Category Archives: Longevity Medicine

One strand of stem cell research is learning how to construct exactly the type of cell needed: "researchers for the first time have transformed a human embryonic stem cell into a critical type of neuron that dies early in Alzheimer's disease and is a major cause of memory loss. This new ability to reprogram stem cells and grow a limitless supply of the human neurons will enable a rapid wave of drug testing for Alzheimer's disease, allow researchers to study why the neurons die and could potentially lead to transplanting the new neurons into people with Alzheimer's. ... These critical neurons, called basal forebrain cholinergic neurons, help the hippocampus retrieve memories in the brain. In early Alzheimer's, the ability to retrieve memories is lost, not the memories themselves. There is a relatively small population of these neurons in the brain, and their loss has a swift and devastating effect on the ability to remember. ... Now that we have learned how to make these cells, we can study them in a tissue culture dish and figure out what we can do to prevent them from dying. ... This technique to produce the neurons allows for an almost infinite number of these cells to be grown in labs, allowing other scientists the ability to study why this one population of cells selectively dies in Alzheimer's disease. ... The ability to make the cells also means researchers can quickly test thousands of different drugs to see which ones may keep the cells alive when they are in a challenging environment. ... [Researchers] demonstrated the newly produced neurons work just like the originals. They transplanted the new neurons into the hippocampus of mice and showed the neurons functioned normally. The neurons produced axons, or connecting fibers, to the hippocampus and pumped out acetylcholine, a chemical needed by the hippocampus to retrieve memories from other parts of the brain."

Link: http://www.eurekalert.org/pub_releases/2011-03/nu-hsc030211.php

Interesting research reported via ScienceDaily: "Unexpected results from a [recent study] could completely alter scientists' ideas about Alzheimer's disease - pointing to the liver instead of the brain as the source of the 'amyloid' that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer's prevention and treatment. ... The product of [the mouse gene corresponding to a gene known to predispose humans carrying particular variations of it to develop early-onset Alzheimer's disease], called Presenilin2, is [involved] in the generation of pathogenic beta amyloid. Unexpectedly, heritable expression of Presenilin2 was found in the liver but not in the brain. Higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer's-like pathology. ... This finding suggested that significant concentrations of beta amyloid might originate in the liver, circulate in the blood, and enter the brain. If true, blocking production of beta amyloid in the liver should protect the brain. ... mice were administered imatinib [which] has poor penetration of the blood-brain barrier in both mice and humans. ... Because it doesn't penetrate the blood-brain barrier, we were able to focus on the production of amyloid outside of the brain and how that production might contribute to amyloid that accumulates in the brain, where it is associated with disease. ... the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate. Thus, an appreciable portion of brain amyloid must originate outside of the brain, and imatinib represents a candidate for preventing and treating Alzheimer's."

Link: http://www.sciencedaily.com/releases/2011/03/110303134435.htm

Interesting research reported via ScienceDaily: "Unexpected results from a [recent study] could completely alter scientists' ideas about Alzheimer's disease - pointing to the liver instead of the brain as the source of the 'amyloid' that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer's prevention and treatment. ... The product of [the mouse gene corresponding to a gene known to predispose humans carrying particular variations of it to develop early-onset Alzheimer's disease], called Presenilin2, is [involved] in the generation of pathogenic beta amyloid. Unexpectedly, heritable expression of Presenilin2 was found in the liver but not in the brain. Higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer's-like pathology. ... This finding suggested that significant concentrations of beta amyloid might originate in the liver, circulate in the blood, and enter the brain. If true, blocking production of beta amyloid in the liver should protect the brain. ... mice were administered imatinib [which] has poor penetration of the blood-brain barrier in both mice and humans. ... Because it doesn't penetrate the blood-brain barrier, we were able to focus on the production of amyloid outside of the brain and how that production might contribute to amyloid that accumulates in the brain, where it is associated with disease. ... the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate. Thus, an appreciable portion of brain amyloid must originate outside of the brain, and imatinib represents a candidate for preventing and treating Alzheimer's."

Link: http://www.sciencedaily.com/releases/2011/03/110303134435.htm

Moderately skilled and experienced operators can make money by creating and maintaining a website on a particular topic. The degree to which money can be made by doing this is, at the highest level, a function of the level of interest in that topic - complicated by how much money flows in associated industries, but in general it is a measure of public interest and engagement.

Out there in the very fluid ecosystem comprised of small-scale entrepreneurs, online advertising networks, and the browsing population, you'll find an ever-changing and adapting group of websites associated with almost any topic that you find interesting. You have the basement level of automated spam blogs and tiny content sites, bottom feeders produced with minimal effort to generate a tiny amount of revenue each - but there are millions of them. Above that there are the institutional versions of those automated spam systems: companies that churn out terrible, banal content according to metrics that measure present interest in particular topics. Above that, the mix of old and young online journalism that does much the same thing, only more slowly and with a more idiosyncratic flavor.

Then you have the entrepreneurs who build and sell websites over the course of years in much the same way that some people buy, renovate, and sell houses. There is a well-established formula: you work on good (or rather good enough) content, pull in an audience, demonstrate worth, and then sell to another player in that marketplace. None of this implies that the entrepreneur has any interest whatsoever in the topic covered by the website - it helps if they do, but it isn't necessary.

This ecosystem, coupled with the vast sums of money that flow through the "anti-aging" marketplace, explains why 99% of the material out there on the topic of human longevity is junk, nonsense, machine-generated, or only present in the hopes that you'll click on a high-value ad. It is worthless garbage, produced by people who have no interest whatsoever in actually attaining the goal of longer lives through medical science. Over the past few years it seems the search engines have largely given up, their indexes clogged with useless pages created by ignorant outsiders for gain that push down the relevance of useful pages created by knowledgeable insiders.

This state of affairs is been a plague upon our houses, a blanket of lies and misdirection that has long made it extremely hard for newcomers to find any sane starting point in learning about longevity science. Discussion of fundraising and serious research can't get a word in edgeways around the jabbering of supplement-pushers and machine-generated sales pitches for the "anti-aging" products of magical thinking.

I mention all of this as I've noticed a slight shift in the strategy of the site-building entrepreneurs over the past year or so. I should mention that it is often the case that it is hard to tell the difference between one of their sites and a spam system, and their modus operandi in matters of aging and longevity has typically been to follow on the coattails of the "anti-aging" marketplace to push whatever expensive, unproven, and ultimately useless supplement is all the rage. Even sites run by people who are genuinely interested in radical life extension have largely made money through supplements - as that, so far as I can see, is the only game in town.

This becomes at some point a self-fulfilling prophecy: the vast majority of the ecosystem spews forth discussion of supplements and "anti-aging" nonsense - and so this is what the community hears, expects, and looks for. The for-profit websites are just as much a tool for education and advocacy as this site is, and sad to say they are generally far more effective at propagating the message they eventually settle on.

But of late, I've been seeing more site-building that incorporates the messages of rejuvenation biotechnology and modern, serious longevity science. Pulling in quotes from well known aging researchers, for example, talking about the Strategies for Engineered Negligible Senescence, and cutting back on the supplement-pushing. I'm not sure where the various entrepreneurs are going with this, but it seems to be a sign that the right sort of message is further spreading thanks to the efforts of advocates in the healthy life extension community. It is, after all, hard to talk up a $20 pitch while selling a $1 technology that looks pretty weak beside the ongoing work that the scientist next door is busy explaining.

Here are a couple of sites I've noticed of late - see if you can decipher the longer-term motivations of the builders. In each case, these are small-scale commercial ventures at various stages of their inception and progress; and I provide no assurances that any of the content you'll find is true, straightforward, or anything other than a hook aimed at your wallet.

Ageless Zoom

For most of my adult life I've had the sense that I was to participate in bringing in the future. But I never clearly knew what that meant. Now we are able, if we choose, to live longer than any life-span humans have ever imagined. That's not mere possibility, it's real and at hand. I think of it as a second lifetime. And for me it's a very real opportunity to move from chance to choice.

Extreme Longevity

Extreme Longevity is an Internet publication dedicated to finding and presenting the latest developments in human longevity research. ... Each day thousands of scientists and researchers around the world are working to gain a greater understanding of what processes make living things age and seek to determine methods to slow down, stop, or even reverse this process. ... At Extreme Longevity you can expect the latest research to be presented regularly in concise easy-to-understand articles which emphasisze how best to put these learnings in to practice.

Immortal Humans

The latest news and developments about humankind's drive towards biological immortality.

That last one is a good example of a site that can be hard to tell apart from a spam blog - but the entrepreneur responsible for it emerged to comment back a ways when I first noted its existence.

There are others I could point out, but a representative set of three is more than enough. Take them for what they are, and ponder what their existence indicates in terms of the present strength and propagation of the message on scientific longevity.

You might recall that studies of centenarians turned up an association between reaching that age and levels of HDL, high density lipoprotein, a form of cholesterol transport mechanism. Here is another study demonstrating the same correlation for younger old people: "No previous researchers have sought to determine whether high-density lipoprotein (HDL) cholesterol levels are associated with survival to 85 years of age in a prospective cohort of aging men. We selected 652 men (mean age 65 years) enrolled in the VA Normative Aging Study who had [at least one] HDL cholesterol level documented during the study and who were old enough on the date of HDL cholesterol measurement to reach 85 years of age by [2008]. ... We used proportional hazards to determine hazard ratios (HRs) for mortality before age 85 years for each category of initial HDL cholesterol compared to the reference adjusting for co-morbidities, calculated low-density lipoprotein cholesterol, medications, smoking, body mass index, and alcohol consumption. Treating HDL cholesterol as a continuous predictor, we also determined the HR for each 10-mg/dl increment in HDL cholesterol. ... Each 10-mg/dl increment in HDL cholesterol was associated with a 14% [decrease] in risk of mortality before 85 years of age. In conclusion, after adjusting for other factors associated with longevity, higher HDL cholesterol levels were significantly associated with survival to 85 years of age." Which leads to the thought that if HDL is so good, why not test to see if artificially creating more of it in the body is beneficial?

Link: http://www.ncbi.nlm.nih.gov/pubmed/21296318

One group of researchers believe that every tissue in the body is supported by a left-over population of fully pluripotent stem cells that might be easily accessible for use in therapies: "From the point of view of regenerative potential, the most important cells are pluripotent stem cells (PSCs). Such cells must fulfill certain in vitro as well as in vivo criteria that have been established by work with PSCs isolated from embryos, which are known as embryonic stem cells (ESCs). According to these criteria, pluripotent stem cells should: (i) give rise to cells from all three germ layers, (ii) complete blastocyst development, and (iii) form teratomas after inoculation into experimental animals. Unfortunately, in contrast to immortalized embryonic ESC lines or induced PSCs (iPSCs), these last two criteria have thus far not been obtained in a reproducible manner for any potential PSC candidates isolated from adult tissues. There are two possible explanations for this failure. The first is that PSCs isolated from adult tissues are not fully pluripotent; the second is that there are some physiological mechanisms involved in keeping these cells quiescent in adult tissues that preclude their 'unleashed proliferation', thereby avoiding the risk of teratoma formation. In this review we present an evidence that adult tissues contain remnants from development; a population of PSCs that is deposited in various organs as a backup for primitive stem cells, plays a role in rejuvenation of the pool of more differentiated tissue-committed stem cells (TCSCs), and is involved in organ regeneration. These cells share several markers with epiblast/germ line cells and have been named very small embryonic-like stem cells (VSELs). We suggest that, on one hand, VSELs maintain mammalian life span but, on the other hand, they may give rise to several malignancies if they mutate. We provide an evidence that the quiescent state of these cells in adult tissues, which prevents teratoma formation, is the result of epigenetic changes in some of the imprinted genes."

Link: http://www.ncbi.nlm.nih.gov/pubmed/21339038