Guitar Lessons in Sherman Oaks

I teach basic chords and songs, reading as well as advanced chord scales utilized in jazz improvisation.

I am patient and like to see my students progress. This brings me much joy! My schedule is flexible and I am willing to work with students especially who show initiative and want to learn.

For teaching, I often use the Alfred books as I find them thorough and logical.I've taught all age groups and am adept at helping students progress.I have many years teaching at music colleges as well as private lessons.I have 3 CDs released internationally and have performed throughout the world.I enjoy it when students bring in a song they want to learn. That is one of the best ways to internalize music.

Source:
http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

Accounting Tutor in Sherman Oaks

I graduated from UCLA magna cum laude with college honors. I possess a Bachelor’s degree in economics as well as a specialization in business and a minor in accounting. I have five years of experience as an educator which includes tutoring students at the graduate, undergraduate, high school, and middle school levels as well as working as a drum teacher.

After college, I spent a year working full time for one of the ‘Big Four’ global public accounting firms while simultaneously studying for and successfully passing all four sections of the CPA exam with an average score of 94%. My rigorous work experience and the balance I had to achieve, between working upwards of 55 hours per week and studying, have allowed me to further hone the organizational skills that I picked up as a student. In addition to tutoring students in specific subjects, I am often consulted to help students with organization, planning, time management, and effective study habits so that they can succeed in rigorous academic environments.

Source:
http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

Daniel Perry of the Alliance for Aging Research was kind enough to send over an article written in conjunction with Brian Kennedy of the Buck Institute for Research on Aging. I take this as a sign that various conjunctions are imminent in the moving spheres of government funding of aging research and the broader pressures on the economy. Organizations like these two have their own cycles of publicity and outreach that ebb and flow in time with potential shifts in public funding:

Bette Davis was right - old age is not for sissies.

One hundred years ago most of us didn't have the luxury of old age. Today, life expectancy is almost 80 years. But while we've gotten very good at adding life-years, we've yet to master how to keep those years healthy and vigorous. Eighty percent of seniors have at least one major chronic condition and half have two or more. Chronic diseases of later life are costing the nation more than $1 trillion per year - a figure expected to increase to $6 trillion by the middle of this century.

Scientists who study aging are in general agreement that the process isn't set in stone - the aging process can be sped up by genetics or poor lifestyle choices, but it can also be slowed down. With sufficient funding and focus, research that slows aging has the potential to do what no drug, surgical procedure, or behavior modification can do - add healthy years of life, and simultaneously postpone the costly and harmful conditions of old age.

Age is the common denominator and number one risk factor to virtually every chronic disease we face. Scientists know that alterations in cell replacement and repair, stress response, and inflammation are the key influencers to the development of cancer, heart disease, diabetes, and other debilitating (and costly) conditions later in life. These are also the essential changes taking place in our aging bodies.

There are currently 10,000 Americans a day turning 65; by 2030, about one in five Americans will be past that age. To afford the eldercare costs that lay ahead our country must invest now in the prevention and postponement of age-related illness. New realities of population aging and chronic disease call for new thinking how we fund biomedical research. The great majority of federal medical research funds goes to studies of diseases of aging such as cancer, heart ailments and diabetes in isolation from each other and largely divorced from the underlying aging processes that lead to all of them. Less than one percent of the National Institutes of Health's (NIH) annual budget funds research into the underlying biology of aging and its role in age-related disease.

Meanwhile privately funded research centers such as the Buck Institute for Research on Aging in California and other centers in universities across the U.S. are probing new understanding of aging in order to defeat diseases from cancer to Alzheimer's. And the private non-profit Alliance for Aging Research is pressing a 'Healthspan Campaign' pointing out the large social and economic rewards to be gained by increasing the federal investment in medical research with a greater focus on the underlying biology of aging.

Already the National Institutes of Health, which is mostly organized by various disease research programs, has initiated a cross-cutting interest group involving 17 separate NIH Institutes to pursue 'geroscience,' a new term for understanding our aging bodies so we might experience more healthy years of life. At a time when even medical research is feeling a funding squeeze, for multiple research institutes to pool expertise and resources in order to confront the mammoth health challenge of an aging population, this is a prudent course and a sound public investment for America's future.

This week, the Director of the NIH, Dr. Francis Collins, will testify before the Senate subcommittee that determines future appropriations. We are encouraged that the promise of more coordinated research into aging will be set before important members of Congress who help determine research priorities. As we have learned from the experience with polio and HIV/AIDS, significant federal investment in biomedical research can have a profound impact on not only reducing mortality and morbidity, but on reducing healthcare costs.

The evidence is strong that the single most effective strategy in "bending the cost curve" on health care is preventing age-related chronic diseases in the first place. It will require courageous and innovative policy-making to step outside the traditional way medical research priorities have been established. Just as old age is not for sissies, neither is forward-looking public policy.

---

Daniel P. Perry is President and CEO of the Alliance for Aging Research.
Brian K. Kennedy, Ph.D. is President and CEO of the Buck Institute for Research on Aging.

It's possible to agree with everything said above about aging and the need for action, and then completely disagree that a wise use of time is chasing tax dollars and playing the lobbying game - putting money into the pockets of politicians and their cronies rather than research institutions. Government funding comes with government regulation and government values: it corrodes everything it touches, destroys the incentives to create progress, blocks clinical applications of research, and turns even the most ambitious ideals into staid jobs programs for the connected that win ever more money by failing to achieve any of their goals.

My view of the ideal future for the funding of medical research is closer to that of Peter Thiel - venture philanthropy, crowdsourcing for research, radical distribution of research collaboration between regions of the world, open biotechnology and science, and big financial risks put on programs like the Strategies for Negligible Engineered Senescence that have massive payoffs on achieving success. This is a future in which the connectivity of the Internet, dirt-cheap biotechnology, crowdsourcing, cheap air travel, and medical tourism combine to make every present institution in medical research irrelevant.

So avoid like the plague the incremental, aim-for-one-little-bit-better, money-chewing philosophy of government expenditures and near-sighted goals, that's what I say. Political culture is unable to look past the present and unable to avoid corruption. If you leave progress up to politicians and the regulatory capture collective that is Big Pharma, all you'll get is waste, "progress" that is one step short of stasis, and the building of institutions that - like the FDA - are incentivized to prevent the future, not unleash it.

So in conclusion, I see folk like the authors above to be in some ways rather like the A4M business leaders, for all that their politics couldn't be any more different. By that I mean that their hearts are in the right place, they have an enthusiasm for the cause of really, actually doing something about aging, but are heading down the wrong road when it comes to achieving significant, game-changing progress in longevity science by the only metric that matters - how long we all live.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Transdifferentiation is showing up more often of late - the ability to switch somatic cells directly between types without having to go through an intermediate stage of reprogramming into stem cells. It should in theory make obtaining specific cells for research and therapy a cheaper and more reliable process in the future: "it has become possible to directly convert cells of the body into one another - without the time-consuming detour via a pluripotent intermediate stage. However, this method has so far been rather inefficient. [Scientists] have now developed the method to the point that it can be used for biomedical applications. ... [Researchers] are interested in the biomedical utilization of artificially produced human nerve cells for disease research, cell replacement, and the development of active substances. ... By blocking the so-called SMAD signaling pathway and inhibiting glycogen synthase kinase 3 beta (GSK3ß), they increased the transformational efficiency [of skin cells to neurons] by several times - and were thus able to even simplify the means of extraction. Using only two instead of previously three transcription factors and three active substances, [the] researchers were able to convert a majority [of] skin cells into neurons. In the end, their cell cultures contained up to more than 80% human neurons. ... We were able to demonstrate how the genes typical for skin fibroblast were gradually down-regulated and nerve-cell-specific genes were activated during the cell transformation. In addition, the nerve cells thus obtained were functionally active, which also makes them interesting as a source for cell replacement."

Link: http://www.sciencedaily.com/releases/2012/04/120411084044.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

As time progresses, researchers are increasingly able to correlate changing mental characteristics in aging with changing structure in the brain. Here is one example: "A brain-mapping study [has] found that people's ability to make decisions in novel situations decreases with age and is associated with a reduction in the integrity of two specific white-matter pathways that connect an area in the cerebral cortex called the medial prefrontal cortex with two other areas deeper in the brain. Grey matter is the part of the brain that contains the bodies of the neurons while white matter contains the cable-like axons that carry signals from one part of the brain to another. In the past, most brain-imaging research has concentrated on the grey matter. Recently, however, neuroscientists have begun looking more closely at white matter. It has been linked to the brain's processing speed and attention span, among other things, but this is the first study to link white matter to learning and decision making. ... The evidence that this decline in decision-making is associated with white-matter integrity suggests that there may be effective ways to intervene. Several studies have shown that white-matter connections can be strengthened by specific forms of cognitive training. ... The critical white-matter connections that the experiment identified run from the thalamus, a highly connected relay center in the brain, to the medial prefrontal cortex, an area of the brain involved with decision making, and from the medial prefrontal cortex to the ventral striatum, which is associated with the emotional and motivational aspects of behavior." You might also look at past research on age-related damage to white matter and its consequences on metal capacity.

Link: http://www.sciencedaily.com/releases/2012/04/120411131917.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Resistance to cancer and increased longevity are thought to be flip sides of the coin when it comes to variations in metabolism and the controlling mechanisms of stem cell action. Either your cells are more ready to divide and repair your tissues, in which case you have increased longevity coupled with increased risk of cancer, or your cells are less ready to divide and repair your tissues and as a consequence you are less likely to suffer cancer, but also less likely to live for as long as your contemporaries in the scenario under which you do evade cancer. The decline of stem cell capacity with age is thought to be an adaptation to resist the increasing risk of cancer due to rising levels of cellular and molecular damage - the less that your stem cells take action, the less likely it is that a cancerous mutation will occur and take hold.

Cancer is a game of odds, in other words. We're all rolling those dice, day in and day out - regardless of how indifferent we are or pretend to be. It's a sobering thought.

On this topic, I noticed an intriguing twin study today that suggests the naturally longer-lived humans amongst us are having their cake and eating it too when it comes to the supposed cancer-longevity balance. There's no balance here at all, just benefits all round from happening to be naturally longer-lived:

BACKGROUND: Animal models and a few human studies have suggested a complex interaction between cancer risk and longevity indicating a trade-off where low cancer risk is associated with accelerating aging phenotypes and, vice versa, that longevity potential comes with the cost of increased cancer risk. This hypothesis predicts that longevity in one twin is associated with increased cancer risk in the cotwin.

METHODS: A total of 4,354 twin pairs born 1900-1918 in Denmark were followed for mortality in the Danish Civil Registration System through 2008 and for cancer incidence in the period 1943-2008 through the Danish Cancer Registry.

RESULTS: The 8,139 twins who provided risk time for cancer occurrence entered the study between ages 24 and 43 (mean 33 years), and each participant was followed up to death, emigration, or at least 90 years of age. The total follow-up time was 353,410 person-years and 2,524 cancers were diagnosed. A negative association between age at death of a twin and cancer incidence in the cotwin was found in the overall analyses as well as in the subanalysis stratified on sex, zygosity, and random selection of one twin from each twin pair.

CONCLUSIONS: This study did not find evidence of a cancer-longevity trade-off in humans. On the contrary, it suggested that longevity in one twin is associated with lower cancer incidence in the cotwin, indicating familial factors associated with both low cancer occurrence and longevity.

It's worth remarking that the ultimate goal for longevity science is to make this and all similarly interesting discoveries absolutely irrelevant - to create a world in which it no longer matters in the slightest which genes we are born with. Sufficiently advanced medical technology - such as that envisaged in the Strategies for Engineered Negligible Senescence, which could be produced within the next twenty to thirty years given the funding - will enable all people to live extremely long lives in good health regardless of their genetic heritage. This is all the more reason to support that research; doing something about the limitations of the human condition beats sitting around listening to the dice roll and your chances of cancer inch upward year by year.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

An article from the Scientist: "Based on new intelligence, oncologists are making informed battle plans to attack a particularly pernicious enemy - the cancer stem cell (CSC). Controversial though they are, cancer stem cells are an incredibly promising target. If treatment-resistant cancer, and the metastases that transplant the cancer throughout the body, could be attributed to the actions of a single cell type, it could explain many of the treatment failures and provide a novel way to attack the disease. The idea that cancers are driven by cells with 'embryonic features' is an old one. Many cancers regress to a less differentiated state, expressing proteins that are usually expressed only in the embryo or during early development. It is only in the past 20 years or so, however, that additional observations led to the hypothesis that these embryonic-like cells were a separate subpopulation that fueled tumor expansion, much the same way that stem cells churn out the cells that make up a particular organ. ... In the past 5 years there has been an exponential increase in CSC research. This research has helped to resolve a number of controversies regarding identification of these cells and their role in driving tumor growth and mediating treatment resistance. Despite these advances, the CSC field is still in its relative infancy, and many questions and challenges remain. More than a dozen biotechnology and pharmaceutical companies are now vigorously pursuing CSC research. As a result, a number of early-phase clinical trials targeting CSCs are in progress. These studies and the later-stage efficacy trials that follow them should indicate whether successful targeting of CSCs significantly improves outcomes in cancer patients. If this is found to be the case, it may usher in the beginning of a new era of cancer therapy."

Link: http://the-scientist.com/2012/04/01/are-cancer-stem-cells-ready-for-prime-time/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A look at why, in this age of biotechnology and great uncertainty over the degree to which life spans will be extended in the next few decades, it is unwise to trust your financial future to large pension and welfare institutions. Any significant progress over the present very modest baseline of incidental life extension through general advances in medicine will likely bring down much of the existing system in the years ahead - which of course suggests that big centralized pension systems should be avoided like the plague, but that won't happen. If today's politics are any guide, politicians will continue to aggressively devalue their national currencies, taking wealth from their broader population to pay for what cannot be afforded until such time as the house of cards cannot be propped up any longer. The lesson to be taken away here: expect to provide for your own financial security in later life, and act accordingly now: "Here's the issue: governments have done their analysis of the aging issue largely based on best guesses of population developments in the future. These developments include further drops in fertility and some further increase in longevity. The trouble is that in the past, longevity has been consistently and substantially underestimated. We all live much longer now than had been expected 30, 20, and even just 10 years ago. So there is a good chance in the future people will live longer than we expect now. We call this longevity risk - the risk we all live longer than anticipated. ... Why is that a risk, you may ask. We all like to live longer, healthy lives. Sure, but let's now return to those pension worries. If you retire at 65 and plan your retirement finances expecting to live another 20 years (assuming you have enough savings for at least that period), you would face a serious personal financial crisis if you actually live to 95, or - well in your 100s. You could rely on your social security system at that point, but the program is also counting on people not living much beyond their mid-80s in most countries. Your personal financial problem multiplies by the size of the population, and, for society as a whole, becomes a very large problem." An example of how the present politics and systems of wealth transfer reward irresponsibility at all levels until such time as growth in collective irresponsibility sinks the whole venture.

Link: http://www.huffingtonpost.com/erik-oppers/seven-billion-reasons-to-_b_1417749.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

By way of a follow-up to an interview last month on what are termed very small embryonic-like stem cells (VSELs), here is a recent open access review paper that outlines the present state of knowledge on this topic - which has some relevance to studies of longevity in addition to the broader field of regenerative medicine:

Very small embryonic/epiblast-like stem cells (VSELs) and their potential role in aging and organ rejuvenation - an update and comparison to other primitive small stem cells isolated from adult tissues:

One of the most intriguing questions in stem cell biology is whether pluripotent stem cells (PSCs) exist in adult tissues. Several groups of investigators employing i) various isolation protocols, ii) detection of surface markers, and iii) experimental in vitro and in vivo models, have reported the presence of cells that possess a pluripotent character in adult tissues. Such cells were assigned various operational abbreviations and names in the literature that added confusion to the field and raised the basic question of whether these are truly distinct or overlapping populations of the same primitive stem cells. Unfortunately, these cells were never characterized side-by-side to address this important issue. Nevertheless, taking into consideration their common features described in the literature, it is very likely that various investigators have described overlapping populations of developmentally early stem cells that are closely related.

...

[We believe that] during embryogenesis, some PSCs give rise to [populations of less potent tissue-committed stem cells (TCSC)s] but some survive in adult tissues as a backup population of PSCs that renews the pool of TCSCs over time. In this scenario, PSCs are precursors of TCSCs during organ/tissue rejuvenation and a source of these cells in emergency situations when organs are damaged (e.g., heart infarct or stroke).

...

a main goal of the molecular analysis studies was to explain why VSELs do not fulfill the in vivo gold-standard criteria expected for PSCs (complementation of blastocyst development and teratoma formation in immunodeficient animals), which are seen with [embryonic stem cells] and [induced pluripotent stem cells]. To explain this discrepancy, we observed that VSELs, in a similar manner as late migratory primordial germ cells (PGCs), modify the methylation of imprinted genes, preventing them from uncontrolled proliferation and explaining their quiescent state in adult tissues

...

we proposed a hypothesis that relates aging, longevity, and insulin/insulin-like growth factors signaling (IIS) to the abundance and function of pluripotent VSELs deposited in adult murine tissues. We postulate that a decrease in the number of these cells due to prolonged IIS negatively affects the pools of TCSCs in various organs and has an impact on tissue rejuvenation and life span. In support of this notion, we observed a significantly higher number of VSELs in long-living murine strains (e.g., Laron dwarfs and Ames dwarfs), whose longevity is explained by low levels of circulating IGF1 and a decrease in IIS. By contrast, the number of VSELs is reduced in mice with high levels of circulating IGF1 and enhanced IIS (e.g., growth hormone-overexpressing transgenic mice) compared to normally aging littermates.

...

a chronic increase in caloric uptake that elevates circulating levels of IGF1 and [insulin] may contribute over time to depletion of [VSELs] from adult tissues, affect the generation of VSEL-derived TCSCs, and thus negatively affect life span. This explains why mice that have high levels of circulating blood plasma IGF1 and enhanced IIS display accelerated depletion of VSELs and have a shorter lifespan than age-matched littermates.

Interestingly, it is often the case that life science researchers spend years investigating the same entity within the body from different directions, working in comparative isolation from one another and developing quite divergent nomenclature. It is only later on that lines are drawn between the dots and some unity imposed on that area of research - this is more or less what happened for lipofuscin, for example, the build up of many mixed harmful chemicals inside cells that occurs with aging. Lipofuscin contributes to many different age-related conditions, and for years went by many different names in different subfields of medical and biological science, and few of the researchers were picking up on parallel and useful research outside their specialty.

So, even aside from the evidence amassed, it is entirely plausible that there is a great deal of this unification and synthesis yet to happen for portions of stem cell research - but on the other hand cells are very complicated beasts. To a certain degree calling something a stem cell or a particular type of stem cell at this time is a form of pidgeonholing in the face of complexity: a cell is quite capable of being sort of a stem cell or somewhat stem cell-like, and different types of stem cell might be as different from each other as they are from non-stem cells - and their categories all blur at the edges. Stemness isn't the result of a single switch, and is rather much more like a collection of linked controlling mechanisms.

Insofar as this all touches upon calorie restriction (CR) and its effects on health and longevity, we should absolutely expect that calorie restriction in some way affects stem cell populations for the better. Stem cells are an integral mechanism of health, and it would be hard to explain how CR improves near every measure of health, slows aging, and extends life in diverse animal species without it causing some improvement in stem cell capacity and operation in addition to its other lower level mechanical effects.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Signs of progress in understanding the mechanisms of induced longevity through altered insulin/IGF-1 signaling are shown in this paper. This is one of the most-studied class of longevity mutations in lower animals, despite there being some debate over whether it is relevant to mammal biochemistry. Here, the basic mechanism is explained as being hormetic, centering on the mitochondria: researchers "elucidate a conserved mechanism through which reduced insulin-IGF1 signaling activates an AMP-kinase-driven metabolic shift toward oxidative proline metabolism. This, in turn, produces an adaptive mitochondrial [reactive oxygen species (ROS)] signal that extends worm life span. These findings further bolster the concept of mitohormesis as a critical component of conserved aging and longevity pathways. ... Impaired insulin and IGF-1 signaling (iIIS) in C. elegans daf-2 mutants extends life span more than 2-fold. Constitutively, iIIS increases mitochondrial activity and reduces reactive oxygen species (ROS) levels. By contrast, acute impairment of daf-2 in adult C. elegans reduces glucose uptake and transiently increases ROS. Consistent with the concept of mitohormesis, this ROS signal causes an adaptive response by inducing ROS defense enzymes, culminating in ultimately reduced ROS levels despite increased mitochondrial activity. Inhibition of this ROS signal by antioxidants reduces iIIS-mediated longevity by up to 60%. ... IIIS upregulates mitochondrial L-proline catabolism, and impairment of the latter impairs the life span-extending capacity of iIIS while L-proline supplementation extends C. elegans life span. Taken together, iIIS promotes L-proline metabolism to generate a ROS signal for the adaptive induction of endogenous stress defense to extend life span."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22482728

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Researchers are comparing the biochemistry of long-lived species to better understand the roots of large differences in life span: "The team looked at the genome of more than 30 mammalian species to identify proteins that evolve in connection with the longevity of a species. They found that a protein, important in responding to DNA damage, evolves and mutates in a non-random way in species that are longer-lived, suggesting that it is changing for a specific purpose. They found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins. Findings show that if certain proteins are being selected by evolution to change in long-lived mammals like humans and elephants, then it is possible that these species have optimized pathways that repair molecular damage, compared to shorter-lived animals, such as mice. ... The genetic basis for longevity differences between species remains a major puzzle of biology. A mouse lives less than five years and yet humans can live to over 100 for example. If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the aging process."

Link: http://esciencenews.com/articles/2012/03/29/study.suggests.why.some.animals.live.longer

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Back in 2006 I had this to say on the topic of what was then the first flush of popular interest in resveratrol, back when far less was known about it:

Our metabolic biochemistry looks like a big wall full of levers. Some of them are painted red, and we think we understand what the instructions beneath these red levers say. Maybe. How much information do you feel you would like before you pull the big red levers in your own personal metabolism? What level of risk due to disease would you presently need to be suffering in order to take the risk represented by a new compound? How do you evaluate these levels of risk?

Resveratrol has turned out, almost predictably, to be another heaped mound of hype that buries a modest kernel of interesting-but-not-terribly-applicable metabolic research. At this stage it seems fairly certain that resveratrol does not extend life in mammals to any great degree - when you find compounds that can do that, there is little uncertainty once the life span studies are in and replicated. See the past couple of years of work on rapamycin in mice as a contrasting example to the uncertainty and lack of verifiable effects for resveratrol and its derived compounds.

In any case, I was reminded of the topic by a recent post at In the Pipeline that echoes many of the same sentiments in my 2006 post:

I've written many times here about sirtuins, and their most famous associated small molecule, resveratrol. And I've been asked more than once by people outside the med-chem field if I take (or would take) resveratrol, given the available evidence. My reply has been the same for several years: no, not yet. Why so cautious, for a compound that's found in red grapes and other foods, and to which I've presumably been exposed many times? Several reasons - I'll lay them out and let readers decide how valid they are and how they'd weight these factors themselves.

...

So what do we know about what resveratrol does? A lot, and not nearly enough. Its pharmacology is very complex indeed, and the one thing that you can clearly draw from the (large) scientific literature is that its (a) a very biochemically active compound and (b) we haven't figured out many of those actions yet. Not even close. Even if all it did was act as on one or more sirtuins, that would be enough to tell us that we didn't understand it.

...

There's room to wonder about the mechanisms of a number of drugs. Indeed, there have been many that have made it to market (and stayed there for many years) without anyone knowing their mechanisms at all. We're still finding things out about aspirin; how much can one expect? Well, one response to that is that aspirin has been used widely in the human population for quite a long time now, and resveratrol hasn't. So the question is, what do we know about what resveratrol actually does in living creatures? If it has beneficial effects, why not go ahead and take advantage of them?

Unfortunately, the situation is wildly confusing (for an overview, see here). The first thing that brought resveratrol into the spotlight was life extension in animal models, so you'd think that that would be well worked out by now, but boy, would you be wrong. The confusion extends up to mouse models, where some of the conclusions - all from respectable groups in respectable publications - seem to flatly contradict each other. No, the animal-model work on resveratrol is such a bubbling swamp that I don't see how anyone can safely draw conclusions from it.

We can conclude that it doesn't straightforwardly extend life at this point. So you have on the one hand a distinct lack of knowledge as to long term effects and on the other hand it clearly isn't doing anything spectacular in laboratory animals. That looks like the worst of both worlds from where I stand.

The sensible thing to do whenever another of these oral-fixation ingested substance hype machines emerges from the juncture of the scientific and business worlds is to balance the purported results against the clear, proven, and solid benefits of exercise and calorie restriction. The risks in moderate exercise and calorie restriction are minimal, while the evidence for great benefit to long-term health is gold-plated and voluminous. When someone is trying to convince you to spend money on something that seems unlikely to produce even a pale shadow of the health benefits of either exercise or calorie restriction, and has largely unknown long term risks - then why even try? It just doesn't make sense.

The research community, and just as importantly the public at large, needs to move beyond their enthusiasm for metabolic manipulation through ingested substances as a path to extending healthy life. It's a grand example of looking for the lost keys under the lamp post - doing something just because it's easier and the path of least resistance, regardless of the likelihood of significant results at the end of the day. Real progress towards longer lives is only going to come through building medical technology capable of repair and rejuvenation at the level cells, organs, and systems within the body: very specific biotechnologies engineered to perform very specific jobs within and around cell structures, and aim to exactly reverse aging by doing so. That couldn't possibly be further removed from the present dominant strategy of mining the natural world for compounds that might or might not cause more minor benefits than minor disadvantages.

It's a common refrain here, but no less true for it: work on rejuvenation biotechnology must displace the present longevity science mainstream if we want to see significant progress towards radical life extension occur before we run out of time, aged to death on the very verge of success.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm