Longevity Medicine » Longevity Medicine

DON’T LEAVE HOME WITHOUT THESE skincare kit

admin — Sun, 05 Feb 2012 16:50:25 +0000

Sophoto has tapped into the antioxidant-laden, pore perfecting power of organic phytotherapy (the study of the use of extracts from natural origin as medicines or health-promoting agents) for their new all inclusive line. Finally, there…

Source:
http://wwww.examiner.com/RSS-3174-Longevity-Examiner

EYE SILK

admin — Sun, 05 Feb 2012 16:50:24 +0000

Sun exposure, cigarette smoke, and stress can all deplete the skin of its elastin – and its resiliency. Tapping into the same repair and protect technology featured in Dermatology Times, relastin has created EYE SILK, an age-fighting elastin…

Source:
http://wwww.examiner.com/RSS-3174-Longevity-Examiner

Some Cells Last as Long as We Do – and Perhaps So Do Some of the Proteins Within Those Cells

admin — Sun, 05 Feb 2012 16:49:49 +0000

It is not unreasonable to regard a cell as a machine that is constantly rebuilding itself – organelles and protein machinery are constantly torn down and replaced. It is also not unreasonable to regard tissue as a collection of cells that is constantly rebuilding itself: cells destroy themselves or are destroyed by watchdog systems, and new cells are created to replace them. This sort of thing happens rapidly indeed in some parts of the body, such as the blood and stomach lining, but there are portions of your nervous system where cells will never be replaced under normal circumstances – the cells you were born with are the very same cells you have now.

These long-lived cells are the most vulnerable to forms of age-related damage involving build up of metabolic waste products, and the related slow failure in the ability of cells to recycle their own damaged components. There is no fallback to replacing cells wholesale in this case, or at least not in our species, so long-lived cells must forge ahead and struggle to do their job no matter how damaged they are. The existence of these cells is a good argument for the need for in situ repair technologies, able to reverse damage and remove other hinderances in order to allow long-lived cells to regain their vigor and function – goals that are hard to attain with the present generation of cell replacement technologies emerging from the field of regenerative medicine.

Now consider this: it may be the case that some of the individual vital proteins in the machinery of long-lived cells are also never replaced. Some of your complex individual proteins, important cogs and gears in important cells, might be as old as you are. The very same sorts of concern about vulnerability surface here as well. Here is news of research in rats:

The scientists discovered that certain proteins, called extremely long-lived proteins (ELLPs), which are found on the surface of the nucleus of neurons, have a remarkably long lifespan. While the lifespan of most proteins totals two days or less, the Salk Institute researchers identified ELLPs in the rat brain that were as old as the organism. … ELLPs make up the transport channels on the surface of the nucleus; gates that control what materials enter and exit. Their long lifespan might be an advantage if not for the wear-and-tear that these proteins experience over time. Unlike other proteins in the body, ELLPs are not replaced when they incur aberrant chemical modifications and other damage.

…

The fundamental defining feature of aging is an overall decline in the functional capacity of various organs such as the heart and the brain. This decline results from deterioration of the homeostasis, or internal stability, within the constituent cells of those organs. Recent research in several laboratories has linked breakdown of protein homeostasis to declining cell function. … Most cells, but not neurons, combat functional deterioration of their protein components through the process of protein turnover, in which the potentially impaired parts of the proteins are replaced with new functional copies. Our results also suggest that nuclear pore deterioration might be a general aging mechanism leading to age-related defects in nuclear function, such as the loss of youthful gene expression programs.

Given how much longer humans live in comparison to rats, it may be that there are no proteins in the human body that never turn over. But I wouldn’t be surprised to find that the situation for old humans is exactly the same as described above for old rats.

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

Rapid Repair of Severed Nerves Demonstrated in Rats

admin — Sun, 05 Feb 2012 16:49:46 +0000

An advance in the methodologies of nerve repair: “scientists believe a new procedure to repair severed nerves could result in patients recovering in days or weeks, rather than months or years. The team used a cellular mechanism similar to that used by many invertebrates to repair damage to nerve axons. … We have developed a procedure which can repair severed nerves within minutes so that the behavior they control can be partially restored within days and often largely restored within two to four weeks. If further developed in clinical trials this approach would be a great advance on current procedures that usually imperfectly restore lost function within months at best. … nerve axons of invertebrates which have been severed from their cell body do not degenerate within days, as happens with mammals, but can survive for months, or even years. The severed proximal nerve axon in invertebrates can also reconnect with its surviving distal nerve axon to produce much quicker and much better restoration of behaviour than occurs in mammals. … Severed invertebrate nerve axons can reconnect proximal and distal ends of severed nerve axons within seven days, allowing a rate of behavioural recovery that is far superior to mammals. In mammals the severed distal axonal stump degenerates within three days and it can take nerve growths from proximal axonal stumps months or years to regenerate and restore use of muscles or sensory areas, often with less accuracy and with much less function being restored. … The team described their success in applying this process to rats … The team were able to repair severed sciatic nerves in the upper thigh, with results showing the rats were able to use their limb within a week and had much function restored within 2 to 4 weeks.”

Link: http://www.eurekalert.org/pub_releases/2012-02/w-npr020112.php

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

A Study of DNA Alterations in the Old

admin — Sun, 05 Feb 2012 16:49:41 +0000

To what degree does nuclear DNA damage contribute to aging? That remains a debated question. Here, researchers show that, at least in immune cells, there are perhaps more forms of large DNA damage than thought in the old: “researchers compared the DNA of identical (monozygotic) twins of different age. They could show that structural modifications of the DNA, where large or small DNA segments change direction, are duplicated or completely lost are more common in older people. The results may in part explain why the immune system is impaired with age. During a person’s life, continuous alterations in the cells’ DNA occur. The alterations can be changes to the individual building blocks of the DNA but more common are rearrangements where large DNA segments change place or direction, or are duplicated or completely lost. … The results showed that large rearrangements were only present in the group older than 60 years. The most common rearrangement was that a DNA region, for instance a part of a chromosome, had been lost in some of the blood cells. … Rearrangements were also found in the younger age group. The changes were smaller and less complex but the researchers could also in this case show that the number of rearrangements correlated with age. … We were surprised to find that as many as 3.5 percent of healthy individuals older than 60 years carry such large genetic alterations. We believe that what we see today is only the tip of the iceberg and that this type of acquired genetic variation might be much more common. … The researchers believe that the increased number of cells with DNA alterations among elderly can have a role in the senescence of the immune system. If the genetic alterations lead to an increased growth of the cells that have acquired them, these cells will increase in number in relation to other white blood cells. The consequence might be a reduced diversity among the white blood cells and thereby an impaired immune system.” Compare that with the other explanations for reduced diversity that involve persistent and pervasive viruses like CMV.

Link: http://www.eurekalert.org/pub_releases/2012-02/uu-itr012612.php

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

SENS5 Video: Immunotherapy to Clear Tau Protein

admin — Sun, 05 Feb 2012 16:49:35 +0000

Immunotherapy is a very broad and active field: there are a great many strategies presently under development, and in various stages of maturity. All aim at making the immune system do the heavy lifting of finding and destroying specific unwanted cells, cellular machinery, and other biochemicals in the body. This is actually the immune system’s evolved purpose, more or less, and so adjusting it to destroy new targets without causing harmful side-effects is a plausible near term technology. Thus there are large segments of the life science community looking into immunotherapies for cancer, immunotherapies to destroy some of the harmful aggregates that build up between cells with age, and so forth.

One of the presentations given at last year’s SENS5 conference was a look at turning the immune system against harmful aggregates of tau protein – as seen in Alzheimer’s disease, for example, but which happens in all brains to some degree:

One of the perils of aging is the accumulation of various protein/peptide aggregates throughout the body, some of which are associated with toxicity. In several age-related disorders, aggregates of certain amino acid sequences are much more prominent than under normal conditions, and define the disease. Harnessing the immune system has emerged in recent years as a promising approach to treat these conditions. My laboratory has worked in this field targeting the amyloid-? peptide, the prion protein, the tau protein, and more recently the islet amyloid polypeptide. The focus of my talk will be on our tau immunotherapy studies. We have shown in tangle mouse models that active or passive immunizations clear pathological tau aggregates from the brain with associated functional benefits.

A thought to leave you with: the more we see the research community working on immunotherapies for age-related conditions, there more likely it becomes that significant investments will be made into reversing the decline of the immune system. The effectiveness of these therapies to a degree depends on the effectiveness of the immune system, and that progressively fails with age – having first generation therapies in the market will ensure that there exists a strong incentive to improve those therapies, and one of the most obvious ways to do that is to rejuvenate the immune system in elderly patients.

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

Considering the Role of Metals in Neurodegeneration

admin — Sun, 05 Feb 2012 16:49:30 +0000

From the Wall Street Journal, a good example of the way in which much of present day research gravitates towards applications that patch over end-stage consequences of disease rather than addressing root causes and prevention: “Research into how iron, copper, zinc and other metals work in the brain may help unlock some of the secrets of degenerative diseases like Alzheimer’s and Parkinson’s. Iron and copper appear to accumulate beyond normal levels in the brains of people with these diseases, and a new [study] shows reducing excess iron in the brain can alleviate Alzheimer’s-like symptoms – at least in mice. … Research into the complicated, invisible roles these metals play in brain diseases has lagged behind study of the more-visible proteins that are damaged or clump together in the brains of Alzheimer’s and Parkinson’s sufferers. But better understanding metals’ role in the brain could help shed light on a range of medical conditions and might offer a new route for developing treatments. … [Researchers] examined the amount of iron in the brains of mice that were bred unable to produce the tau protein, which helps stabilize the structure of neurons. Tau damage is associated with Alzheimer’s and Parkinson’s. As the mice aged, they suffered symptoms similar to people with both diseases, including impaired short-term memory, and also exhibited an accumulation of iron in their brains. When the researchers gave them a drug removing excess iron, the symptoms reversed. This means normally functioning tau is necessary for removing iron in the brain … The finding bolsters previous research showing that bringing down iron may be a path to new treatments. … An accumulation of iron in neurons seems to be a final end-stage event in neurodegeneration, whether it be Alzheimer’s or Parkinson’s, [or] any [condition] related to tau abnormalities.”

Link: http://online.wsj.com/article/SB10001424052970204740904577192901072611524.html

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

Investigating Sodium Channels in the Aging Brain

admin — Sun, 05 Feb 2012 16:49:24 +0000

Researches find another way in which the brain declines with age: “New findings [reveal] a novel mechanism through which the brain may become more reluctant to function as we grow older. … researchers examined the brain’s electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. In this way they characterised what is known as “neuronal excitability” – this is a descriptor of how easy it is to produce brief, but very large, electrical signals called action potentials; these occur in practically all nerve cells and are absolutely essential for communication within all the circuits of the nervous system. … The [researchers] identified that in the aged brain it is more difficult to make hippocampal neurons generate action potentials. Furthermore they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels, which mediate the rapid upstroke of the action potential by allowing a flow of sodium ions into neurons. … Much of our work is about understanding dysfunctional electrical signalling in the diseased brain, in particular Alzheimer’s disease. We began to question, however, why even the healthy brain can slow down … Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells. Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability.” You might compare this with past work on potassium channels and memory in aging.

Link: http://www.sciencedaily.com/releases/2012/02/120201105124.htm

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

Intern at the SENS Foundation this Summer

admin — Sun, 05 Feb 2012 16:49:17 +0000

Are you presently working on a life science or medical degree? Are you interested in advancing aging and longevity science – research that aims to extend the healthy human life span and reverse the causes of age-related disease? Do you want to intern this summer at the SENS Foundation, one of the most important young non-profits in the world?

In the summer of 2012, the Academic Initiative will bring as many as three students to the SENS Foundation Research Center in Mountain View, California to participate in SENS research for three months. These students will receive monthly stipends and, if they are not local to the San Francisco Bay Area, a credit towards airfare.

Undergraduate, graduate, and medical students may apply, as may students who have graduated immediately prior to the summer. After an initial selection process, the most promising candidates will be interviewed over the phone by the SENS researchers they would work with. Each major research program at the Research Center will limit itself to one intern, such that each intern will be working on a different project and will be selected by different researchers. It will be important for applicants to have prior lab experience, and more experienced applicants are more likely to be accepted than relatively inexperienced ones.

The application is available online here. Applications are due by March 31, 2012. The most promising applicants will be interviewed in April. As always, if you have any questions, you can contact us.

Chances to work on the foundations of world-changing research programs don’t wander past the window every day. Beyond that, the SENS Foundation is a great place for younger researchers – people who are serious about longevity science and have a genuine interest in advancing the state of the art – to come into contact with a network of more experienced peers, fundraisers, and advocates that will serve well in later years. Connections are what makes the world go round, and certainly what advances careers and opens doors.

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

Age Changes the Extracellular Matrix

admin — Sun, 05 Feb 2012 16:49:10 +0000

The extracellular matrix (ECM) surrounds and supports cells, both structurally and in a range of other ways, such as by mediating cell signalling. With age, however, the ECM changes for a variety of reasons – it is damaged by the actions of senescent cells, for example. This has consequences, such as on the capacity of stem cells to maintain tissue. Here is a review paper: “Aging is characterized by reduced tissue and organ function, regenerative capacity, and accompanied by a decrease in tissue resident stem cell numbers and a loss of potency. The impact of aging on stem cell populations differs between tissues and depends on a number of non cell-intrinsic factors, including systemic changes associated with immune system alterations, as well as senescence related changes of the local cytoarchitecture. The latter has been studied in the context of environmental niche properties required for stem cell maintenance. Here, we will discuss the impact of the extracellular matrix (ECM) on stem cell maintenance, its changes during aging and its significance for stem cell therapy. … It is concluded that a remodeled ECM due to age related inflammation, fibrosis or oxidative stress provides an inadequate environment for endogenous regeneration or stem cell therapies.” The question of whether an old body can fully benefit from stem cell therapies continues to arise – eventually the stem cell research community will have to start addressing the damage of aging in order to assure the performance of their therapies when treating the old.

Link: http://www.ncbi.nlm.nih.gov/pubmed/22285947

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

Understanding the Mechanisms of Autophagy

admin — Sun, 05 Feb 2012 16:49:02 +0000

Autophagy is very important to long term health, and shows up again and again as a pivotal part of the way in which various genetic manipulations and lifestyle choices can improve health and extend life. Here is a good article that delves into the mechanisms of autophagy and the present limits of scientific understanding: “Cells live longer than their internal components. To keep their cytoplasm clear of excess or damaged organelles, as well as invading pathogens, or to feed themselves in time of nutrient deprivation, cells degrade these unwanted or potentially harmful structures, and produce needed food and fuel, using a process they have honed over millions of years. Known as autophagy, this catabolic process involves the selection and the sequestration of the targeted structures into unique transport vesicles called autophagosomes, which then deliver the contents to lysosomes where they are degraded by lytic enzymes. … Experimental evidence indicates that autophagosome biogenesis is probably a very complex process on several levels, including its regulation in response to different cellular and environmental cues, and the factors governing the choice of membrane sources. Is there any therapeutic value in determining the origin of the autophagosomal membranes? We think that elucidating this process could ultimately provide new drug targets for the treatment of diseases that can be alleviated or cured by the activation of autophagy, including specific muscular dystrophies, persistent infections, and neurodegenerative disorders (ataxias, Huntington’s, and Parkinson’s diseases). Understanding the sources and processes by which the autophagosome’s lipid bilayers are delivered will undoubtedly reveal critical new proteins and articulate their functions, allowing researchers to pinpoint specific parts of the pathway.”

Link: http://the-scientist.com/2012/02/01/the-enigmatic-membrane/

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

Heterochromatin Levels in Flies Can Raise and Lower Lifespan

admin — Sun, 05 Feb 2012 16:48:55 +0000

Heterochromatin is the name given to the more tightly packaged structural forms of DNA and proteins found in the cell nucleus. It has been shown to be involved in cellular senescence, and is a part of the way in which genes are turned on or off, but like most things in the nucleus it is also involved in the deep, dark depths of many other mechanisms – down there in the basement clockwork of the tall towers of machinery that run a cell. Modern day research tools are making it ever easier to catalog the cogs, gears, and operations that take place on any one level of one particular machine-tower, but it is still very hard and time-consuming to turn localized, disconnected understandings into realizations about the mechanism as a whole.

So researchers can presently say a great deal about heterochromatin and its localized behavior, but far less about how these descriptions of structure and low-level operations relate to higher level cellular mechanisms, and never mind how that all ties into trajectories of health and longevity for organisms as a whole. Cells are complicated, exceedingly so, and as a consequence the life sciences are at a point of simultaneously drowning in data while being unable to answer even a tiny fraction of all the questions about biology that are presently asked. This won’t last, given the pace of progress in computational technologies, but it is rather like the prospect of starving amidst plenty for the near future.

You might recall that – in my opinion – the acid test as to whether a biological mechanism is interesting to those us who follow longevity science is not whether you can use it to shorten life span, but rather whether you can use it to extend health life. Even better is a case in which researchers can demonstrate both of those goals: turn the dial one way and life shortens, turn it the other and it lengthens – these are indications that there might be something worthy of further investigation in that research.

That all said, here is a demonstration that heterochromatin levels in flies can be used to dial lifespan up and down:

To understand the role of heterochromatin in animal aging, and the underlying molecular mechanisms, we altered heterochromatin levels in Drosophila by genetically manipulating Heterochromatin Protein 1 (HP1) levels … we examined the life spans of flies with reduced or increased levels of HP1. These flies exhibit reduced or increased levels of heterochromatin, respectively, during development, as HP1 is an integral component of heterochromatin and controls heterochromatin levels.

We found that reducing HP1 levels by half [caused] a dramatic shortening of life span compared to isogenic controls. … Conversely, a moderate overexpression of HP1, caused by basal activity of the hsp70 promoter, significantly extended life span, resulting in a 23% increase in median life span and a 12% increase in maximum life span. Similarly, at non-heat shock conditions (25°C), a second (independent) line of hsp70-HP1 flies also lived significantly longer than their control flies.

…

These results suggest that heterochromatin levels significantly influence life span, and moderately higher levels of heterochromatin promote longevity.

Too much boosting of heterochromatin via the methods the researchers used is fatal to flies, unfortunately. The full paper offers some thoughts on the potential mechanisms of increased longevity with increased heterochromatin levels, but there is no definitive line item to point to – at this stage, only plausible hypotheses about cellular integrity, a slower rate of decline in muscle strength, and so forth.

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

How to Live to 100 – Health

admin — Sun, 29 Jan 2012 16:50:40 +0000

Source:
http://www.usnews.com/Topics/tag/Subject/l/longevity/rss

The Big Chill: Winter Skincare

admin — Sun, 29 Jan 2012 16:50:38 +0000

Seeing dry patches on your skin? Does your skin feel blotchy and unsightly? Are you waking up looking older than you feel? If you have answered yes to some of the above you are suffering from &ldquo…Source:
http://wwww.examiner.com/RSS-3174-Longevity-Examiner

An Online Chat With Aubrey de Grey and S. Jay Olshansky

admin — Sun, 29 Jan 2012 16:50:06 +0000

Science recently hosted a live chat event with researchers Aubrey de Grey and S. Jay Olshansky, public figures who have debated their views on longevity science a number of times over the last seven years or so. The logs and viewer comments from the event remain available for those interested in viewing the discussion, but note that it takes a little while for the widget containing them to load.

Live Chat: The Science of Antiaging

Jennifer Couzin-Frankel: And here’s a question from Roy: Does the paper titled “Clearance of p16 positive senescent cells delays ageing-associate disorder” published in Nature January, 2011, prove the Strategies for Engineered Negligible Senescence (SENS’s) validity, i.e. extend lifespan by remediating damage? If so, are their other examples of experimental validation of SENS in animal models?

Aubrey: Roy: that paper is a great proof of concept for one component of SENS, the benefits of removing “death-resistant” cells. The experiment didn’t show life extension, but it wasn’t expected to, because to do that you have to fix all the things that limit lifespan, not just one of them. Yes, there are various other examples, such as the elimination of amyloid in mouse models of Alzheimer’s and the introduction of stem cells (or the stimulation of their division) in various tissues. We’ll see more of this soon, that’s for sure.

…

Jennifer Couzin-Frankel: An interesting question from Morten: Why do you want to live longer (as I understand it at least de Grey is after living longer)? What can’t you accomplish in a life time?

Aubrey: Morten: this is the most insidious misunderstanding of the work that I and other biomedical gerontologists do. We are NOT working to extend life for the sake of extending life. We are working to postpone the ill-health of old age, which will probably have the side-effect of extending life, but it’s no more than that, a side-effect. I personally have no idea how long I want to live, [any] more than I have an opinion on what time I want to go to the toilet next Sunday. In both cases I know I’m going to have better information nearer the time, so it’s idiotic to even think about it. However, I can tell you that I have at least 1000 years of backlog already (books to read, films to se…) – don’t you? If not, why not?

S. Jay Olshansky: Morton. The goal of research in this area in my view is not to extend life. The goal is to extend healthy life. If we live longer, I consider that a bonus. However, I would encourage you to be asking the same question of those now working to combat heart disease, cancer, and stroke, and those who experience these conditions. Why [do] we all want to live longer? I believe what we are talking about here are interventions that enable us to live our lives healthy for as long as possible.

…

Comment From Guest: Couldn’t you guys be focusing on pain control, quality-of-life and ending poverty and depression in the elderly?

S. Jay Olshansky: [Think] about this for a moment. In 1900 life expectancy at birth was about 45. Now it’s about 80 for women and 76 for men. We gained 30 years of life — most healthy. Wasn’t that worth it? It’s hard to imagine the goal of extending healthy life as being harmful in any way — it would enable people to remain working longer if they want, or retire healthier for a longer time period. Health also begets wealth for individuals and populations. Goodness — why are we working so hard to combat heart disease and cancer then?

There’s a lot more there to look through; you should certainly read the whole thing.

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

Falling Heart Disease Rates

admin — Sun, 29 Jan 2012 16:50:03 +0000

From the Independent: “It is one of medicine’s mysteries: what has caused Britain’s plummeting rate of heart disease over the last decade? Deaths from heart attacks have halved since 2002 and no one is quite sure why. Similar changes have occurred in countries around the world but the death rate in England, especially, has fallen further and faster than almost anywhere. … The researchers looked at 840,000 men and women in England who had suffered a total of 861,000 heart attacks between 2002 and 2010. Overall, the death rates fell by 50 per cent in men and 53 per cent in women. … For the last 70 years we have been in the grip of a heart disease epidemic that began in the 1940s, rose to a peak in the 1970s and then began to fall. All Western countries were affected and all followed broadly the same pattern. … researchers conclude that just under half the decline in heart attack death rates in England over the last decade is due to better hospital treatment; the rest is due to changes in lifestyle and the widespread use of pills to lower cholesterol and blood pressure.” One might theorize that – at the high level – increased heart disease across the last seven decades is a consequence of the fat and sedentary lifestyles that tend to accompany increases in wealth across the board, while reductions are largely due to improvements in medical technology.

Link: http://www.independent.co.uk/life-style/health-and-families/health-news/the-curious-case-of-the-vanishing-killer-6294626.html

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

On Growth Hormone and "Smaller is Better"

admin — Sun, 29 Jan 2012 16:49:56 +0000

Here is an open access PDF format mini-review on what is known of growth hormone and aging – that less of it is generally better: “A recent report of virtually complete protection from diabetes and cancer in a population of people with hereditary dwarfism revived interest in elucidating the relationships between growth, adult body size, age-related disease and longevity. In many species, smaller individuals outlive those that are larger and a similar relationship was shown in studies of various human populations. Adult body size is strongly dependent on the actions of growth hormone (GH) and the absence of GH or GH receptor in mice leads to a remarkable extension of longevity. Many mechanisms that may account for, or contribute to, this association have been identified. It is suggested that modest modifications of the diet at different ages may extend human healthspan and lifespan by reducing levels of hormones that stimulate growth.”

Link: http://www.ncbi.nlm.nih.gov/pubmed/22261798

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

A Culture of Controlling, Malicious Timidity

admin — Sun, 29 Jan 2012 16:49:53 +0000

The course of our future lives, our health and longevity, is swayed by a population of timid mice – but malicious mice, ever ready to use state force to punish and hold back anyone they see as being insufficiently timid. These are people who support the ball and chain of centralized regulation of medical research, people who fear all change, people who fear everything they don’t understand, and people who rush to prevent anyone else from enjoying the freedom to undertake personal risk in the course of advancing progress. This describes the vocal mainstream of Western culture: risk-averse, ignorant, and enamored of control for its own sake: a dangerous combination for those who pull upon the strings of law and regulation.

As I have often remarked in the past, freedom is absolutely essential to progress in medicine: the freedom for researchers to attempt goals as they see fit; the freedom for anyone to fund the research and clinical development they desire; the freedom for people to take personal risks in the use of medical technology; the freedom for groups to create an unhampered marketplace in medicine, in which technologies are rapidly sifted for those with the greatest benefit. These are all simply parts of economic and personal liberty, something that is in extremely short supply in the medical industry.

So the mice stamp their little feet, and the impersonal engines of government – the unaccountable employees of bureaucratic bodies such as the FDA – move to prevent us all from undertaking rapid development in medicine, on penalty of jail. For our own good, supposedly.

If anti-aging drugs are possible, they will require dangerous – and ethically troubling – clinical trials. … If anti-aging medicine is to become a reality, then the various theories about how to halt or reverse the aging process will require testing on human subjects. Carrying out such tests will place unprecedented pressure on the rules protecting human participants in clinical trials. I suspect, then, that human guinea pigs for anti-aging trials will come disproportionately from the poor and disempowered. … The rich and powerful will be looking to do away with rules that they perceive as denying them millennial life spans.

Those would be the rules preventing terminal cancer patients from choosing to up and pay for their own personal trial of a promising therapy-in-development – forcing them to die without any recourse. The rules that make formal clinical trials so lengthy and expensive that many potential therapies are simply never developed or tried by humans, and those that are might be a decade in the slow regulatory grind from readiness to actual availability. The rules that raise the costs of medicine too high for those poor folk that the author seems to be concerned about. Regulation of medicine, which raises costs, disrupts the effective market mechanisms of progress, and prevents people from using potential therapies that are technologically feasible and ready to field-test, is a morally bankrupt affair.

But this is the culture we live in, sad to say: one in which vague and poorly articulated discomfort with potential future inequities are given more consideration than the ongoing massive toll of death and suffering that we should be working day and night, as fast as possible, to prevent. A toll of 100,000 lives every day, and the hundreds of millions who are crippled, diminished, and in pain. Instead we get institutions like the FDA, whose staff toil to prevent new medicine from ever seeing the light of day. The mice would close their eyes and drown the world in blood just to feel a little better in their own vague sense of disquiet: they are the very worst of humanity, not even willing to acknowledge the fearsome costs of their own timidity.

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

Creating Smooth Muscle Cells from Skin Cells

admin — Sun, 29 Jan 2012 16:49:48 +0000

Here is another example of work on creating patient-specific cells to order, one of the necessary building block technologies needed for an industry that constructs organs and other larger masses of tissue in the body: researchers have “discovered a method of generating different types of vascular smooth muscle cells (SMCs) – the cells which make up the walls of blood vessels – using cells from patients’ skin. … Cardiovascular disease is the leading cause of death in the world. These deaths are mainly caused by the hardening and subsequent blockage of blood vessels due to the accumulation of fatty materials, a condition called atherosclerosis. As not all patients are suitable for conventional stenting or bypass treatment, an option in the future may be to grow new blood vessels to bypass their own blocked vessels. The [team] worked with embryonic stem cells and reprogrammed skin cells, collectively known as human pluripotent stem cells (hPSCs), which have the potential to form any cell type in the body. They discovered a method of creating all the major vascular smooth muscle cells in high purity using hPSCs which can also be easily scaled up for production of clinical-grade SMCs. This is the first time that such a system has been developed and will open the door for comparative studies on different subtypes of SMCs to be carried out, which are otherwise extremely difficult to obtain from patients.”

Link: http://medicalxpress.com/news/2012-01-cambridge-team-smooth-muscle-cells.html

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

Creating Alzheimer’s Neurons from Stem Cells

admin — Sun, 29 Jan 2012 16:49:43 +0000

The principle use of stem cells in the near future is actually research, not therapy – generating diseased cells to order will lower the cost of better understanding the mechanisms of disease and age-related conditions. For example: “scientists have, for the first time, created stem cell-derived, in vitro models of sporadic and hereditary Alzheimer’s disease (AD), using induced pluripotent stem cells from patients with the much-dreaded neurodegenerative disorder. … It’s a first step. These aren’t perfect models. They’re proof of concept. But now we know how to make them. It requires extraordinary care and diligence, really rigorous quality controls to induce consistent behavior, but we can do it. … We’re dealing with the human brain. You can’t just do a biopsy on living patients. Instead, researchers have had to work around, mimicking some aspects of the disease in non-neuronal human cells or using limited animal models. Neither approach is really satisfactory. … With the in vitro Alzheimer’s neurons, scientists can more deeply investigate how AD begins and chart the biochemical processes that eventually destroy brain cells associated with elemental cognitive functions like memory. Currently, AD research depends heavily upon studies of post-mortem tissues, long after the damage has been done. … The differences between a healthy neuron and an Alzheimer’s neuron are subtle. It basically comes down to low-level mischief accumulating over a very long time, with catastrophic results. … The researchers have already produced some surprising findings. … In this work, we show that one of the early changes in Alzheimer’s neurons thought to be an initiating event in the course of the disease turns out not to be that significant.”

Link: http://www.sciencedaily.com/releases/2012/01/120125131029.htm

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