>experiments with \u201cmosaic worms\u201d<\/span><\/a> have shown that the benefits of IGF-1 can be separated from the costs. \u00a0\u201cMosaic\u201d means that the worms have been grown with different genetics in different tissues. \u00a0With this technique, it was shown that the pro-aging costs of IGF-1 are confined to expression in the nervous system, while the benefits come from expressing IGF-1 in muscle tissue. \u00a0Why, then, has nature not found the optimal solution, and evolved worms to express IGF-1 only in muscle tissue?<\/span><\/p>\n

 <\/p>\n

HGH to Regrow the Thymus<\/b><\/p>\n

The thymus is a tiny gland where our white blood cells (T-cells) are trained to distinguish self from invader. \u00a0The <\/span>thymus shrinks through our lifetime<\/span><\/a>, and its loss has broad consequences for all the diseases of old age–autoimmunity, weaker defense against infectious disease, failure of the immune system to eliminate cancer in its earliest stages. \u00a0<\/span><\/p>\n

Greg Fahy is an innovative biochemist and personal friend. \u00a0When he was 46, he successfully regrew his own thymus in a short, one-man experiment using HGH and DHEA. \u00a0The procedure was written up as a journal article <\/span>here<\/span><\/a>, and his patent on the procedure is <\/span>here<\/span><\/a>. \u00a0For safety, he monitored IGF-1 levels to assure that they did not exceed those in a healthy, young adult. \u00a0This year, Fahy is conducting a tiny clinical trial based on this experience.<\/span><\/p>\n

 <\/p>\n

Safe ways to enhance IGF-1? \u00a0Maybe.<\/b><\/p>\n

Rhonda Patrick<\/span><\/a> gives a succinct and powerful case for an IGF trade-off: \u00a0Better physical and mental performance vs shorter life span. She hints that you might be able to get the benefits without the costs with natural means of enhancing IGF: \u00a0physical exercise and <\/span>saunas<\/span><\/a>. \u00a0Physical Exercise is a safe bet, because we know there is a net benefit for longevity, as well as abundant health benefits in the here and now. \u00a0Saunas (\u201chyperthermic conditioning\u201d) also boost the body\u2019s own HGH without injecting anything. \u00a0Heat shock has a hormetic benefit for life span in rodents and especially in worms; but I know of no epidemiological evidence linking the result to either a longer or shorter life span in humans.<\/span><\/p>\n

Creatine<\/span><\/a> is a small molecule, a substance that we all have lots of in our bodies already, though less as we age. \u00a0It is a popular supplement among body-builders. \u00a0Creatine acts in some of the same anabolic pathways as GH, promoting muscle growth. \u00a0Creatine acts by inhibiting <\/span>myostatin<\/span><\/a>, which is a growth inhibitor, so it is the sort of double negative that makes for grammatical awkwardness. \u00a0Eating creatine triggers a <\/span>burst of GH release<\/span><\/a>. \u00a0Regular use of creatine boosts the background level of GH, but actually suppresses the burst of GH that comes with exercise.<\/span><\/p>\n

In an an <\/span>article from researchers at the Reynolds Oklahoma Center on Aging and National Inst of Aging<\/span><\/a>, researchers suggest that it should be feasible to tease apart the benefits and costs of IGF-1 by raising IGF-1 preferentially in some tissues and not others. \u00a0<\/span>DAF-2 was an early life extension gene in worms–disable it and the worm lives twice as long. \u00a0So what\u2019s the counterpart of DAF-2 in humans? \u00a0Turns out it\u2019s an IGF-1 receptor. \u00a0A few years later, <\/span>Gary Ruvkun discovered<\/span><\/a> that disabling DAF-2 in just the worm\u2019s nervous system was sufficient to extend life span. \u00a0This suggests that it might be possible to de-couple the anabolic benefits of IGF-1 from the life-shortening consequences. \u00a0If people are like worms, that is\u2026<\/span><\/p>\n

—————
\n*named for Ames, Iowa, not Bruce Ames<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"

In the 1980s, Growth Hormone was explored by athletes to build muscles and by aging men to…build muscles. \u00a0GH made them feel younger, revived energy and sex drive and even cognitive performance. \u00a0Then the other shoe dropped: \u00a0Animals without the GH receptor lived longer, while animals with extra copies of the GH gene die early. … 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-421","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nHGH and IGF-Promise and Danger - 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\/2015\/09\/04\/hgh-and-igf-promise-and-danger\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"HGH and IGF--Promise and Danger\" \/>\n<meta property=\"og:description\" content=\"In the 1980s, Growth Hormone was explored by athletes to build muscles and by aging men to…build muscles. \u00a0GH made them feel younger, revived energy and sex drive and even cognitive performance. \u00a0Then the other shoe dropped: \u00a0Animals without the GH receptor lived longer, while animals with extra copies of the GH gene die early. ... 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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":"HGH and IGF-Promise and Danger - 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\/2015\/09\/04\/hgh-and-igf-promise-and-danger\/","og_locale":"en_US","og_type":"article","og_title":"HGH and IGF--Promise and Danger","og_description":"In the 1980s, Growth Hormone was explored by athletes to build muscles and by aging men to…build muscles. \u00a0GH made them feel younger, revived energy and sex drive and even cognitive performance. \u00a0Then the other shoe dropped: \u00a0Animals without the GH receptor lived longer, while animals with extra copies of the GH gene die early. ... 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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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