{"id":164,"date":"2013-10-29T02:55:18","date_gmt":"2013-10-29T02:55:18","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=164"},"modified":"2013-10-29T12:58:30","modified_gmt":"2013-10-29T12:58:30","slug":"signal-molecules-in-the-blood-what-do-we-lose-with-age","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/10\/29\/signal-molecules-in-the-blood-what-do-we-lose-with-age\/","title":{"rendered":"Signal Molecules in the Blood: What do we lose with age?"},"content":{"rendered":"

Two weeks ago I wrote about the hypothesis of Harold Katcher<\/a> (and others) that aging may be mediated by signaling molecules that circulate in the blood \u2013 hormones among them. \u00a0Katcher\u2019s idea for rejuvenation is to give older folks transfusions of blood plasma (with the white and red blood cells filtered out) from younger folks. \u00a0This could require a large number of young volunteers, I said, so maybe we could make a start by identifying some of the differences between hormones in blood from older and younger humans. \u00a0There are some hormones we have too much of, and others we have too little of as we age. \u00a0<\/em><\/p>\n

A timely news item: Steve Horvath<\/a>, a biostatistician from UCLA, published an article<\/a> last week in which he analyzed the way gene expression changes with age. A semi-permanent factor in gene expression is methylation of the DNA<\/a>, and Horvath showed that you can pretty much tell how old a person is by using a statistical template he developed to analyze which genes are methylated.<\/em><\/strong><\/p>\n

This week, I explore a few hormones that decline with age. \u00a0(Next week, I\u2019ll cover those that increase with age.) \u00a0Of those I\u2019ve investigated, melatonin offers the best prospect for life extension benefits.<\/em><\/p>\n

– – – – – – – – – – – – – – –<\/p>\n

<\/em>I take the position that aging is not a passive process of accumulated damage<\/a>, but a genetic program, centrally orchestrated through the body on a schedule. \u00a0It follows that signaling molecules that broadcast instructions through the bloodstream are likely to be messengers of death as we get older. \u00a0There are too many signals to catalog, and biochemists are just beginning to unravel the web of their interactions. Some may be small RNAs<\/a> and micro-proteins<\/a>, in addition to the better-known hormones. \u00a0Nevertheless, it\u2019s worthwhile looking at those we know about.<\/p>\n

Melatonin:<\/strong><\/p>\n

Melatonin is just the kind of circulating factor we\u2019d like to evaluate. It is produced in the brain (specifically the pineal gland), and it is a high-level signaling hormone<\/a> that affects gene transcription, with a cascade of lower-level effects.<\/p>\n

\"\"This was the first hormone to be studied for anti-aging potential, and there is good evidence that supplementing with melatonin works to modestly extend rodents\u2019 life span. \u00a0Melatonin is an anti-oxidant, but in the tiny quantities that the deploys it, this is probably not significant. \u00a0It is best known as a regulator of our diurnal sleep cycle. \u00a0Young people generate melatonin in their bloodstream around the same time each evening, signaling the body to prepare for sleep; and melatonin levels stay high through the night, dropping off before it\u2019s time to wake up. \u00a0Older people have less melatonin at night. \u00a0More older people than younger people suffer from sleep disorders. \u00a0And some people who travel between time zones find that taking melatonin at the (new) bedtime helps their bodies to reset their clocks.<\/p>\n

(In my personal experience, I find that 1 mg of melatonin helps me fall asleep at night. Side effects include morning “sand” in my eyes, exacerbation of apnea, and possibly an effect on dreaming – it\u2019s hard to tell.)<\/p>\n

\u201cIt may be that melatonin, when taken as a supplement, can stop or slow the spread of cancer<\/a>, make the immune system<\/a> stronger, or slow down the aging process. But these areas need more research,\u201d says WebMD<\/a> – a properly conservative assessment.<\/p>\n

I\u2019ve mentioned Vladimir Anisimov in the past – a Russian biochemist who has studied a large number of anti-aging interventions in his lab, and reports optimistic results, only some of which have been replicated outside his St Petersburg lab. \u00a0He may be the world\u2019s authority on the association between melatonin and slower aging. \u00a0Here is his 2006 review<\/a> of studies up to that time.<\/p>\n

Melatonin is a potent neuroprotective agent<\/a>, demonstrated in tests where animals brains are subjected to ischemia (oxygen deprivation). It has been proposed as a no-brainer for Alzheimer’s treatment\u00a0[Ref1<\/a>, Ref2<\/a>, Ref3<\/a>], and for Parkinson\u2019s there is preliminary data [Ref1<\/a>,\u00a0Ref2<\/a>,\u00a0Ref3<\/a>], though clinical evidence remains shaky.<\/p>\n

Taken orally, it is easily absorbed and quickly boosts blood levels. \u00a0Melatonin is cheap and convenient. \u00a0In the mid 1990s, several books were published promoting broad benefits. Walter Pierpaoli<\/a> led the charge. There followed the inevitable backlash<\/a>, but when I review the warnings in these papers now, I find they have little substance. \u00a0The worst they had to say was that melatonin needs more study. \u00a0This remains true today, and melatonin\u2019s chief drawback in this area is that it is unpatentable and too cheap to motivate any capitalist entity to invest in research.<\/p>\n

Thyroxine and thyrotropin<\/strong><\/p>\n

Thyroxin is a hormone generated by the thyroid. \u00a0Bet you knew that. \u00a0Like melatonin, it is a high-level signal with lots of downstream effects. \u00a0And as with melatonin, levels of thyroxine decline with age<\/a>. \u00a0A few studies<\/a> have found association between low thyroxine levels and mortality, and with risk of brain aging diseases (PD and AD); but others find the opposite.\"\"<\/p>\n

Thyrotropin is a related hormone, which stimulates the thyroid to produce thyroxine. \u00a0There is better data associating low thyrotropin levels with disease in the elderly than there is for thyroxine. \u00a0The Leiden 85+<\/a> study of mortality in the elderly found that mortality rates were higher in people who had high thyroxine, low thyrotropin. (Yes, that’s not a misprint: high thyroxine levels in older people might be a liability.)<\/p>\n

There is no question there is such a thing as too much thyroxine as well as too little, and it is regulated in the body from moment to moment. \u00a0Symptoms of too much thyroxine include anxiety, tremors and heart irregularity. So thyroxine is tricky, and it is wisely classed as a prescription drug, though it is a natural hormone. \u00a0But there are thyroxine pills, available by prescription, prescribed for hypothyroid conditions; some people also use them for weight loss. Daily dosages in tens of micrograms. \u00a0We rarely stop to think how exquisitely sensitive is our bodies\u2019 homeostasis, that a signal far smaller than a pinhead can have major effects.<\/p>\n

Carnitine and carnosine are two popular supplements taken for potential life extension benefits that can interfere with thyroxine uptake<\/a>. \u00a0A number of other supplements stimulate and support the thyroid<\/a>. \u00a0\u00a0Without clinical symptoms, these may be more practical alternatives to thyroxine for now, but maybe someday we will know better how to optimize thyroxine levels in the body.<\/p>\n

 <\/p>\n

DHEA \u00a0(dehydroepiandrosterone)<\/strong><\/p>\n

The most abundant hormone in the body when we are in our 20\u2019s declines to a small fraction of its prevalence when we are old. \u00a0At any age, males have more than females. \u00a0Manuractured in the adrenals, DHEA is chemically related to sex hormones and steroids, and there is evidence that they are transformed into these forms in our bodies.<\/p>\n

\"\"<\/p>\n

There are some studies showing cancer suppression in mice from DHEA. But DHEA is peculiar to human biochemistry, and it is scarce in mice and rats. \u00a0This is a reason to question whether there is a basic relationship to aging, and also whether we can extrapolate from studies of DHEA in rodents.<\/p>\n

Some human studies show lower rates of heart disease<\/a> and cancer when DHEA levels are higher; others find no effect. \u00a0\u00a0If there is a benefit, it may be small enough or contingent enough that it is difficult to disentangle from secondary associations. \u00a0Smokers tend to have higher DHEA levels.<\/p>\n

\u201cAn early human study that pointed to possible benefits for DHEA came from Dr. Barrett-Connor’s group. They measured DHEA levels in blood samples taken from almost 2,000 men and women between 1972 and 1974 and looked at how many died from heart disease. In 1986, they reported that men with high DHEA levels were far less likely to have died of heart disease, while women with high DHEA levels were at greater risk. A more detailed analysis published late last year, however, showed that men with above-average DHEA levels back in the early 1970s were only 15% less likely to have died of heart disease, while there was no association between DHEA levels and heart disease in women.\u201d (Ray Sahelian, 1996<\/a>)<\/p>\n

There is better evicence that DHEA has, for some people, a positive effect on mood and energy and possibly favorable body composition (more muscle, less fat). \u00a0Life Extension Foundation emphasizes that dosing should be done in conjunction with blood tests<\/a>, because of individual differences in absorption and in natural DHEA levels.<\/p>\n

Mayo clinic says<\/a>: \u201cNo studies on the long-term effects of DHEA have been conducted. DHEA can cause higher than normal levels of androgens and estrogens in the body, and theoretically may increase the risk of prostate, breast, ovarian, and other hormone-sensitive cancers. Therefore, it is not recommended for regular use without supervision by a licensed health professional.\u201d \u00a0Nevertheless, it\u2019s sold over-the-counter.<\/p>\n

Men and women respond differently to DHEA because it has a greater propensity to be turned into male hormones. \u00a0In a UCSD clinical study<\/a>, hormone levels were monitored in men and women during a six-month course of DHEA. \u00a0Male hormones in the women but not the men rose to unnaturally high levels,<\/p>\n

 <\/p>\n

Others:<\/strong><\/p>\n

I\u2019m not going to talk about growth hormone. \u00a0HGH can make you feel good in the short run, but it is a life-shortener in the end. \u00a0\u201cDespite more than a decade of finding numerous ways to slow aging in mice, the longest-lived genetically altered mice are still those that lack the genes for growth hormone receptor (GHR),\u201d [Source<\/a>]<\/p>\n

Sex hormones decrease with age, but from a theoretical perspective the evolutionary function is to cut off fertility, not to raise mortality. \u00a0A lot of study has been done of post-menopausal hormone replacement therapy and mortality from cancer and heart disease, and the story has no simple message<\/a>. \u00a0\u00a0The same is true for (male and female) sex hormone levels in males<\/a>.<\/p>\n

Some of the biochemical changes with age take place within the cell, unrelated to whole-body signaling. \u00a0For example, CoQ10 (ubiquinone) is manufactured and consumed in each cell. \u00a0It does not qualify as a hormone or signaling chemical because it is not circulated. \u00a0As for CoQ10, there is less of it as we age, and probably the body suffers for that. \u00a0Certainly the capacity of mitochondra to generate energy for us diminishes with age, and a shortage of CoQ10 is a logical candidate. \u00a0Oral administration of CoQ10 has not produced life extension<\/a> in animal experiments. \u00a0Vladimir Skulachev (University of Moscow) has an ingenious way to target CoQ10 to the mitochondria, and he has succeeded in increasing life span in lab rodents using what he calls SkQ<\/a>, which is a CoQ10 molecule modified with a mitochondrion-seeking tugboat on the front.<\/p>\n

 <\/p>\n

Respecting the wisdom of the body – not!<\/strong><\/p>\n

Editorial comment: There\u2019s a habit of conservatism in medical thinking that has imposed too high a burden of proof for DHEA and melatonin and thyroxine, based on a vague notion that the body knows what it is doing, so if we have less of it as we age, then probably less of it is good for us. \u00a0This is the way people think before they realize that the body\u2019s purpose is to kill itself<\/a>, slowly but surely as we get older. \u00a0If we want to live longer, we are going to have to oppose programmed biochemical changes that come with age.<\/p>\n

Today and tomorrow<\/strong><\/p>\n

I can recommend melatonin for now, and hope that study in coming years focuses on other promising targets for intervention, especially Anisimov\u2019s small peptides. \u00a0There is no barrier to studying difference between blood factors in young and old people. \u00a0It could be done now at modest cost. \u00a0For example, small peptides could be catalogued in blood samples from 100 young people and 100 old people, and consistent differences would be easy to spot. \u00a0The same could be done with short RNAs. \u00a0What else to look for? \u00a0I\u2019m sure the biochemists have better ideas than I have.<\/p>\n","protected":false},"excerpt":{"rendered":"

Two weeks ago I wrote about the hypothesis of Harold Katcher (and others) that aging may be mediated by signaling molecules that circulate in the blood \u2013 hormones among them. \u00a0Katcher\u2019s idea for rejuvenation is to give older folks transfusions of blood plasma (with the white and red blood cells filtered out) from younger folks. … 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-164","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nSignal Molecules in the Blood: What do we lose with age? - 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\/2013\/10\/29\/signal-molecules-in-the-blood-what-do-we-lose-with-age\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Signal Molecules in the Blood: What do we lose with age?\" \/>\n<meta property=\"og:description\" content=\"Two weeks ago I wrote about the hypothesis of Harold Katcher (and others) that aging may be mediated by signaling molecules that circulate in the blood \u2013 hormones among them. \u00a0Katcher\u2019s idea for rejuvenation is to give older folks transfusions of blood plasma (with the white and red blood cells filtered out) from younger folks. ... 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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":"Signal Molecules in the Blood: What do we lose with age? - 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\/2013\/10\/29\/signal-molecules-in-the-blood-what-do-we-lose-with-age\/","og_locale":"en_US","og_type":"article","og_title":"Signal Molecules in the Blood: What do we lose with age?","og_description":"Two weeks ago I wrote about the hypothesis of Harold Katcher (and others) that aging may be mediated by signaling molecules that circulate in the blood \u2013 hormones among them. \u00a0Katcher\u2019s idea for rejuvenation is to give older folks transfusions of blood plasma (with the white and red blood cells filtered out) from younger folks. ... 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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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