{"id":417,"date":"2015-08-24T22:40:37","date_gmt":"2015-08-24T22:40:37","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=417"},"modified":"2015-08-26T14:35:08","modified_gmt":"2015-08-26T14:35:08","slug":"report-from-rejuvention-biotech-2015","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/08\/24\/report-from-rejuvention-biotech-2015\/","title":{"rendered":"Report from Rejuvenation Biotech Conference"},"content":{"rendered":"

Fifteen years ago, Aubrey de Grey organized the first SENS roundtable–<\/span>S<\/b>trategies for <\/span>E<\/b>ngineering <\/span>N<\/b>egligble <\/span>S<\/b>enescence<\/span><\/a>. \u00a0It was a small group of out-of-the-box thinkers, heretics who talked about attacking head-on the idea that aging is just part of the human condition, looking for medical (and beyond-medical) treatments that would restore strength, stamina, and alertness, and lower the risk of all the diseases of old age at once.<\/span><\/p>\n

There followed five more SENS conferences in Cambridge, UK. \u00a0Now, SENS HQ has moved to Silicon Valley the series has been absorbed as a summer Rejuvenation Biotech conference<\/a>\u00a0in California.<\/span><\/p>\n

This is the mainstreaming of anti-aging science, the product of many long years of work and relationship-building, largely by Aubrey himself. \u00a0As <\/span>Joni Mitchell<\/span><\/a> wisely warns, \u201cSomething\u2019s lost and something\u2019s gained…our dreams have lost their grandeur coming true.\u201d \u00a0<\/span>There is a lot more money, a lot more data, well-established\u00a0people and funders are involved. \u00a0But there is less daring, out-of-the-box risk-taking than in the past, and my personal judgment is that we are still at a stage of understanding where high-risk science is essential.<\/span><\/p>\n

At one point, a young man posed a question in a session devoted to cancer strategies. \u00a0The most common cancers attract the most funding, he said, and there has been little progress over the years in survival percentages in these cases. \u00a0Meanwhile, there has been dramatic progress in rare cancers, though they are the province of fringe research with little mainstream funding. \u00a0Perhaps there is an inverse correlation between funding and scientific progress. \u00a0Perhaps funding distortions favor repeat funding of long-term projects, with a resulting bias toward failed ideas. \u00a0Perhaps funding makes scientists more conservative, and impedes discovery. \u00a0This was a perspective that no one could digest, and audience and speaker moved on with embarrassed laughter. \u00a0<\/span><\/p>\n

At the end of this page<\/a> is the most exciting thing I learned at the conference, which is also the most far-flung and likely to be an artifact.<\/span><\/p>\n

 <\/p>\n

Alzheimer\u2019s Trial using Infusion of Blood Plasma from Young Donors<\/b><\/p>\n

Tony Wyss-Coray<\/span><\/a> of Stanford has what I consider the boldest and most promising program for rejuvenation today. \u00a0He discovered last year<\/a> that mice given 8 infusions of 0.1 ml blood plasma from a young mouse\u00a0showed dramatic improvements in cognitive performance. \u00a0(This is the equivalent of about \u00bd\u00a0pint of blood per infusion in human scale.) \u00a0Tony told us that there was an unpublished experiment in which similar benefits were achieved with blood from young\u00a0humans infused into older mice. \u00a0The cognitive improvements last at least a few weeks, but were not tested beyond that time frame.<\/span><\/p>\n

Take a moment to appreciate how unexpected this was. \u00a0Even for those of us who are enthusiastic about the ability of blood factors to reprogram the body\u2019s age, we expected that many repeated treatments would be needed, and that it would be necessary to remove pro-inflammatory factors from old blood as well as adding pro-growth factors from young blood. \u00a0Most blood factors are constantly being generated and destroyed, so their lifetime in the bloodstream is only a few hours or even minutes. \u00a0It was beyond optimistic to think that so short a course of treatment would\u00a0have a measurable effect.<\/span><\/p>\n

The result was so promising that Wyss-Coray is leapfrogging over the animal testing phase. \u00a0He has formed a <\/span>for-profit spinoff<\/span><\/a>, proceding right to <\/span>clinical trials<\/span><\/a>. \u00a0(This is possible because plasma transfusion is already a mature technology, long approved for safety in other contexts.)<\/span><\/p>\n

 <\/p>\n

Thymus Regeneration<\/b><\/p>\n

Georg Hollander<\/span><\/a> presented a cogent and enlightening\u00a0exegesis of the thymus, from basic function to ongoing projects. \u00a0The thymus is a small gland under the breastbone that is responsible for a crucial function of the immune system: \u00a0traing white blood cells (T-cells) to distinguish between self and other, so they can consistently attack the latter and spare the former. \u00a0In adulthood, the thymus atrophies (\u201cthymic involution<\/span><\/a>\u201d)<\/span>, and in old age there is almost no thymus left, with the disastrous result that T-cells not only fail to protect our bodies from invaders, but treat our bodies as the enemy, leading to autoimmunity<\/span>. \u00a0The training is performed by web-like epithelial cells, shaped like crumpled blankets, each epithelial cell in contact with up to 60 developing T-cells. \u00a0Epithelial cells must express every single protein in the genome, and there is a transcription factor called AIRE that binds to DNA, promoting \u201cpromiscuous expression.\u201d \u00a0Curiously, AIRE works best for genes that are normally turned off by methylation or acetylation. \u00a015% of genes are expressed <\/span>only<\/i><\/b> in the presence of AIRE. \u00a0There are micro-RNAs that are also necessary for promiscuous expression of all genes. \u00a0<\/span><\/p>\n

Hollander has been working on the hypothesis that each epithelial cell succeeds in programming only a random subset of the genome, so if you have fewer epithelial cells late in life, the cells collectively will not express every single gene in the body; there will be holes in the set of all genes represented in the thymus, and as a result there will be autoimmunity. \u00a0He said we need a minimum 200-300 epithelial cells for a fully-functioning thymus that protects the body against itself.<\/span><\/p>\n

At Wake Forest Inst, <\/span>John Jackson<\/span><\/a> is working on growing epithelial cells in a petri dish, then forming them on a scaffold, integrating blood vessels (<\/span>vascularization<\/span><\/a>) and structural (<\/span>stromal<\/span><\/a>) cells. \u00a0His intern <\/span>Blake Johnson<\/span><\/a> made remarkable progress in a single summer toward creating a functional mouse thymus. \u00a0Mice (like other small animals) have much larger thymi in relation to body size; and (like humans), they lose most of their thymic volume over their short lifetimes, with the result that their immune systems are disabled and they are vulnerable especially to cancer.<\/span><\/p>\n

FOXN1<\/a>\u00a0is a transcription factor that may be a key to thymic reactivation. \u00a0Last year, a Scottish group<\/a> announced growing\u00a0a fully-functional thymus and transplanting it into a mouse. \u00a0A\u00a0Pittsburgh group<\/a>\u00a0is working on similar techniques<\/span>. \u00a0Greg Fahy of <\/span>21st Century Medicine<\/span><\/a> is conducting a tiny clinical trial in the coming year, using growth hormone and other blood factors to regrow the thymus in people 50-65 yo. \u00a0(Enrollment is closed; they are <\/span>not<\/i><\/b> seeking test subjects.)<\/span><\/p>\n

 <\/p>\n

Two paths to longevity<\/b>
\n<\/b>(Dataheads can skip this and the following section. They are just philosophy.)<\/span><\/p>\n

Very broadly, there are two approaches to anti-aging medicine, which might be called \u201cbioengineering\u201d and \u201cendocrinology\u201d. \u00a0The question is, how much of the change that takes place with age can the body reverse with its internal resources, given the appropriate chemical signals (that\u2019s endocrinology)? \u00a0And how much remains that must be rebuilt or replaced with prosthetics (bioengineering)? \u00a0From the beginning, SENS has emphasized the bioengineering approach–its middle name is \u201cengineering\u201d. \u00a0I am more optimistic about what the body might be able to do on its own, if only we can master its biochemical language. \u00a0<\/span><\/p>\n

Significant advances have been made in bioengineering in the 15 year history of SENS. \u00a0A prosthetic limb no longer needs to be a peg leg, but can be designed to <\/span>respond to neural signals<\/span><\/a>. \u00a0Prosthetic <\/span>eyes<\/span><\/a> and <\/span>ears<\/span><\/a> have come down from the clouds into the realm of the feasible. \u00a0The first <\/span>organs grown cell-by-cell on scaffolds<\/span><\/a> in the lab have been re-implanted successfully in human patients. <\/span><\/p>\n

But even more stunning and promising breakthroughs have appeared in the realm of chemical signaling. \u00a0In 2000, before the Bush Ban, all stem cell research depended on embryonic stem cells harvested from foetal tissue; but turning muscle or skin cells back into stem cells has turned out to be surprisingly easy (though the process is still being refined). \u00a0\u201cEpigenetics\u201d was an abstract noun in 2000, and it is now the fastest-growing area of biological science. \u00a0Epigenetic signaling may be the organizing principle of whole-body aging [<\/span>ref<\/span><\/a>, <\/span>ref<\/a>, ref<\/a><\/span>]. \u00a0Signal proteins have been identified that turn on whole systems of genes that retard aging. \u00a0Better yet, <\/span>pathways that promote inflammation<\/span><\/a> (e.g. <\/span>TGF-\u03b2, NF<\/span>k<\/span>B<\/span>) can be blocked, while some blood factors\u00a0(e.g. FOXn1, oxytocin) <\/span>turn on regenerative pathways<\/span><\/a>, with the promise of rejuvenation. \u00a0<\/span>Steve Horvath<\/span><\/a> has pioneered a bioinformatic approach to identifying the epigenetic differences between old and young humans.<\/span><\/p>\n

 <\/p>\n

Broad strategies <\/b><\/p>\n

Business is averse to risk. \u00a0Science is all about exploring the unknown. \u00a0It’s not exactly a match made in heaven.<\/span><\/p>\n

Chas Bountra<\/span><\/a> is deeply tied to the establishment, but radical in his own way. \u00a0He is a veteran of many years as head of research at Glaxo Smithkline, and now directs the Structural Genomics Unit at Oxford. \u00a0His focus is Alzheimer\u2019s Disease, and tells us why: \u00a0We have a basic understanding of cancer, stroke and heart disease, and are making steady, incremental progress toward prevention and higher survival rates. \u00a0If current trends continue, dementia will be the scourge of the next generation, exacting an unaffordable social cost as patients survive for years, unable to contribute to society, to care for themselves or even to enjoy social interactions with others.<\/span><\/p>\n

He is interested in \u201cnovel targets\u201d. \u00a0He will not consider amyloid beta or Tau protein aggregates because, \u201cwe have spent tens of billions of dollars researching A-beta plaques and we still can\u2019t Bountra makes an impassioned plea for open source researching. \u00a0He boasts of doing research that drug companies shun as too risky, and having succeeded in identifying more than 40 new targets that drug manufacturers have pursued and brought to the market. \u00a0His research unit publishes all data, takes no patents, and shares all ideas in academic journals. \u00a0\u00a0His model: Universities take all the risk, using public monies; pharmaceutical giants make all the profits. \u00a0(Big Pharma then uses its considerable leverage in lobbying Congress to increase funding for biochemical research.)<\/span><\/p>\n

For a commie like me, this model is tainted with corporate welfare, but while I choke on the social injustice, I admit that it is practical and effective in today\u2019s political environment.<\/span><\/p>\n

 <\/p>\n

Oldest\u00a0Aging Scientist Still Active<\/b><\/p>\n

That title probably goes to George Martin<\/a>, at 88 still deeply thoughtful\u00a0and open to new ideas in his U Washington lab.\u00a0I visited George a week earlier, on my way to San Francisco. \u00a0<\/span>Len Hayflick<\/a>,<\/span>\u00a087, works at UCSF. \u00a0 At 86, <\/span>Bruce Ames<\/span><\/a> is still active and doing good work. \u00a0After the conference, I was privileged to visit his lab in Children\u2019s Hospital Oakland Research Institute (CHORI). \u00a0Ames has been doing innovative biochemistry since the 1960s, and by now has persevered to see some of his heresies absorbed into the canon of public health. \u00a0After a 32-year career at UC Berkeley, he moved to emeritus status and opened his present lab in 2000. \u00a0\u00a0<\/span><\/p>\n

\"\"
Bruce Ames<\/figcaption><\/figure>\n

In 1972, Ames launched his career by investing a <\/span>quick and easy lab test for mutaogenicity<\/span><\/a>\u00a0(and presumptive carcinogenicity) that has saved millions of dollars and countless rabbits and mice. \u00a0<\/span><\/p>\n

In the 1980s, Ames was an early influence on my diet and helped form my understanding of aging. \u00a0In that era, we all thought about buildup of toxins and cumulative effect of carcinogens. \u00a0Ames was at the forefront, ranking carcinogens by a scheme he called <\/span>HERP<\/span><\/a>, which took proper account of potency and average public exposure. \u00a0The conclusion that surprised him and alienated many advocates of natural medicine was that natural carcinogens are common in the foods we eat, overwhelming the risk from pesticides and preservatives for which we were seeking tighter regulation. \u00a0Always an evolutionary thinker, Ames headed off the argument that we might be evolved to deal with natural carcinogens but not manufactured carcinogens, demonstrating that diets and lifespans of our hominid forbears made that conclusion unsupportable.<\/span><\/p>\n

Ames was one of an elite group at the first SENS roundtable discussion in 2000, forerunner of the <\/span>RB2015<\/span><\/a> conference that I attended last week.<\/span><\/p>\n

Today, <\/span>Ames argues that dozens of micronutrients<\/span><\/a> are essential for both day-to-day metabolism and for long-term health. \u00a0When any of these micronutrients are in short supply, the body prioritizes the former, and the latter is shortchanged, with consequences for longevity.<\/span><\/p>\n

In Bruce\u2019s lab, I met Rhonda Patrick, a dynamic young post-doc who both does innovative nutritional science and has a uniquely nerdy and well-informed video blog,\u00a0<\/span>FoundMyFitness.com<\/span><\/a>\u00a0of health advice, broadcasting biochemistry, nutrition and metabolism for the masses. \u00a0<\/span><\/p>\n

I can\u2019t resist noting how pleased I was to find support in Bruce’s lab for my contrarian idea that aging is controlled\u00a0in part by an evolved genetic program.<\/span><\/p>\n

 <\/p>\n

Metformin Update<\/b><\/p>\n

I have been an advocate of metformin for everyone, and enthusiastic about <\/span>Nir Barzilai\u2019s trial<\/span><\/a> of metformin as an anti-aging drug. \u00a0Last week, I learned from <\/span>Brian Hanley<\/span><\/a> that metformin has a dark side, to wit, a statistical association with higher frequency of Alzheimer\u2019s disease [<\/span>ref<\/span><\/a>, <\/span>ref<\/span><\/a>]. \u00a0There is a <\/span>biochemical mechanism<\/span><\/a> that makes the epidemiology more compelling. \u00a0B12 supplementation <\/span>may mitigate<\/span><\/a> the risk.<\/span><\/p>\n

Other studies [<\/span>ref<\/span><\/a>, <\/span>ref<\/span><\/a>] \u00a0have found that diabetes patients have elevated risk of dementia, and that that risk is <\/span>reduced<\/i><\/b> when they take metformin. \u00a0So it\u2019s fair to say that there is contradictory evidence, and the direction of the effect may depend on individual variation. \u00a0Here is a <\/span>balanced view<\/span><\/a> of both sides.<\/span><\/p>\n

A reader of this blog, George Goldsmith has written to me that <\/span>berberine<\/span><\/a> is a good herbal substitute for metformin. \u00a0Everything we know about berberine looks really good–it is an anti-inflammatory as well as helping preserve insulin sensitivity, acting through the AMPK pathway. \u00a0But we have much more experience with metformin, both clinically and in the lab. \u00a0Metformin increases life span in mice, and to my knowledge, this test has yet to be performed with berberine. \u00a0<\/span>Magnesium supplements<\/span><\/a> also can help prevent insulin resistance, and there are other good reasons to take magnesium. \u00a0<\/span><\/p>\n

Gynostemma pentaphyllum<\/span><\/i><\/a>, sold by LEF under the brand name <\/span>AMPK Activator<\/span><\/a>, is another herbal alternative to metformin.<\/span><\/p>\n

\u00a0<\/span><\/p>\n

Telomeres<\/b><\/p>\n

Bill Andrews<\/span><\/a> was a major sponsor of the conference and a ubiquitous presence, though he did not make a presentation. \u00a0Curiously enough, the only spokesperson for telomere biology was <\/span>Judith Campisi<\/span><\/a>. \u00a0While Andrews has taken the position that lengthening telomeres is more than a good thing, possibly a key to reversing aging, Campisi has cautioned us that telomerase is rationed by the body, and there must be a good reason for this. \u00a0For two decades, Campisi has been the principal advocate of the thesis that telomeres are permitted to shorten in order to protect us from runaway replication of tumor cells. \u00a0<\/span><\/p>\n

My judgment is that Andrews has it right, and Campisi is clinging to a flawed theory \u00a0\u00a0At this point, overwhelming evidence tells us that <\/span>short telomeres cause many more cancers than they prevent<\/span><\/a>. \u00a0To her credit, Campisi has backed away from the cancer theory which she had so long propounded. \u00a0\u00a0But she has yet to embrace the radical truth that telomere shortening is an evolved mechanism of programmed death (and <\/span>has been since the dawn of eukaryotic life<\/span><\/a>). \u00a0Campisi is a good scientist who knows as much about telomere biology as anyone on the planet; but she has afforded too much deference to the prevailing evolutionary perspective, though it is contradicted by evidence that she can (and does) recite from memory. \u00a0So her more recent papers stress the (sometimes) beneficial role of inflammatory signals in promoting wound healing, and she pursues a theory that she hopes will someday explain the devastating consequences of telomere shortening as a necessary price to pay for the signals that call forth repair and renewal.<\/span><\/p>\n

Meanwhile, flawed evolutionary theory continues to be the principal obstruction that impedes progress toward an effective telomerase activator which, I believe, will add years to our lives. \u00a0Neither VC investors nor NIH funders have given this subject the priority it deserves.<\/span><\/p>\n

 <\/p>\n

 <\/p>\n

Rejuvenation from an extract of umbilical blood<\/b>
\n<\/b>(Here is the promised most exciting, and most speculative thing I learned.)<\/span><\/p>\n

Wuyi Kong is a researcher in regenerative medicine who spent 15 years at Stanford before returning to her native China five years ago. \u00a0She now has a <\/span>private for-profit business<\/span><\/a>, incorporated in Silicon Valley and relocated to China, with enough funding from the Chinese government to get tantalizing results, but not enough to do clinical trials.<\/span><\/p>\n

She describes particles in umbilical blood that confound a basic principle of biology: that every cell comes from another cell. \u00a0She calls these medium-size particles <\/span>NPRCP<\/span><\/a>, for non-plasma RNA-containing particles, and has observed them in electron micrographs, as they agglomerate into stem cells. \u00a0<\/span><\/p>\n

\"Time<\/a>
Time sequence shows particles aggregating into cells. This is either a Nobel Prize or an anomaly.<\/figcaption><\/figure>\n

For 15 years, Kong has been filtering these particles from umbilical blood and injecting them intravenously, first into mice and then into humans, with spectacular results. \u00a0<\/span>In her <\/span>most complete and convincing paper<\/span><\/a>, she damages the kidneys of mice by cutting off blood supply, then demonstrates regrowth of the kidneys after infusion with NPRCPs. \u00a0The problematic claim is that NPRCPs are non-living particles, yet they agglomerate to form stem cells, which are then ennucleated with DNA from the recipient mouse. \u00a0This is indeed strange science, but isn’t this all the more reason to replicate her experiments? \u00a0 \u00a0<\/span><\/p>\n

Kong claims anecdotal evidence for erasing wrinkles and white hair turned to black. \u00a0More substantively, she says patients have improved energy and faster healing. \u00a0One semi-comatose patient with advanced AD recovered not just her consciousness but also her short-term memory.<\/span><\/p>\n

This is the kind of speculative, creative science that I have come to expect at SENS conferences. \u00a0Most such\u00a0reports do not pan out, but some of them\u00a0lead to spectacularly disruptive technologies. \u00a0We can survive with no less.<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"

Fifteen years ago, Aubrey de Grey organized the first SENS roundtable–Strategies for Engineering Negligble Senescence. \u00a0It was a small group of out-of-the-box thinkers, heretics who talked about attacking head-on the idea that aging is just part of the human condition, looking for medical (and beyond-medical) treatments that would restore strength, stamina, and alertness, and lower … 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-417","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nReport from Rejuvenation Biotech Conference - 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\/08\/24\/report-from-rejuvention-biotech-2015\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Report from Rejuvenation Biotech Conference\" \/>\n<meta property=\"og:description\" content=\"Fifteen years ago, Aubrey de Grey organized the first SENS roundtable–Strategies for Engineering Negligble Senescence. \u00a0It was a small group of out-of-the-box thinkers, heretics who talked about attacking head-on the idea that aging is just part of the human condition, looking for medical (and beyond-medical) treatments that would restore strength, stamina, and alertness, and lower ... 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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. 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