Following on from the release of their 2010 research report, the SENS Foundation folk have issued their 2010 year-end report. Just as for the earlier research report, it is an interesting and closer look at the finances and research activities of the organization - one of the very few groups in the world whose leaders have the right idea when it comes to aging, longevity, and biotechnology.

In 2009 we launched SENS Foundation. We did it to drive biomedical research towards a functional and cost-effective approach to extending individual health. We did it to raise awareness for an alternative to an increasingly complex and problematic pathology chase in medicine; to redefine regenerative medicine as applied to aging; to enable doctors to think about fixing patients before they were sick.

We did it to transform the way you think about medicine. We knew it was a big agenda when we set out, and we were fully conscious of how small a public charity we were. We recognized that our first successful steps would depend upon our demonstration of fundamental credibility to the medical science community.

That is why I am especially pleased to present this 2010 end of year report. As you will read, we have created a mature organization and delivered the networks and collaborations needed to build the rejuvenation biotechnology field. We've expanded our own research programs and have used that expansion to develop collaborations with leading universities and research institutions in regenerative medicine, around the nation and the world. We have, in short, found our voice with a substantial and mainstream scientific community. Rejuvenation biotechnology, as a research field, is emerging, and SENS Foundation has led that charge.

If you like what you see, then help the Foundation achieve its mission. Donate, tell your friends, and write about what might be achieved soon through advanced biotechnology if there were just the will and the funding to do it. Bootstrapping a new industry and new view of medicine is a slow process, but every helping hand makes it faster.

Metabolism is complex - very, very complex. In areas that have been well studied for more than a decade, researchers are still pushing back and forth on whether well known genes and pathways are actually important in longevity. In this sort of environment a single study in a few dozen mice isn't worth much, as the results from these various studies are either are all over the map, or prone to being overturned by a more careful, well-funded, and larger research project. That is what seems to have happened here for IGF-1 and longevity:

One of the major discoveries in aging during the past decade has been the observation that mutations in insulin/IGF-1 signaling led to increased longevity in various invertebrate models.

...

The most direct evidence that mutations affecting the insulin/IGF-1 signaling pathway lead to increased longevity in mammals has come from studies with Igf1r+/? mice ... i.e., mice lacking one copy of the gene coding for IGF-1 receptor ... In 2003, Holzenberger et al. reported that female Igf1r+/? mice exhibited a 33% increase in lifespan. ... However, the lifespan data in the Holzenberger study are problematic because of the small sample size and the very short lifespan of both the wild type (WT) and Igf1r+/? mice studied.

...

therefore, we have reassessed the effect of reduced expression of the IGF-1R on lifespan using the rigorous criteria recommended by Ladiges et al., e.g., lifespan and end-of-life pathology were assessed using large sample sizes and husbandry conditions that permitted the control lifespan to approach its full potential, which are necessary if the longevity differences in the experimental group are to be relevant to healthy aging.

In agreement with Holzenberger et al., we found that the female Igf1r+/? mice were more resistant to the oxidative stress than were WT female mice while no difference was observed between the male Igf1r+/? and WT mice. However, there was only a modest increase in the mean lifespan (4.7%) of female Igf1r+/? mice compared to their WT littermates and no significant change in end-of-life pathology. Thus, our data show [that] reduced IGF-1R signaling in mammals does not play the same major role in aging that is observed in invertebrates.

And so it goes - sometimes the early results achieved in small, prospective studies with small budgets don't hold up to closer inspection. Some fundamental processes relating to the link between operation of metabolism and longevity are very similar between lower animals (like worms) and higher animals (like mammals). You might think of the effects of calorie restriction, for example. But clearly other processes are significantly different between species, and this is one more layer of complexity that will increase the cost and slow the progress of efforts to slow aging by manipulating metabolism - such as by altering IGF-1.

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

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

Researchers recently demonstrated that increased cellular housekeeping could slow neurodegeneration, and here a different group show the same outcome: "Cells, which employ a process called autophagy to clean up and reuse protein debris leftover from biological processes, were the original recyclers. A team of scientists [have] linked a molecule that stimulates autophagy with the reduction of one of Alzheimer's disease's major hallmarks, amyloid peptide. Their finding suggests a mechanism that could be used to eliminate built-up proteins in diseases such as Alzheimer's, Down syndrome, Huntingdon's and <a href="http://en.wikipedia.org/wiki/Beta_amylo&quot; the="The" molecule,="molecule," called="called" smer28,="SMER28," spurs="spurs" autophagy,="autophagy," which="which" in="in" turn="turn" eliminates="eliminates" unwanted="unwanted" materials="materials" such="such" as="as" amyloid-beta, the protein aggregates that cause Alzheimer's plaques. Increasing autophagy, either through a drug or a natural process such as diet, could improve the outcome for people with neurodegenerative diseases ... The researchers [tested] various compounds for their ability to reduce the buildup of amyloid-beta by exposing cultured cells to compounds known to activate autophagy. They then compared the effect of these compounds by removing growth factors from the culture medium, a well-established stimulant of autophagy known as 'starvation.' The researchers found that SMER28 was the most effective compound, and focused their studies on it to characterize the cellular components involved in this phenomenon. They compared the effect of SMER28 on amyloid-beta formation using normal cells or cells where the expression of genes known to be involved in autophagy was reduced or abolished. They found that three important autophagic players were involved, and one of them was essential for SMER28's effect."

Link: http://www.eurekalert.org/pub_releases/2011-03/ru-mts031611.php

It is unfortunate and noteworthy that the loudest institutional voices in Western culture seem to have an aversion to human enhancement. It is the ideal of equality run rampant, heading for its inevitable Harrison Bergeron endpoint - equality by leveling down to the lowest and preventing new heights from being achieved. Destruction is the only thing that politicians are really good at, sad to say, and egalitarianism, much like communism, is pretty in its abstract ideals but horrific when put into practice:

• The Terrible Urge to Tear Down the Successful
• Shunning Advances Through the Instinct to Equality

This rejection of human enhancement is in essence a rejection of the urge to improvement - and is thus one of a number of important hurdles standing in the way of widespread support for the development of rejuvenation biotechnology. Living longer than your parents did? That's an enhancement, and a great many talking heads would like to see laws written to prevent such technologies from ever seeing the light of day.

Yet the urge to improvement is everywhere else in evidence in our societies, as noted in this subtle injection of transhumanist ideals into the Discover Magazine website:

Just because I'm not ill [and] not injured, doesn't mean that I am, by default, as healthy as I could be. For some bizarre reason, we don't think about our bodies that way when it comes to health care and self improvement. We don't pursue excellent health the way we strive to be better in our hobbies and work. So, where did we get the idea that mediocre health is good enough?

...

But here's the interesting thing: neither the US nor the UK have regulations in place for prescription pharmaceuticals that are not therapeutic. Drugs that don't cure an illness but still have a beneficial effect have one of two paths: either find an illness they do cure or invent an illness that the drug seems to cure. An example of the latter is Viagra. I don't care what the DSM says, erectile dysfunction is not real illness. But Viagra works. It doesn't "cure" anything, but it sure makes a lot of people's lives better, which is [a] great thing. But it's a massive problem that there is no way for drugs that make our health better to find their way onto the market. And there in lies the problem. Save vaccines, modern medicine just doesn't know what to do with medicine that prevents disease or improves a person's life.

...

Prevent and improve. Those are the two words I'd argue are most underused in every other aspect of human health care. Why does self-improvement not include pharmaceuticals that make us smarter or stronger or happier? Because we've been convinced and told and reminded and scolded that taking a pill means something is wrong with you.

And so to aging and longevity. The bureaucrats of the FDA do not recognize aging as a disease, and so will not approve treatments for it. In a culture that is hostile to human enhancement, winning support for the reversal of aging will be that much harder. This is one of many ways in which freedom matters greatly in medical research. Under the systems of regulation in place in the largest markets of the world, researchers and commercial developers are far from free to turn proven science into commercial products, and far from free to convince their fellow countrymen to try something new.

We humans are the species that improves ourselves and creates value from our surroundings. That is our defining characteristic - and yet, paradoxically, so much time and effort in this day and age is devoted to sabotaging the engines of progress.

CALERIE is the largest present study of calorie restriction in humans: "In a robust and consistent manner, sustained caloric restriction (CR) has been shown to retard the aging process in a variety of animal species. Nonhuman primate studies suggest that CR may have similar effects in longer-lived species. The CALERIE (Comprehensive Assessment of the Long-term Effects of Reducing Intake of Energy) research program is the first systematic investigation of CR in nonobese human beings. In the phase 2 study, it is hypothesized that 2 years of sustained CR, involving a 25% reduction of ad libitum energy intake, results in beneficial effects similar to those observed in animal studies. ... The study is a multicenter, parallel-group, randomized controlled trial. A sample of 225 participants [is] being enrolled with 2:1 allocation to CR. ... An intensive dietary and behavioral intervention was developed to achieve 25% CR and sustain it over the 2 years. Adherence is monitored using a doubly labeled water technique. Primary outcomes are resting metabolic rate and core temperature, and are assessed at baseline and at 6-month intervals. Secondary outcomes address oxyradical formation, cardiovascular risk markers, insulin sensitivity and secretion, immune function, neuroendocrine function, quality of life and cognitive function. ... The results will provide insight into the detrimental changes associated with the human aging process and how CR mitigates these effects."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20923909

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

A study conducted by a team of researchers from London found that drinking cherry juice rich in polyphenols can boost recovery after exercise.

The body experiences a series of interconnected metabolic processes during exercise. You will begin to notice heavier and faster breathing, faster heart rate and your muscles will begin to heat up and feel sore. This is the body’s natural response to mild and extreme physical activities, and this can intensify to higher levels depending on the intensity of the physical activity. Exercise demands different systems in the body to respond according to the increased demand for energy. Body heat, breathing and blood circulation will be affected.

Different forms of exercise call for the action of specific muscle groups. Other more strenuous forms of exercise may require the use of multiple muscle groups. But in any case, exercise means muscle activity. The muscles will demand other systems in the body to respond and produce energy. Each system in the body will either work more, work less or focus on muscle activity. The heart, for example will start beating faster to speed up the circulation of blood and energy throughout the body while the stomach temporarily slows down in digesting food in order to channel more energy into the muscles.

Adenosine triphosphate, or ATP, is an essential biochemical fuel needed by the body to supply the muscles with energy. ATP needs to be burned in order for it to be transformed into usable energy. And this process will require oxygen, the elimination of metabolic wastes like lactic acid and carbon dioxide which are produced in the process, and the omission of heat out of the body.

After about 30 minutes to an hour of exercise, the body is tired and exhausted. And recovery is needed before doing the same routine all over again. The body will need at least 24 to 48 hours of recovery for muscle and tissue repair, especially when weight lifting. There are natural techniques to hasten and improve recovery after performing an exercise. A study conducted by a team of researchers from London found that the simple habit of drinking cherry juice can help the muscles recover faster.

Cherry Juice for Faster and Better Recovery

Researchers from London found that cherry juice can boost the muscle recovery after strenuous exercise. Previous studies had reported that the antioxidants in cherries can help the body overcome the oxidative damage caused by exercise. The study, conducted from the London South Bank University Sports and Exercise Science Research Center, focused and looked at the antioxidant property of cherry juice and its potential in hastening muscle recovery.

The study was published in the Medicine and Science in Sports Exercise. The researchers observed that people who were subjected to a week of drinking a certain branded cherry juice after a series of intensive exercise routines can help speed up recovery time and create better results compared to those who consumed control beverage. The cherry juice used in the study was from Montmerency beverage company. Lead researcher, Dr Joanna Bowtell, said that Montmorency cherry juice can improve the recovery of isometric muscles after exercise due to its strong antioxidant property.

A related study published in the Journal of Nutrition reported that the consumption of at least 45 cherries in a day can reduce the circulation of inflammatory markers in the body. This is due to the anthocyanin and flavonoid content of cherries, the researchers said. Reducing the amount of inflammatory compounds in the body can help reduce the muscle damage caused by exercise and lessen recovery time.

The researchers gathered a group of 10 competitive weight lifters to participate in the study and divided them in half. The first group was asked to drink cherry juice 7 days before and 2 weeks after a series of single leg knee extensions. The second group was subjected to the same process but with fruit concentrate in place of the cherry juice. At the end of the study, the researchers found that the recovery of the first group was faster than that of the control group but there was no noticeable difference between their energy production.

The industry of food nutrition in North America costs around $3.2 billion while Western Europe accounts for $713.6 billion of the industry. Researchers and sports scientists are continuously on the lookout for better ways of improving the performance of athletes by creating new exercise programs and products that promote better and faster recovery. But for individuals who simply want to improve their performance and enjoy a healthy life, there are several natural ways of hastening recovery time without spending too much.

Natural Ways to Speed Up Recovery after Exercise

The body needs time to recover. The length of time needed for the muscles to repair may vary depending on the intensity of the exercise. Resting between exercise days will not only let the body perform its natural recovery process but this will also help avoid injuries in the future. So make it a point to get enough sleep and sufficient nutrition after each exercise.

Stretching is not only needed before doing any form of physical activity, but stretching after each exercise can also help the muscles recover faster. Moving around or maintaining the same exercise but at a lower intensity for a few minutes will help remove lactic acid from the body. Lactic acid substances are produced in the combustion of ATP and may result to muscle stiffness.

Get enough nutrients from the food you eat and replace lost fluids. During exercise, the body makes use of available and stored energy. Refueling by eating the right kinds of food will help the body recover better and faster. Drinking a lot of fluids during and after exercise is also recommended to avoid dehydration, promote the flow of nutrients and support certain metabolic processes.

Taking an alternation of cold and hot baths a few hours after heavy exercise will help in alleviating muscle soreness and prevent injury. Contrast water therapy will help get rid of waste products faster by repeatedly dilating and constricting the blood vessels. Some athletes alternate 30 seconds of cold water with 2 minutes of hot water for four times with a short rest in between.

The key to faster recovery is using an exercise routine that allows time for recovery. Over-training without sufficient rest may only defeat the purpose of exercising.

Sources
nutraingredients.com
sportsmedicine.about.com
health.howstuffworks.com

Discuss this post in Frank Mangano’s forum!

Vitamin D has been linked to many health conditions before. A recent study links insufficient levels of the vitamin with the disabling condition depression

In a recent study performed by researchers from the National Institute of Aging in the United States, insufficient levels of vitamin D may be the reason why many individuals over the age of 65 are experiencing symptoms of depression.

Senior individuals often have low levels of the important vitamin because they tend to stay indoors more often, as opposed to younger, more sprightly individuals with more active lifestyles. The study was published in a medical journal on endocrinology this year.

According to Luigi Ferrucci, the lead researcher, the emerging link between vitamin D deficiency and the occurrence of depression must be further investigated.  The study involved a follow-up testing of nearly one thousand male and female respondents within a six-year period.

The researchers used a specialized scale that measured the symptoms of depression called CES-D.  The researchers discovered that those with lower levels of vitamin D in their blood tended to have poorer score in the CES-D test.  Those with higher vitamin D percentages in their blood scored better in the same test.

Alarming, global trend

Depression is fast becoming one of the leading causes of disability around the world, not just in the United States.  It is estimated that today, there are 120 million people afflicted with the condition.  Ferrucci’s study is not the first to point at the possible link between the vitamin and depression.

In an earlier study carried out two years ago, Dutch researchers reported that insufficient levels of the vitamin in the body resulted in a higher percentage of the parathyroid hormone.

This hormone, which is used by the body to regulate calcium loss, has been directly linked to a higher incidence of depression in some one thousand two hundred respondents in yet another independent study.  This is the reason why a causal pathway must be mapped out to determine just how this vitamin affects the human brain.

In a fourth related study, researchers McCann and Arnes noted that vitamin D is important for the proper functioning and health of the human brain.  The widespread presence of vitamin D receptors throughout the human brain is evidence of the vital role of the nutrient in brain health.

According to yet another scientific review, vitamin D has been associated with affecting proteins in the human brain that are responsible for governing the learning process and remembering.  If an imbalance occurs in these areas, you can just imagine a chain reaction occurring throughout the brain.

Benefits of vitamin D

There are several ways that you can get vitamin D: natural exposure to sunlight, food (like dairy products, e.g. yogurt, milk, etc.) and through vitamin supplementation.  The body only needs about 10 – 15 minutes of exposure to natural sunlight to produce vitamin D on its own.

If this is not possible, people with low levels of vitamin D should explore vitamin supplementation; this applies most especially to senior individuals who may not be eating well or are unable to engage in a more active lifestyle.  Instead of using sunscreen when going out to get your healthy dose of sunshine, you can protect your skin naturally by taking natural antioxidants like fresh wheatgrass juice and citrus fruits.

The usual recommended dose for adults is between 400 to 800 IU (international units) of vitamin D everyday. Pregnant women should be given a higher dose (800 IU) to ensure optimum bone health and proper development of the fetus.

And there are more reasons to love vitamin D! Here are some of the most important benefits:

1. It is needed for proper absorption and utilization of calcium and phosphorous.  It is needed for the proper maintenance and repair of the bones and skin.

2. It strengthens and helps maintain the immune function of the body. Conditions like flu and the common cold can be warded off more efficiently if the immune system is strengthened by vitamin D.

3. It is an important nutrient that prevents the occurrence of MS (multiple sclerosis).  According to researchers from the Oregon Health & Science University, MS is less frequent in tropical countries because there is more available sunshine in these places than in temperate regions.

4. Vitamin D has also been linked to the maintenance of normal body weight (according to research from the Medical College of Georgia).

5. Vitamin D is important for brain health in the later years (60 – 79 years of age).

6. In a recent study from the Harvard Medical School, vitamin D can also reduce asthma attacks in asthmatic individuals.

7. We are exposed continually to low levels of radiation.  The good news is vitamin D can also help protect us from such exposures.

According to US cancer researchers, people with adequate levels of vitamin D have a lower risk for many types of cancer than people with low or inadequate levels of the vitamin.

Sources:
nutraingredients.com
healthvitaminsguide.com
medicalnewstoday.com

Discuss this post in Frank Mangano’s forum!

Exposure to secondhand smoke produces psychological stress and predisposes individuals to a higher risk of being hospitalized due to psychiatric illnesses.

In a study performed by researchers from the University College London, it was found that individuals who were exposed to secondhand smoke were more likely to suffer from psychological distress than people who were not exposed. The risk of psychological distress from secondhand smoke exposure is a staggering 50% – a significant risk percentage.

In addition to psychological stress, it was also found that people who regularly inhaled other people’s smoke were 3 times more likely to be admitted to a psychiatric facility in less than 7 years.  Smokers on the other hand, are four times more likely to be hospitalized due to psychological distress and other psychiatric problems.

The dangers of passive smoking

The researchers were able to measure the degree of a person’s exposure to nicotine by marking and measuring the compound cotinine, which is the chemical byproduct of nicotine after it has been metabolized/processed by the body.  The compound cotinine can be found in a person’s saliva.  The UK study tracked more than 5,000 smokers and 2,000+ non-smokers; all respondents of the study had no prior history of mental illnesses.

Within six years of the study, forty-one individuals from both the groups were admitted to a psychiatric facility.  More than fourteen percent of all the subjects of the UK study reported some degree of psychological stress.  After filters were applied, the researchers stated that despite differences in social circumstance, the risk factors still applied to both smoker and non-smokers. The study made use of a general questionnaire, which allowed the researchers to measure the exposure of secondhand smoke.

Based on the study, “passive smoking” or mere exposure to secondhand smoke increases  a person’s risk for psychological stress by more sixty percent. Prior to the more recent UK study, earlier animal studies showed that tobacco can alter an animal’s mood, which suggested a link between tobacco use and clinical depression in humans.

Tobacco: a poor stress reliever

This study shows that tobacco use is not a good coping strategy – instead of providing stress relief, it actually produces psychological stress. In a study published by the Journal of Pediatric Psychology (Oxford University Press) it was found that younger individuals are more prone to using tobacco as a coping strategy against stress.  It was found that smoking did not provide any significant stress relief to the respondents.

Sources:
reuters.com
archpsyc.ama-assn.org
jpepsy.oxfordjournals.org

Discuss this post in Frank Mangano’s forum!

The FDA is the only reason that we don't see dozens of different serious commercial efforts to treat people using early-stage stem cell therapies within the US. One of the few groups to try is presently under pressure, as this press release notes: "Regenerative Sciences, Inc., a Colorado medical practice that specializes in the use of a person's own stem cells to help patients avoid more invasive orthopedic surgery, announced today that the US Food and Drug Administration (FDA) is seeking to enjoin the clinic physicians from practicing medicine using patients' own stem cells. The lawsuit will allow Regenerative Sciences to question the FDA's policy that adult stem cells can be classified as drugs when used as part of a medical practice. ... The FDA will finally answer our questions, in court, about their claims and jurisdiction as opposed to doing everything in their power to avoid the issue that we are not a drug manufacturer, but simply a medical practice." The FDA has a long history of abuse and overreach, and this is simply more of the same - exactly what we should expect of bureaucrats left largely unaccountable for their actions. Progress and discovery becomes entirely secondary to the urge to power. When everything that is not explicitly permitted is forbidden, there is no innovation, no progress. This age of biotechnology could be far further advanced if not for the short-sighted fools who write and enact medical regulations.

View the Article Under Discussion: http://www.prnewswire.com/news-releases/colorado-medical-clinic-welcomes-opportunity-to-fight-fda-in-court-100247969.html

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

The Tithonus Error is the widespread and mistaken belief that extending the human life span will result in us being aged and decrepit for longer. This is not the case, however: engineered longevity can only be accomplished by repairing or reducing cellular and biochemical damage - which means you will be younger for longer. At In Search of Enlightenment, you'll find an examination of the roots of the Tithonus Error: "There is an irrational public predisposition to regard research on specific late-life diseases as marvelous but to regard research on aging, and thus all late-life diseases together, as a public menace bound to produce a world filled with nonproductive, chronically disabled, unhappy senior citizens consuming more resources than they produce. ... I am working on a new paper [that] examines how misperceptions about the present and future state of global health are themselves major obstacles to tackling aging. Because [imagined simulations of the future] are based on memories, medical research that proposes to eliminate a disease is much more likely to invoke hedonic experiences in our simulations then is a medical intervention that retards aging. ... our inability to make accurate, sensible simulations of what a future of retarding human aging would entail (for both the developed and developing world) is itself one of the greatest obstacles to prioritizing aging research. And this problem needs to be redressed."

View the Article Under Discussion: http://colinfarrelly.blogspot.com/2010/04/prospection-errors-are-obstacles-to.html

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Beta-glucan sourced from the barley plant and barley-based products can help improve the digestive tracts of people over 50 because of its probiotic potential.

Beta-glucan is a fibrous compound that naturally occurs in the cell walls of food such as the fiber of the barley plant and edible yeast.

Beta-glucan is also present in food mushrooms, such as the maitake mushroom.  Since it is nearly everywhere, eating food that has lots of beta-glucan may improve digestion, new study says.  Better digestion results from its seemingly probiotic effect, which is more noticeable in individuals fifty years old and above.

The study was published this year in Food Research International and is led by Adamantini Kyriacou, a researcher from the Harokopio University, which is based in Athens, Greece.

There should be no confusion with the term “probiotic”. According to Gibson et.al. in a related study on the human digestive process, probiotics is defined as non-digestible materials that have a positive or beneficial effect on the metabolism of the whole digestive tract.

Beta-glucan from oats & barley

The most widespread form of beta-glucan is found in oats. For many years now, this type of beta-glucan has already been associated with lower bad cholesterol (low-density lipoproteins) and has been tagged as a potential preventive for coronary heart disease.

The US Food and Drug Administration has already declared the link between specific oat products and better heart health.  More than a decade ago, the FDA established that a person only needs 3 grams of the compound to help lower cholesterol.

The Greek study endeavored to find out if beta-glucan derived from the barley plant produced the same positive effects.  The randomized study that involved more than fifty individuals (between the age of thirty-nine and seventy-two) showed that the positive probiotic effect was more apparent in the individuals over the age of fifty.

Some positive effects were also seen in younger respondents, but their response to the beta-glucan was not as statistically significant as the response of the fifty-plus year old respondents.

Other benefits of beta-glucan

Beta-glucan has also other established health benefits:

1. It binds to low-density lipoproteins (“bad cholesterol”) and removes them from the body, effectively reducing the cholesterol level in the body.
2. Beta-glucan has also been used to support the medical treatment of diabetes and obesity.  It may have some positive effects on weight loss efforts because it reduces cholesterol and improves heart health.
3. Beta-glucan can also be used as an immunostimulant.
4. For cancer patients, the addition of beta-glucan may help improve the digestive process and strengthen the immune system.
5. Beta-glucan is also capable of reducing the blood sugar level of diabetics.

Sources:
nutrasanus.com
nutraingredients.com
naturalmedicine.about.com

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Crowdfunding of commercial products is having a lengthy day in the sun at the moment. It has emerged from years of great success in small markets, such as the pen and paper gaming and indie publishing industries, and people are now applying the same models to fields where much more money is involved. Quite successfully too, some raising millions in what amount to well-run and timely preorder campaigns for products yet to be built. The range of endeavors open to crowdfunding of course includes scientific research, which is why it is a topic that shows up here every now and again:

If you can raise money for books, art projects, and widgets, why not for discrete life science research projects with determined goals? The LongeCity (previously the Immortality Institute) crowd have been trying this for some years, with a great deal of success considering the limited audience of this community in comparison to the audience available through Kickstarter. It is sad but true that far more people are brought to a state of excitedly opening their wallets for the development of an iPhone widget than for any sort of biotechnology project, even one that will contribute to the reversal of aging.

If you have a dedicated community, then you want to turn that dedication into professional organizations and the funds to run them. This is always going to be a messy, organic process of development, but which perhaps may be open to improvement through the spread of a more formalized crowdfunding culture. But in any case, I wanted to expand on the point made in the quote above - that crowdfunding for scientific research is a radically different undertaking from crowdfunding for development of a commercial product. This seems worth emphasizing, given that a whole range of startups and new ventures seem to be trying to port over crowdfunding into the sciences pretty much as-is, or with just a few embellishments. Like these, for example:

• EurekaFund
• FundaGeek
• GeekFunder
• Microryza
• Petridish
• Rockethub
• Sciflies

What we can hope for from this wealth of effort is that some groups figure out the magic formula that will make science funding work in this environment - and make it work with the same degree of liquidity and interest as in commercial projects. Experimentation is clearly needed, however.

The basic point of divergence between crowdfunding a product versus crowdfunding research is that in the former case the funders are definitively buying something concrete: that is their motivation and incentive. They are putting down money in expectation that what they are doing is submitting a preorder. Variations on the preorder theme are legion, but they all boil down to paying for a definitive item, a which will usually have fairly solid delivery date. Scientific research is notoriously bad when it comes to delivering on both those points, however. The work that is most amenable to crowdfunding consists of small projects that only incrementally add value to their fields - and which may not even do that, given the necessarily high failure rate for research.

The challenge facing science crowdfunding is the same challenge faced by scientific advocates at all times: they do their part to grow communities of supporters and encourage those supporters to pay for research work. That work will give no immediate result, the eventual result may be hard for supporters to understand, it will likely not benefit them for some time, if ever, and in addition to all of that the undertaking will quite likely fail. Science is a high risk endeavor, with few short-term payoffs that people find rewarding - and thus it is a hard sell when held up against the allure of immediate gratification, candy, and shiny objects.

But technological progress is the only thing that matters, not today's pretty baubles that are made possible by past successes in science. Funding of science has to be made to work if we want to continue on this upward curve to longevity, wealth, and expansion of what it means to be human.

Despite all of the challenges, the old messy, organic way of funneling money into scientific projects does in fact make progress. People who care about the end result, something decades away, do step up to fund science. You might look at our little community of longevity science enthusiasts for example, making noise and raising somewhere north of $14 million over the past eight years for organizations and initiatives like the Methuselah Foundation, the New Organ Prize, and the SENS Foundation. Knowing that this is possible, and regardless of the fact that it is hard, very hard, to convince people to open their wallets for science, you have to look at what's happening in the crowdfunding space right now and think that fundraising for science could all be made easier - if someone just goes about it in the right way, builds the right tools, hits the right business model, pulls together the right sort of seed community.

And maybe so. I've watched most of a decade of a small community funding research, and the cryonics advocates have watched much the same thing for far longer, but I don't have any good answers - and I'm not sure that they do either. So it is a good thing that a number of venture funded and bootstrapped groups are working on this; they'll have a few years of runway to work on finding the key to the problem, and we'll all benefit should one of them come up with a good way forward.

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

The first generation of the modern cryonics community, people who were middle-aged in the 1970s, is benefiting from the technologies and visions that they built. They founded a movement that has sustained itself for four decades in providing steadily improved cryopreservation services through organizations such as Alcor and the Cryonics Institute. The growth that would remake cryonics as from a non-profit community into a for-profit business with a healthy research and development arm has yet to happen, unfortunately, despite the clear need for the ability to preserve the brains and minds of those who will age to death before the advent of working rejuvenation biotechnology. But the present level of success is enough to provide a shot at renewed life in the future for the few who are determined enough and organized enough to take it.

I see that another of the early cryonics pioneers was cryopreserved recently:

Alcor Co-Founder Fred Chamberlain is Cryopreserved

Fred Chamberlain III who, with his wife Linda, incorporated Alcor in 1972, was cryopreserved by Alcor on March 22, 2012. One week earlier, Fred relocated from Florida to a Scottsdale hospice. This allowed us to watch over him and respond immediately when needed. We believe that Fred received an excellent cryopreservation. More details will be released later.

Linda Chamberlain has released a document to announce his cryopreservation and honor him.

Bon Voyage, Fred Chamberlain

Fred Chamberlain was a NASA-JPL electrical engineer working on the Mariner-Jupiter-Saturn mission in 1973 [and] was and is of absolutely critical importance to cryonics. While most people with more than a passing acquaintance with cryonics will associate his importance with the founding of Alcor, that is in reality only a surrogate marker for his deeper importance. Fred came on the scene in cryonics in what was unarguably its darkest hour. It had degenerated into little more than a fraudulent cult in California and, everywhere in the US, it had lost all vestiges of technical and scientific rigor.

When Fred discovered this in his role as Vice President of the Cryonics Society of California (CSC) he not only left CSC and founded Alcor, he and Linda Chamberlain established, for the first time anywhere, the practice of scientific, evidence based cryonics; cryonics based on the scientific method, on documentation of procedures, policies, cryopreservation protocols and rigorous patient case reports. He and Linda mandated not only scientific and technical accountability, but administrative, financial and legal accountability as well.

Until it does become an earnestly growing industry of many competing companies and millions of cryopreservations every year, cryonics can only work - in the sense of providing a good chance at safe preservation until such time as molecular nanotechnology and other advanced medical technologies can rebuilt and revive cryopreserved individuals - if the movement acts as a community. Maintaining the means of brain preservation for the long term is simply a new option in the general category of caring for elders whose bodies are failing them: this is something that well-balanced communities of humans have accomplished for a long time indeed. So provided that the cryonics movement can persevere as an ordinary, standard community of people with shared interests, as it has for the past 40 years, it should offer those who are cryopreserved a good chance of stability and safety for the decades between now and the advent of restorative technologies of the future.

But that growth is still a better option all round. So very many people go to the grave every day, people who might have chosen cryonics or plastination if those were options backed by a large, vocal industry with millions of customers.

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

It has been a number of years since researchers started to investigate the role of DJ-1 in Parkinson's disease. Here, the work has made it to the stage of a possible therapy: "As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. ... Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age. The ability to modify the activity of DJ-1 could change the progress of the disease. [Researchers have] now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine- producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch. Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. ... We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain. ... In pre-clinical trials, the treatment was tested on mice ... From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain. Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not."

Link: http://www.aftau.org/site/News2?page=NewsArticle&id=16503

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

Resveratrol in and of itself is likely not terribly interesting for work on longevity - and certainly not worthy of the hype surrounding it. The same probably goes for sirtuins in general. This, however, is still a good example of work on tracing back the pathways of action of a metabolic change agent: "Research has previously suggested that resveratrol acts through activation of the sirtuin (SIR) gene family. This gene pathway, though controversial, has been implicated in life extension across several species. It has been reported that SIR extends lifespan in much the same way as caloric restriction which itself in turn may activate SIR. It has remained unclear however if resevertrol directly activates SIR or if it acts on SIR indirectly via another intermediary biochemical pathway. The current study successfully answered that question. Using several cell biology techniques the authors were able to demonstrate that resveratrol actually functions to activate SIR indirectly. They showed that resveratrol is really a phosphodiesterase inhibitor (PDE4). They demonstrated that reducing PDE4 allows cyclic AMP (cAMP) levels in the cells to rise. cAMP then increases the activity of AMPK which next increases NAD+ which finally increases SIR. This elegant study then went on to prove that the same life extending benefits of resveratrol could be achieved in rats by administering them the PDE4 inhibitor rolipram. ... inhibiting PDE4 with rolipram reproduces all of the metabolic bene?ts of resveratrol, including prevention of diet-induced obesity and an increase in mitochondrial function, physical stamina, and glucose tolerance in mice. "

Link: http://extremelongevity.net/2012/02/13/resveratrol-study-finds-new-class-of-life-extension-molecules/

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

Resources in research and medical development seems to be the unifying topic here for the past week or so. It is interesting to these accidental thematic collections of content come and go in passing, all without any deliberate intent; a reminder that we take small samples from a much broader, many-threaded conversation of millions of people, one that spans all media and has its tides and fashions at every timescale. So continuing the theme, here is a newly processed and posted video from the SENS5 conference:

Since rejuvenation therapies will ultimately offer many more years of life than traditional life-saving interventions, a problem emerges for existing principles of medical decision-making. Justice demands that all patients are due an equal standard of medical care. But if we measure medical care in terms of the amount of life it saves, or in terms of its cost relative to its effectiveness, or even in terms of its ability to save identified individuals rather than reduce statistical risk in groups, rejuvenation will eventually be far more valuable than life-saving. More broadly, effective rejuvenation medicines will effectively erode the boundary between curative and prophylactic medicines, as well as the boundary between treatment and enhancement.

The quote above is the more reasonable part of the abstract, which concurs with the sensible view that the dominant strategies in medicine must change: what happens today largely takes the form of trying to patch over late stage consequences without addressing root causes, and will thus always be expensive and ultimately unsuccessful. It is poor value in comparison to a strategy of consistently repairing low-level biological damage and thus effecting rejuvenation.

That said, I should note that the whole is a viewpoint I cannot agree with. The presentation builds upon an idealized, and already incorrect, view of the British governmental heath monolith on the one hand, and the meaning of "justice" that roughly translates to "equality maintained through theft, coercion, and destruction of progress is better than honestly earned inequality" on the other. The end result is just moving deckchairs on the Titanic, painting a poisonous, failing system a different color. It'll all come to the same in the end. All systems, like the government health services in Western nations, that divorce themselves from price signaling and patient accountability for costs incurred ultimately create shortages, enforce rationing, and stagnate. They turn relationships between patient and provider from mutually beneficial trade to hostile engagement at arms length, then remove the market incentives for participants to develop and offer better services and technologies, and later the incentives that cause people to offer any form of service at all. Finally, you reach the unhappy truth about other people's money: it runs out.

While they last, the current incarnation of government-run health systems will continue to greatly harm the progression of medical technology - the pace of development, the cost-effectiveness, and the directions taken. The effects of the FDA on research directions - such as the institutional discouragement of work on therapies for aging - are but one facet of this problem. The laws that remove freedom of choice in funding research and development, freedom to practice medicine, and the freedom to try new medical technologies are but another.

These systems are rotten to the core, and the best thing we can do is find practical ways to work around their constraints: engaging them, trying to change them by working within the system, will only prop up these corroded, toxic hulks for that little while longer. We will all be better off when the current regime of regulation and centralized control collapses.

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

Average telomere length in at least some tissues makes a good marker for general health, but the progressive shortening of telomeres may or may not be a root cause of aging. Telomere length results from a dynamic system of lengthening and shortening processes, which seems more likely to be a reflection of underlying function and dysfunction: "In an ongoing study of almost 20,000 Danes, a team of researchers [have] isolated each individual's DNA to analyse their specific telomere length - a measurement of cellular aging. ... The risk of heart attack or early death is present whether your telomeres are shortened due to lifestyle or due to high age ... The recent Copenhagen General Population Study involved almost 20,000 people, some of which were followed during almost 19 years, and the conclusion was clear: If the telomere length was short, the risk of heart attack and early death was increased by 50 and 25 per cent, respectively. ... That smoking and obesity increases the risk of heart disease has been known for a while. We have now shown, as has been speculated, that the increased risk is directly related to the shortening of the protective telomeres - so you can say that smoking and obesity ages the body on a cellular level, just as surely as the passing of time. ... one in four Danes has telomeres with such short length that not only will they statistically die before their time, but their risk of heart attack is also increased by almost 50 per cent. Future studies will have to reveal the actual molecular mechanism by which the short telomere length causes heart attacks. Does one cause the other or is the telomere length and the coronary event both indicative of a third - yet unknown - mechanism?" I lean towards the latter hypothesis, that both risk of catastrophic failure in bodily systems and telomere length reflect levels of accumulated damage at the level of cells and macromolecules in the body.

Link: http://news.ku.dk/all_news/2012/2012.2/cellular-aging-increases-risk-of-heart-attack/

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

A viewpoint from Vladimir Skulachev, whose research group works on mitochondrially targeted antioxidant compounds: "'It is recognized that in exceptional circumstances the possibility exists for selection to favor limiting survival. In acknowledging that at least in theory, aging might occasionally be adaptive, however, the high barriers to validating actual instances of adaptive ageing are made clear' ... A few years ago it was hardly possible to find the latter statement in an article written by the most famous proponents of non-programmed aging. Certainly, this conclusion is accompanied by some reservations. Nevertheless, the balance between concepts of programmed and non-programmed aging seems to be really shifted to the programmed one. ... The idea that programmed death was invented by biological evolution was introduced in the end of nineteenth century by August Weismann, who suggested that such a death is useful for evolution as a mechanism which (i) purifies the population from weak individuals and (ii) promotes succession of generations. For sure, both these roles may be inherent in aging. However, they failed to explain why aging represents slow and concerted decline of many physiological functions (slow phenoptosis) rather than simple fast switching off of a single function of vital importance (acute phenoptosis). ... There is, it must be acknowledged, an instinctive attraction to the idea that aging is programmed. Aging is widespread across species and applies universally to all individuals within a species in which it is observed. There is also reproducibility about changes that occur with aging .... I may only add that, if aging is programmed, it can be retarded, prevented, and perhaps even reversed by treatments interrupting execution of this program, just as we already can interrupt programs of cell death. In other words, programmed aging can be cured like a disease. As for the concept of non-programmed aging, assuming occasional accumulation of stochastic injuries as its reason, it is quite pessimistic for finding any way of successful treatment. Here we simply observe and describe such a process without the possibility of improving the situation." This last viewpoint is exactly the wrong way around - repair of damage is likely to be far easier through SENS and similar programs than safely altering the exceedingly complex systems of metabolism to change the way in which aging happens. We should hope that genetic programs are of limited and narrow influence as a driver of aging - that they are merely reactions to underlying accumulations of damage where they exist at all. Because otherwise we're in for a long, slow road when it comes to extending healthy life.

Link: http://impactaging.com/papers/v3/n11/full/100403.html

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

I had been meaning to point out video of Cynthia Kenyon's TEDGlobal presentation recorded earlier this year and posted online last month:

Kenyon, as you might know, leads the Kenyon Lab at UCSF, and was one of the first to demonstrate meaningful life extension in lower animals through single gene mutations back in the 1990s. We've come a long way since then, even if progress towards longevity-enhancing biotechnology and growth in public acceptance of that goal seems painfully slow while you're living through it a day at a time. As Maria Konovalenko of the Science for Life Extension Foundation points out, it is sometimes encouraging to read the public comments on a presentation like this one and see a great many generally positive opinions expressed:

The more TED Talks about ways to intervene in aging processes we have, the faster people all around the world would understand the feasibility of life extension therapies. By the way, I was glad to see that there are quite a lot of folks, advocating for longevity in the comments discussion about the video. I think this is another sign of TED audience becoming more and more educated and open-minded in regard to the idea of radical life extension. I would like to address the TED events organizers and ask them to do more talks on the topic of aging.

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