Found: genes that make kids smart

http://www.theaustralian.com.au/news/nation/found-genes-that-make-kids-smart/story-e6frg6nf-1225926421510

SCIENTISTS have identified more than 200 genes potentially associated with academic performance in schoolchildren.

Those schoolchildren possessing the "right" combinations achieved significantly better results in numeracy, literacy and science.

The finding emerged from a study of more than 4000 British children to pinpoint the genes and genetic combinations that influence reasoning skills and general intelligence.

One of its main conclusions is that intelligence is controlled by a network of thousands of genes with each making just a small contribution to overall intelligence, rather than the handful of powerful genes that scientists once predicted.

The researchers believe their work could eventually lead to genetic tests to predict babies' academic potential.

"This kind of research could help us develop genetic tests to predict which kids are at risk of developing problems with their schooling, so that we could intervene to help them," said Robert Plomin, professor of behavioural genetics at the Institute of Psychiatry at King's College London, who will describe his work today at a meeting of the Royal Society.

In his research, Professor Plomin built up a database on the academic ability of 4000 children, partly from teacher assessments and partly by having the youngsters sit a battery of cognitive tests. Then he and his colleagues analysed the children's DNA, looking for tiny variations in their genes.

There are potentially many millions of these variations, but the team restricted their search to looking at the million or so of the most common, to find out which gene variants were most frequently found in children with either a high or low level of academic achievement.

"Out of the gene variants we looked at, a couple of hundred are emerging which seem to have a small but significant relationship with ability in maths and English," said Professor Plomin.

Such research reflects a long-term trend away from the idea that particular aspects of human physiology, appearance and behaviour are controlled by just a few genes.

This idea arose from early breakthroughs in which illnesses such as multiple sclerosis and breast cancer, or features such as hair and eye colour, were found to be strongly influenced by variations in the structure of just one or a few genes. Some scientists then predicted similar results for anything from heart disease to intelligence.

In recent years, however, it has become clear that most aspects of human development, health and behaviour are controlled by huge networks of individual genes, of which humans have about 25,000.

Research into height, for example, has picked out 300 genes that affect how tall people will grow, but even these genes can only explain 15 per cent of the total variations in human height. It implies that hundreds more genes must also play a part.

The scale of the search needed to track down all the genes involved in complex areas such as intelligence was beyond scientists' abilities until recently. The deployment of computers means they can now begin to work out the interactions of these genes.

THE SUNDAY TIMES

Sex Makes You Smarter- Can 'Virtual Sex' Do The Same?

http://www.science20.com/rogue_neuron/sex_makes_you_smarter_can_virtual_sex_do_same

It has been known for quite some time that exercise promotes neurogenesis, but now astudy by Leuner, Glasper, and Gould, published by PLoS ONE this month, claims that the most intimate form of exercise - sexual activity - can produce the same effects.  And better yet- having multiple, repeated sexual experiences results in a greater positive effect than a single experience alone. Added bonus: it reduces anxiety as well.  I love that kind of data!

A lot of bloggers have been buzzing about this study for a few days now.  I mean, understandably so.  Who doesn't want to hear that lots of sex is beneficial on multiple cognitive levels?   I can practically hear the cheers rising up from college campuses everywhere. 

Here's a question to ponder: If sex makes you smarter via changes in synaptic strength  following the act, can you get the same benefit from virtual sex, as long as your brain is convinced it is real at the time?  I'll discuss this idea in a bit, but first let's look at the methods and the data from the actual study.

From the abstract:

"Aversive stressful experiences are typically associated with increased anxiety and a predisposition to develop mood disorders. Negative stress also suppresses adult neurogenesis and restricts dendritic architecture in the hippocampus, a brain region associated with anxiety regulation. The effects of aversive stress on hippocampal structure and function have been linked to stress-induced elevations in glucocorticoids. Normalizing corticosterone levels prevents some of the deleterious consequences of stress, including increased anxiety and suppressed structural plasticity in the hippocampus."

Previous studies have shown that high stress levels have a negative impact on learning and memory.  However, not all stress is bad.  I have stated before, namely in my recent presentation at the H+Summit, that some amount of stress, of a specific type, can actually be good for you, and can improve your cognitive functioning.  In this study, they decided to use a fan favorite as their "good stress" variable: Sex.  Additionally, they wanted to see if all sex was created equal in terms of beneficial outcome.  Specifically, whether or not one novel sexual experience (acute condition) had the same impact as repeated sexual experiences (chronic condition).

Here we examined whether a rewarding stressor, namely sexual experience, also adversely affects hippocampal structure and function in adult rats. Adult male rats were exposed to a sexually-receptive female once (acute) or once daily for 14 consecutive days (chronic) and levels of circulating glucocorticoids were measured.

Separate cohorts of sexually experienced rats were injected with the thymidine analog bromodeoxyuridine in order to measure cell proliferation and neurogenesis in the hippocampus. In addition, brains were processed using Golgi impregnation to assess the effects of sexual experience on dendritic spines and dendritic complexity in the hippocampus.

Finally, to evaluate whether sexual experience alters hippocampal function, rats were tested on two tests of anxiety-like behavior: novelty suppressed feeding
and the elevated plus maze.

To sum up, going on the previously discovered knowledge about exercise promoting neural growth, and negative stress impairing neural activity, they wanted to see if positive stress (a happy sexual experience) had a positive or negative impact on neurogenesis.  They also wanted to know what effects this type of stress had on anxiety levels.  Here's what they found:

We found that acute sexual experience increased circulating corticosterone levels and the number of new neurons in the hippocampus. Chronic sexual experience no longer produced an increase in corticosterone levels but continued to promote adult neurogenesis and stimulate the growth of dendritic spines and dendritic architecture. Chronic sexual experience also reduced anxiety-like behavior. These findings suggest that a rewarding experience not only buffers against the deleterious actions of early elevated glucocorticoids but actually promotes neuronal growth and reduces anxiety.

Yay! Good news! So what does all of this really mean?

Well, the fact that repeated sexual experiences can reduce anxiety is no big surprise.  I think most of us knew that already.  But what is interesting to me is the extent, the type, and the conditions of the neural growth that occurred following the sexual experiences.

*to see all of the detailed graphs and data points, go to the original article here.* 

Let's look at all of the things we already know, based on this study's results, past research and basic knowledge about neurological functioning:

• Exercise- for example, running- while it increases stress levels, it is "good stress".  Exercise has been shown in the past to promote neurogenesis.  In other words, this type of good stress actuallypromotes neural growth, rather than impairing it.
• It is suggested that if the stressful event has a hedonic value, or a pleasant outcome, it
  cancels out the negative effects of the raised glucocorticoid levels.  Even though stress levels in this study were raised in the acute (one-night-stand) condition, the brain was buffered from aversive damage due to the positive nature of the stress, and still allowed for neural growth.  This means that there is some sort of protective quality from good stress. 
• This would conclude that sexual activity, in this case, is similar in function to exercise, as it relates to neural growth and the protective features of good stress.
• The one-night-standers (acute condition), had an increase in anxiety following the experience, which was evidenced by results of the training tasks, but this did not hinder the neural growth.
• The one-night-stand condition yielded significant neural growth, but the chronic (female-a-day-for-fourteen-days) condition showed even more neural growth, plus nixed any of the anxiety effects after about day 4 or 5 of having consistent sex. 
• It would stand to reason that the more sex you have, the less anxiety you'll have, plus you'll increase your neural growth, ie., get smarter.  Awesome.

Mini-summary: According to these results, sex is indeed a good form of stress, and it induced neural growth. Additionally, more frequent sex is even better than a one-hit-wonder when it comes to maximizing the growth and easing anxiety.  All good stuff.  I am definitely adding "Have more sex" to my "Maximizing Your Cognitive Potential" checklist.

Now- here is where I want to touch on the more interesting theoretical concepts.  These points have not been discussed as much, but they should be.  First, why is sex rewarding and pleasurable? And why does it enhance learning?

One word: Dopamine.

Why aren't more people discussing the dopamine factor?!? Dopamine! My BFF! Dopamine ties everything together.

Cited by the authors of this paper, a previous study's results suggest that ICSS (Intracranial Self-Stimulation- translate: press a lever, an electrical impulse is sent to an implanted electrode to artificially stimulate an area of the brain) was enough to increase adult neurogenesis.

Another study, Dynamic Changes in Accumbens Dopamine Correlate With Learning During Intracranial Self-Stimulation ( Owesson-White et al, 2008), looked at the action of dopaminergic neurons in response to cues of a rewarding stimulus.  Basically, they wanted to see if they could condition the activation of dopamine D1 receptors by merely presenting a cue for a stimulus, without actually having to stimulate the neurons directly.

This phenomenon is similar to seeing a slice of lemon and salivating without tasting it; you have paired an actual lemon with a sour taste in the past, and now the visual cue of the lemon is enough to induce salivation on its own.  Well, that is what happened here, only the induced response wasn't salivation, it was activation of dopamine receptors.  Even better!

Dopamine, as you may know, has many wonderful functions in the brain: reward, motivation, pleasure, focus and attention- just to name a few.  The fact that the subjects in the ICSS study were able to activate those specific dopamine receptors merely in response to a cue was a pretty significant discovery. 

According to the authors, "This D1 activation is highly significant because it has been linked to neural processing related to LTP (Long-Term Potentiation), a change in synaptic strength related to learning."  In other words, they were able to stimulate neural growth just by seeing a cue for the stimulus, without actually having to engage in the activity.  Subsequent research has shown this same result.

This is a pretty big deal.

Basically, you can get the neural benefits of engaging in a pleasurable activity without actually having to do anything other than trick your brain into thinking it is getting the reward.  This can be done via conditioning or paired association learning, like in the mentioned ICSS study, but what about more technologically induced ways?  Like Virtual Reality?

Get smarter and learn to talk to women?  This is not my World of Warcraft avatar,  mine has longer hair.

Some of my transhumanist friends swear that by the time we perfect Full-Immersion Virtual Reality, humans will no longer need or want to have sexual intercourse.  Now, I am not saying that is my personal stance on the issue, but they do have a point in some respects.

Leuner, et al claim that the pleasure component of the activity is crucial to the maximum benefit derived from engaging in it.  If this is the case, does bad sex induce the same levels of growth and anti-anxiety benefit as great sex?  Is it a continuum of minimum to maximum benefit based on how good the experience is?

For example, exercise promotes neural growth, but I haven't seen any studies that rate the quality of the exercise experience and then compare the amount of resulting neurogenesis as a function of the good or bad rating of the activity.  But if the emotional valence of the activity is important in its ability to neutralize the negative impact of the stress, one would assume the more enjoyable, the better.

So now look at Virtual Reality (VR) sex.  In theory, it is perfect in every way, tailored exactly to your utmost desires, so ultimately, it is the best sex of your life every time you switch on your little device.  Your brain actually believes it is engaging in this activity, so you would expect to see the same types of reward response in the neurons, activation of the dopamine receptors, following the simulation.  If this is true, in theory, you would also experience neural growth as a result of engaging in VR sex, even though your body is passive.

In fact, if the amount of neurogenesis achieved is in any way related to the quality of the sex or the amount of pleasure experienced, would you get even MORE neural growth from virtual sex than you would in actual sex?

Looking at the brain in this way opens the door for all kinds of artificial enhancements.  If we could trick the brain into perceiving an activity as pleasurable, activating those addictive little dopamine receptors, we could potentially enhance learning capacity merely by experiencing a simulation in our mind.  How many people do you think would spend all weekend having virtual sex if this were possible?

(I personally know of MANY who would, incidentally)

I wonder, though, after the VR sex simulation is over, and you consciously understand that it was not real, does this impact any of the positive effects that may result?  I guess the only way to really know is to conduct original research and see what results of it.

Is there any funding out there for such a project? I'm sure I could round up several hundred volunteer subjects...

The Mathematical Probability Of Life On Other Earth-Like Planets

http://www.science20.com/news_releases/the_mathematical_probability_of_life_on_other_earth_like_planets

Infinity was invented to account for the possibility that in a never-ending universe, anything can happen. Life on other Earth-like planets, for example, is possible in an infinite universe, but not probable, according to a scientist from the University of East Anglia.

The mathematical model produced by Prof Andrew Watson suggests that the odds of finding new life on other Earth-like planets are low because of the time it has taken for beings such as humans to evolve and the remaining life span of the Earth. Structurally complex and intelligent life evolved late on Earth and this process might be governed by a small number of very difficult evolutionary steps.

Prof Watson, from the School of Environmental Sciences, takes this idea further by looking at the probability of each of these critical steps occurring in relation to the life span of the Earth, giving an improved mathematical model for the evolution of intelligent life.

According to Prof Watson a limit to evolution is the habitability of Earth, and any other Earth-like planets, which will end as the sun brightens. Solar models predict that the brightness of the sun is increasing, while temperature models suggest that because of this the future life span of Earth will be ‘only’ about another billion years, a short time compared to the four billion years since life first appeared on the planet.

“The Earth’s biosphere is now in its old age and this has implications for our understanding of the likelihood of complex life and intelligence arising on any given planet,” said Prof Watson.

“At present, Earth is the only example we have of a planet with life. If we learned the planet would be habitable for a set period and that we had evolved early in this period, then even with a sample of one, we’d suspect that evolution from simple to complex and intelligent life was quite likely to occur. By contrast, we now believe that we evolved late in the habitable period, and this suggests that our evolution is rather unlikely. In fact, the timing of events is consistent with it being very rare indeed.”

Prof Watson suggests the number of evolutionary steps needed to create intelligent life, in the case of humans, is four. These probably include the emergence of single-celled bacteria, complex cells, specialized cells allowing complex life forms, and intelligent life with an established language.

“Complex life is separated from the simplest life forms by several very unlikely steps and therefore will be much less common. Intelligence is one step further, so it is much less common still,” said Prof Watson.

His model, published in the journal Astrobiology, suggests an upper limit for the probability of each step occurring is 10 per cent or less, so the chances of intelligent life emerging is low – less than 0.01 per cent over four billion years.

Each step is independent of the other and can only take place after the previous steps in the sequence have occurred. They tend to be evenly spaced through Earth’s history and this is consistent with some of the major transitions identified in the evolution of life on Earth.

Glucosamine And Chondroitin Don't Work For Joint Pain - Study

Η γλουκοσαμίνη και η χονδροϊτίνη δε βοηθούν στην ελάττωση του πόνου σε ασθενείς με οστεοαρθρίτιδα. Κοινώς δεν αξίζει να δίνεις τόσα λεφτά για να προστατεύεις τα γόνατα σου από την έντονη καταπόνηση (bodybuilding, strength training, πολεμικές τέχνες και άλλα δυναμικά αθλήματα).

Link

Άρθρο:

Τwo popular supplements taken by millions of people around the world to combat joint pain, glucosamine and chondroitin, do not work, according to research published today - but they don't hurt you either.  Basically, they are expensive placebos.

Glucosamine and chondroitin are either taken on their own or in combination to reduce the pain caused by osteoarthritis in hips and knees.  The researchers, led by Professor Peter Jüni at the University of Bern in Switzerland, state that although they don't work these supplements are not dangerous - "we see no harm in having patients continue these preparations as long as they perceive a benefit and cover the cost of treatment themselves."

However, they note, "Health authorities and health insurers should not cover the costs for these preparations, and new prescriptions to patients who have not received treatment should be discouraged."   So buy them if you are convinced they work, but don't ask insurance to cover it.

Osteoarthritis of the hip or knee is a chronic condition which is mainly treated with painkillers and anti-inflammatory drugs but these can cause stomach and heart problems, especially if used long-term. Treatments that not only reduce pain but slow the progression of the disease would be desirable, say the authors.

In the last decade, general practitioners and rheumatologists have increasingly prescribed glucosamine and chondroitin to their patients and many have also purchased them over the counter. In 2008 global sales of glucosamine supplements reached almost $2 billion, an increase of about 60% since 2003.   But studies related to the benefit of that $2 billion spent on glucosamine and chondroitin were conflicting so a large scale review of studies was needed to determine whether or not the supplements actually work.

Professor Jüni and colleagues analyzed the results of 10 published trials involving 3,803 patients with knee or hip osteoarthritis. They assessed changes in levels of pain after patients took glucosamine, chondroitin, or their combination with placebo or head to head.

Result: No clinically relevant effect of chondroitin, glucosamine, or their combination on perceived joint pain or on joint space narrowing.  Despite that, some patients are convinced that these preparations are beneficial, say the authors, and they suggest this might be instead because of the natural course of osteoarthritis or the well-discussed placebo effect.

"Compared with placebo, glucosamine, chondroitin, and their combination do not reduce joint pain or have an impact on narrowing of joint space. Health authorities and health insurers should be discouraged from funding glucosamine and chondroitin treatment," they conclude.

Some quick links:

The Secret Lives of Big Pharma's 'Thought Leaders'
Alzheimer's Drug Boosts Perceptual Learning in Healthy Adults
How to find the perfect relationship - don't follow dating rules
The price of love? Losing two of your closest friends
Why Women Prefer 'Chill' Guys
Revenge of the nerds: Should we listen to futurists or are they leading us towards ‘nerdocalypse’?
Being lonely 'can kill you', research shows
How Football Playing Robots Have the Future of Artificial Intelligence at Their Feet
Depression Drugs Affect Personality
Can a supplement boost immunity, slow aging?
Anti-Aging Medicine: Longevity & Life Extension
Laws of Physics Vary Throughout the Universe, New Study Suggests
Vitamin B could delay onset of Alzheimer's: study
Good dancing may be sign of male health, scientists say
Prescription for a Healthier Brain: Coffee and Cigarettes?
The Neurobiology of Evil
Playboys have shorter lives

Bottled tea beverages may contain fewer polyphenols than brewed tea

Link

OSTON, August 22, 2010 — The first measurements of healthful antioxidant levels in commercial bottled tea beverages has concluded that health-conscious consumers may not be getting what they pay for: healthful doses of those antioxidants, or “poylphenols,” that may ward off a range of diseases.

Scientists reported here today at the 240th National Meeting of the American Chemical Society (ACS) that many of the increasingly popular beverages included in their study, beverages that account for $1 billion in annual sales in the United States alone, contain fewer polyphenols than a single cup of home-brewed green or black tea. Some contain such small amounts that consumers would have to drink 20 bottles to get the polyphenols present in one cup of tea.

Many commercial bottled tea beverages

contain little or no healthful antioxidants,

new research suggests.

Credit: Wikimedia Commons

“Consumers understand very well the concept of the health benefits from drinking tea or consuming other tea products,” said Shiming Li, Ph.D., who reported on the new study with Professor Chi-Tang Ho and his colleagues. “However, there is a huge gap between the perception that tea consumption is healthy and the actual amount of the healthful nutrients — polyphenols — found in bottled tea beverages. Our analysis of tea beverages found that the polyphenol content is extremely low.”

Li pointed out that in addition to the low polyphenol content, bottled commercial tea contains other substances, including large amounts of sugar and the accompanying calories that health-conscious consumers may be trying to avoid. He is an analytical and natural product chemist at WellGen, Inc., a biotechnology company in North Brunswick, N.J., that discovers and develops medical foods for patients with diseases, including a proprietary black tea product that will be marketed for its anti-inflammatory benefits, which are due in part to a high polyphenol content.

Li and colleagues measured the level of polyphenols — a group of natural antioxidants linked to anti-cancer, anti-inflammatory, and anti-diabetic properties — of six brands of tea purchased from supermarkets. Half of them contained what Li characterized as “virtually no” antioxidants. The rest had small amounts of polyphenols that Li said probably would carry little health benefit, especially when considering the high sugar intake from tea beverages.

“Someone would have to drink bottle after bottle of these teas in some cases to receive health benefits,” he said. “I was surprised at the low polyphenol content. I didn’t expect it to be at such a low level.”

The six teas Li analyzed contained 81, 43, 40, 13, 4, and 3 milligrams (mg) of polyphenols per 16-ounce bottle. One average cup of home-brewed green or black tea, which costs only a few cents, contains 50-150 mg of polyphenols.

After water, tea is the world’s most widely consumed beverage. Tea sales in the United States have quadrupled since 1990 and now total about $7 billion annually. The major reason: Scientific evidence that the polyphenols and other antioxidants in tea, may reduce the risk of cancer, heart disease, and other afflictions.

Li said that some manufacturers do list polyphenol content on the bottle label. But the amounts may be incorrect because there are no industry or government standards or guidelines for measuring and listing the polyphenolic compounds in a given product. A regular tea bag, for example, weighs about 2.2 grams and could contain as much as 175 mg of polyphenols, Li said. But polyphenols degrade and disappear as the tea bag is steeped in hot water. The polyphenol content also may vary as manufacturers change their processes, including the quantity and quality of tea used to prepare a batch and the tea brewing time.

“Polyphenols are bitter and astringent, but to target as many consumers as they can, manufacturers want to keep the bitterness and astringency at a minimum,” Li explained. “The simplest way is to add less tea, which makes the tea polyphenol content low, but tastes smoother and sweeter.”

Li used a standard laboratory technique, termed high-performance liquid chromatography (HPLC), to make what he described as the first measurements of polyphenols in bottled tea beverages. He hopes the research will encourage similar use of HPLC by manufacturers and others to provide consumers with better nutritional information.

S-Adenosyl Methionine (SAMe) για την κατάθλιψη

Diet Supplement Helps With Depression

Drug Discovery & Development - September 01, 2010

A new study conducted by investigators at Harvard Medical School and Massachusetts General Hospital (MGH) suggests that S-Adenosyl Methionine (SAMe), an over-the-counter dietary supplement, can be an effective, relatively well-tolerated, adjunctive treatment for adults with major depressive disorders who do not respond to their treatment with antidepressant medication. This first-of-its-kind study was published in the August 2010 American Journal of Psychiatry. According to the National Institute of Mental Health, there are approximately 14.8 million people with major depressive disorders in the United States.

The study, "S-Adenosyl Methionine (SAMe) Augmentation of Serotonin Reuptake Inhibitors for Antidepressant Nonresponders With Major Depressive Disorder: A Double-Blind, Randomized Clinical Trial," is the first randomized, placebo-controlled clinical trial conducted on SAMe in a population of patients with major depressive disorders. A total of 73 adults were enrolled in this six week study and randomly assigned to the placebo control group or the SAMe treatment group. SAMe, in combination with standard depression treatment, was more effective than antidepressant treatment alone in improving measures of depression and remission rates of patients with significant clinical depression. SAMe-treated subjects had a greater response and remission rate to treatment than the placebo-treated group. SAMe was well-tolerated with no reported adverse reactions.

"With each study we continue to gain a better understanding of SAMe's role in treating depression. This new finding, albeit preliminary and in urgent need of replication, suggests significant, clinically meaningful differences in outcome among patients who had SAMe added to their antidepressant medication treatment compared to those taking a placebo with their medication," said George Papakostas, M.D., associate professor of psychiatry at Harvard Medical School, director of treatment-resistant depression studies in the Department of Psychiatry at MGH, lead author of the current study. "These findings provide preliminary support for the efficacy, safety, and tolerability of SAMe as an additive therapy for patients with major depressive disorders who do not respond to antidepressant treatment alone. Continued research, however, is urgently needed to more definitively further our understanding of the role of SAMe in the treatment of adults diagnosed with depression. Adjunctive SAMe therapy is promising, but cannot yet be recommended for wide-spread clinical use," said Papakostas.

The National Institute of Mental Health funded the study. Pharmavite LLC, the manufacturer of Nature Made SAM-e Complete and the leading distributor of SAMe supplements in the United States, provided the SAMe supplements and placebo pills used in the study.

To date, at least 40 clinical trials have been conducted on SAMe directly and in combination with traditional antidepressant medications. Studies have evaluated SAMe's use in naturally restoring a healthy mood to the most recent research for treating major depressive disorders. This current study follows a pilot study published in 2004 in the Journal of Clinical Psychopharmacology, which concluded that antidepressants used in combination with SAMe were significantly more effective in relieving depression than medication alone.

In an accompanying editorial, J. Craig Nelson, M.D., professor of psychiatry at the University California, San Francisco, wrote, "The study of Papakostas, et al. is persuasive. It is the first adjunctive treatment trial of SAMe and the first placebo-controlled trial of oral SAMe since 1993. The era of development for new amine reuptake inhibitors appears to be coming to a close. Some novel approaches appear to be dead ends. SAMe offers a novel mechanism of treatment action and opens up a new area for future exploration. Of course this clinical trial requires replication. And there are numerous other questions about long-term safety and efficacy, comparisons with other adjunctive agents, and selection of appropriate patients. But demonstration of a new treatment for depression with a novel mechanism is exciting news."

Date: August 31, 2010
Source: Porter Novelli

Telomerase-activating compound may help reverse aging

From Sentient Developments blog:

Researchers have discovered a telomerase-activating compound which could eventually be used to reverse aging in humans.

Specifically, a naturally derived compound known as TA-65 has been shown to activate the telomerase gene in humans. The researchers, a collaboration of scientists from Sierra Sciences, TA Sciences, Geron Corporation, PhysioAge, and the Spanish National Cancer Research Center, discovered that activating this gene could prevent the shortening of telomeres at the ends of chromosomes, thereby slowing or even stopping the cellular aging process.

While TA-65 is probably too weak to completely arrest the aging process, it is the first telomerase activator recognized as safe for human use.

"We are on the cusp of curing aging," said William Andrews, Ph.D., co-author of this study and President and CEO of Sierra Sciences, LLC. "TA-65 is going to go down in history as the first supplement you can take that doesn't merely extend your life a few years by improving your health, but actually affects the underlying mechanisms of aging. Better telomerase inducers will be developed in the coming years, but TA-65 is the first of a whole new family of telomerase-activating therapies that could eventually keep us young and healthy forever."

As excited as I am by this discovery, I believe Andrews's statement is considerably overstated. We are still quite a ways off from having interventions that will "keep us young and healthy forever," and it will unlikely be accomplished through the exclusive use of telomerase-activating therapies. Aging is a multi-faceted process that will inevitably require a cocktail of therapies. Moreover, as healthy life span is continually extended, new and unanticipated age-related diseases will crop up.

It's worth noting that, in addition to slowing the cellular aging process, the researchers hope that TA-65 may also help treat diseases which attack the immune system such as HIV/AIDS.

Press release.