Dr Mercola Interviews Dr Villeponteau the Formulator of Stem Cell 100

Dr Bryant Villeponteau the formulator of Stem Cell 100 and other Life Code nutraceuticals was recently interviewed by Dr Mercola who owns the largest health web site on the internet. Dr. Villeponteau is also the author of Decoding Longevity a new book which will be released during December. He is a leading researcher in novel anti-aging therapies involving stem cells an area in which he has been a pioneer for over three decades.

Stem cell technology could have a dramatic influence on our ability to live longer and replace some of our failing parts, which is the inevitable result of the aging process. With an interest in aging and longevity, Dr. Villeponteau started out by studying developmental biology. If we could understand development, we could understand aging, he says. Later, his interest turned more toward the gene regulation aspects. While working as a professor at the University of Michigan at the Institute of Gerontology, he received, and accepted, a job offer from Geron Corporation a Bay Area startup, in the early 90s.

They were working on telomerase, which I was pretty excited about at the time. I joined them when they first started, he says. We had an all-out engagement there to clone human telomerase. It had been cloned in other animals but not in humans or mammals.

If you were to unravel the tip of the chromosome, a telomere is about 15,000 bases long at the moment of conception in the womb. Immediately after conception, your cells begin to divide, and your telomeres begin to shorten each time the cell divides. Once your telomeres have been reduced to about 5,000 bases, you essentially die of old age.

What you have to know about telomerase is that it’s only on in embryonic cells. In adult cells, it’s totally, for the most part, turned off, with the exception of adult stem cells, Dr. Villeponteau explains. Adult stem cells have some telomerase not full and not like the embryonic stem cells, but they do have some telomerase activity.

Most of the research currently being done, both in academia and industrial labs, revolves around either embryonic stem cells, or a second type called induced pluripotent stem cells (iPS). Dr. Villeponteau, on the other hand, believes adult stem cells are the easiest and most efficient way to achieve results.

That said, adult stem cells do have their drawbacks. While they’re your own cells, which eliminates the problem of immune-related issues, there’s just not enough of them. Especially as you get older, there are fewer and fewer adult stem cells, and they tend to become increasingly dysfunctional too. Yet another hurdle is that they don’t form the tissues that they need to form…

To solve such issues, Dr. Villeponteau has created a company with the technology and expertise to amplify your adult stem cells a million-fold or more, while still maintaining their ability to differentiate all the different cell types, and without causing the cells to age. Again, it is the adult stem cells ability to potentially cure, or at least ameliorate, many of our age-related diseases by regenerating tissue that makes this field so exciting.

Dr Villeponteau believes you can add many years, likely decades, to your life simply by eating right, exercising (which promotes the production of muscle stem cells, by the way) and living an otherwise clean and healthy lifestyle. Extreme life extension, on the other hand, is a different matter.

His book, Decoding Longevity, covers preventive strategies to prolong your life, mainly diet, exercise, and supplements. A portion of the book also covers future developments in the area of more radical life extension, such as stem cell technology.

If you would like to read the entire interview here is a link to the text version:

Click here for more information about Stem Cell 100

Transcript of Interview With Dr. Bryant Villeponteau by Dr. Joseph Mercola

Aging Reversed / ABC News

Now researchers have found a way not just to stop, but, reverse the aging process. The key is something called a telomere. We all have them. They are the tips or caps of your chromosomes. They are long and stable in young adults, but, as we age they become shorter, damaged and frayed. When they stop working we start aging and experience things like hearing and memory loss.

In a recent study published in the peer reviewed journal Nature scientists took mice that were prematurely aged to the equivalent of 80-year-old humans, added an enzyme and essentially turned their telomeres back on. After the treatment they were the physiological equivalent of young adults. You can see the before and after pictures in the videos above. Brain function improved, their fertility was restored it was a remarkable reversal of the aging process. In the top video the untreated mouse shows bad skin, gray hair and it is balding. The mouse with it’s telomeres switched back on has a dark coat color, the hair is restored and the coat has a nice healthy sheen to it. Even more dramatic is the change in brain size. Before treatment the aged mice had 75% of a normal size brain like a patient with severe Alzheimers. After the telomeres were reactivated the brain returned to normal size. As for humans while it is just one factor scientists say the longer the telomeres the better the chances for a more graceful aging.

The formal study Telomere dysfunction induces metabolic and mitochondrial compromise was published in Nature.

Additional information published by Harvard can be found in the following articles.

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

While scientists are not yet able to accomplish the same results in humans we believe we have developed a nutraceutical to help prolong youth and possibly extend life until age reversal therapy for humans becomes available.

Stem Cells Secret’s of 115 Year Old Woman

New evidence that adult stem cells are critical to human aging has recently been published on a study done on a super-centenarian woman that lived to be 115 years. At death, her circulating stem cell pool had declined to just two active stem cells from stem cell counts that are typically more than a thousand in younger adults. Super-centenarians have survived all the normal diseases that kill 99.9% of us before 100 years of age, so it has been a mystery as to what actually kills these hardy individuals. This recent data suggest that stem cell decline may be the main contributor to aging. If so, stabilizing stem cells may be the best thing one can do to slow your rate of aging.

There are many theories of aging that have been proposed. For example, damage to cells and tissues from oxidative stress has been one of the most popular fundamental theories of aging for more than half a century. Yet antioxidant substances or genes that code antioxidant enzymes have proven largely ineffective in slowing aging when tested in model animals. Thus, interest by scientists has shifted to other hypotheses that might provide a better explanation for the slow declines in function with age.

Stem cells provide one such promising mechanism of aging. Of course, we all know that babies are young and vigorous, independent of the age of their parents. This is because adults have embryonic stem cells that can generate young new cells needed to form a complete young baby. Indeed, these embryonic stem cells are the product of continuously evolving stem cell populations that go back to the beginning of life on earth over 3.5 billion years ago!

In adults, the mostly immortal embryonic stem cells give rise to mortal adult stem cells in all the tissues of the body. These adult stem cells can regenerate your cells and tissues as they wear out and need replacement. Unfortunate, adult stem cells also age, which leads to fewer cells and/or loss of function in cell replacement. As functional stem cells decline, skin and organs decline with age.

Blood from world’s oldest woman suggests life limit

Time Magazine: Long-Life Secrets From The 115-Year-Old Woman

Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis

Abstract
The somatic mutation burden in healthy white blood cells (WBCs) is not well known. Based on deep whole-genome sequencing, we estimate that approximately 450 somatic mutations accumulated in the nonrepetitive genome within the healthy blood compartment of a 115-yr-old woman. The detected mutations appear to have been harmless passenger mutations: They were enriched in noncoding, AT-rich regions that are not evolutionarily conserved, and they were depleted for genomic elements where mutations might have favorable or adverse effects on cellular fitness, such as regions with actively transcribed genes. The distribution of variant allele frequencies of these mutations suggests that the majority of the peripheral white blood cells were offspring of two related hematopoietic stem cell (HSC) clones. Moreover, telomere lengths of the WBCs were significantly shorter than telomere lengths from other tissues. Together, this suggests that the finite lifespan of HSCs, rather than somatic mutation effects, may lead to hematopoietic clonal evolution at extreme ages.

Blue Light can Accelerate Aging Even if it Doesn’t Reach Your Eyes

Although blue light may not be shining in someones eyes, it can still affect a person’s longevity. A new study has suggested that the blue wavelengths which are produced by light emitting diodes from phones, household fixtures and computers damage cells in the brain and in the retinas.

The research conducted at Oregon State University utilized the common fruit fly in its study as it is an important model organism due to its developmental and cellular mechanisms which it shares with other animals and also humans.

The team examined how fruit flies respond to daily 12 hour exposure periods to blue LED light. This is light that is similar to the blue wavelengths in devices such as tablets and phones. They found that the blue accelerated aging in the fruit flies.

Flies that were subjected to the daily 12 hours in light and then 12 hours in darkness had shorter lives when compared to flies that were kept in total darkness or those that had been kept in light with the blue wavelengths filtered out. The fruit flies that had been exposed to blue light showed damage to their brain neurons and retinal cells and also had impaired locomotion. Their ability to climb the walls in their enclosures which is a common behavior, was diminished.

Some of the flies used in the study were mutants that do not develop eyes and those eyeless flies also experienced locomotion impairments and brain damage. This suggests that flies don’t have to see the blue light to become harmed by it.

The team was initially surprised that the blue light accelerated the aging process in the flies. They measured expression of genes in the older flies and discovered that stress response, protective genes were expressed when the flies were kept in the light. They hypothesized that light was regulating the genes. They then wondered if it is the light that is harmful so they looked at the spectrum of light. It was quite clear that although light without the blue light slightly shortened the flies lifespan, blue light alone shortened their lifespan quite dramatically.

Natural light is critical for the body’s circadian rhythm which is the 24 hour cycle of physiological processes such as hormone production, brain wave activity, and cell regeneration which are important to sleeping and feeding patterns. There is evidence that suggests that increased exposure to artificial light is a risk factor for circadian and sleep disorders. With the widespread use of LED device displays and lighting, people are exposed to increasing amountsof light in the blue spectrum. Commonly used LEDs emit a high fraction of blue light. However, LED lighting has not been used for a long enough period to know its effects across the lifespan of humans.

Flies when given a choice avoid blue light. The team is going to test to see if the same signaling that causes them to escape blue light in involved in longevity. Advances in medicine and technology could work together to address the damaging effects of blue light if the research in flies proves applicable to humans.

As science looks for a variety of ways to help people stay healthy as they live longer, creating a healthier spectrum of light may be a possibility, not only in terms of better sleep, but in terms of overall health.

There are a few things people can do to protect themselves that do not involve being in darkness for hours. Eyeglasses that have amber lenses will filter out blue light and will protect the retinas. Some laptops, phones and other devices can be set to reduce blue emissions. Blue light screen filters can be purchased and cut to size for almost any device including LED televisions. Special light bulbs are available that are filtered to reduce or eliminate blue light. These products can be found on Amazon.com or LowBlueLights.com. In the future there might be phones that auto adjust their display depending on length of usage which the phone perceives. This kind of phone while most likely difficult to create, would have a big impact on health.

To view the original scientific study click below

Daily blue-light exposure shortens lifespan and causes brain neurodegeneration in Drosophila.

Improved Cardiac Regeneration Developed

A novel multi pronged approach for concurrently rejuvenating both the vasculature and cardiac muscle of the heart has been recently developed. The results give hope to developing a new treatment for repairing hearts that have been damaged by myocardial infarction. This new therapy could serve as an alternative to heart transplants

The joint research team consisted of scientists and researchers from City University of Hong Kong along with other organizations, conducted the first study that involved two distinct stem cell effects for cardiac repair. The aim was to concurrently rejuvenate both the vasculatures and heart muscles by using two major stem cell types – bone marrow derived mesenchymal stem cells (hMSCs) and cardiomyocytes which were derived from induced pluripotent stem cells. (hiPSC-CMs).

The hMSCs was used in the study because of their prominent paracrine activity of secreting good proteins which promote the regeneration of blood vessels and endothelial cell survival. The other stem cell type, hiPSC-CMs, was used because of their similarities with human primary CMs in terms of their expressions of structural proteins, cardiac specific genes, ion channels and most importantly their spontaneous contraction.

Earlier studies describe the beneficial effects of either hMSCs or hiPSC-CMs on a myocardial infarction (MI) separately. The recent study was the first to simultaneously study the effects of these two distinct stem cells for cardiac repair. The team used a dual approach in which the hiPSC-CMs and hMSCs were delivered by two distinct routes. The hiPSC-CMs were injected intramyocardially directly into a border zone of a rat’s heart. The hMSCs loaded patch was implanted on top of the infarct area similar to a bandage.

The results of the study indicate that this dual approach showed a significant improvement in cardiac function and enhancement of vessel formation on a MI heart. The hMSC loaded patch not only provided a micro environment which enhanced vascular regeneration which was expected, but in addition showed improvement in the retention of hiPSC-CMs. Ultimately this augmented heart function and also restored the injured myocardium.

In addition, histological analysis demonstrated that the implanted hMSC loaded patch promoted the functional maturation of injected hiPSC-CMs. They became more rectangular and elongated in cell shape and appeared to be more organized in order which are typical morphological characteristics of mature adult CMs. Functional maturation of intramyocardially hiPSC-CMs is very important because it can reduce the potential risk of arrhythmia’s which are a major cause of sudden cardiac death.

The team believe the novel dual approach could potentially provide clinical and translational benefits to the field of cardiac regeneration. Using the same principle, the protocol could be utilized in repair of other organs including the liver, pancreas and brain where multiple types of stem cells co exist.

The team is now working on additional studies using larger animals such as pigs and they have applied for a patent.

To view the original scientific study click below

Dual stem cell therapy synergistically improves cardiac function and vascular regeneration following myocardial infarction.

Transplanted Brain Cells Survive without Anti-Rejections Drugs

Through experiments using mice, researchers have developed a method to successfully transplant a particular kind of protective brain cells without the use for life long anti-rejection drugs. The team at Johns Hopkins Medicine, have selectively circumvented the immune response against foreign cells which allows for transplanted cells to survive and even thrive and protect brain tissue after immune suppressing drugs have been discontinued.

A significant obstacle to the ability to replace brain cells is the mammalian immune system. The immune systems works by quickly identifying non self or self tissues and then mounting attacks to destroy foreign or non self invaders. This is beneficial when targeting viruses and bacteria, however it is a significant hurdle for transplanted organs, tissues or cells which are also flagged for destruction.

Traditional anti rejection medications that unspecifically and broadly tamp down the immune system at once frequently work to fend off tissue rejection. This leaves the patient vulnerable to infection and a variety of other side effects. Patients need to continue with these drugs indefinitely.

The Johns Hopkins Medicine team sought out ways to manipulate T cells which are the immune system’s elite infection fighting force that goes after foreign invaders. Specifically, they focused on a series of so called costimulatory signals that T cells must encounter in order to start an attack.

These particular signals are in place to help ensure the immune system cells don’t go rogue by attacking the body’s own healthy tissues. The idea is to exploit the normal tendencies of these signals as a means of training the immune system to eventually accept transplanted cells as self permanently.

To accomplish this, the team used two antibodies, CTLA4-lf and anti-CD154 which keep T cells from initiating an attack when they encounter foreign particles by binding to the surface of the T cell which essentially blocks the go signal. This particular combination was previously used successfully to block the rejection of solid organ transplants in animals, however had not been tested for cell transplants to repair the myelin in the brain.

In a significant set of experiments, the team injected the brains of mice with the protection glial cells which produce the myelin sheath that surrounds neurons. These very specific cells were genetically engineered to glow so that the team could keep track of them.

The glial cells were transplanted into three mice types. This included mice that were genetically engineered to not form the glial cells which create the myelin sheath, normal mice and mice that were bred to be able to mount a response of the immune system. They used the antibodies to block an immune response, concluding treatment after six days.

Each day the team used a specialized camera that could detect the glowing cells and capture pictures of the mice brains. They were particularly looking for the relative absence or presence of the transplanted glial cells. Cells that had been transplanted in the control mice that had not received the antibody treatment immediately started to die off. Their glow was no longer seen by the camera by day 21.

The mice which had received the antibody treatment were able to maintain significant levels of the transplanted glial cells for more than 203 days. This indicated they were not killed by the mouse’s T cells even in treatment absence.

The fact that any glow had remained showed the team that cells had survived the transplantation even long after stopping the treatment. This was interpreted as a success in selectively blocking the immune system’s T cells from killing the cells that had been transplanted.

The next step for the team was to see whether the transplanted glial cells would survive well enough to do what glial cells typically do in the brain which is create the myelin sheath. To accomplish this, the team looked for key structural differences between the mouse brains which contained thriving glial cells and those without using MRI imaging. The team discovered in the images the cells in the treatment mice were indeed populating the appropriate portions of the brain.

The results confirmed that the cells that had been transplanted had the ability to thrive and assume their normal function which is to protect the brain neurons. The results are preliminary, however the team was able to deliver these cells and allow them to thrive in a localized part of the mice brains.

For the future, the teams hopes to combine their findings with additional studies on cell delivery methods to the brain to help in repairing the brain on a more global scale.

To view the original scientific study click below

Induction of immunological tolerance to myelinogenic glial-restricted progenitor allografts.

Is it Better to Work Out Before or After Breakfast?

A new study has found that just be changing when you eat and exercise, you can have achieve better control of blood sugar levels. The study by health scientists at the Universities of Birmingham and Bath, shows that exercising before breakfast burns more fat which improves the body’s response to insulin and can lower people’s risk of cardiovascular disease and type 2 diabetes.

This six week study involved thirty men who were classified as overweight or obese and compared the results from two intervention groups. One group were those who are breakfast then exercised. The other control group were those who made no lifestyle changes. The results showed that people who exercised before breakfast burned double the amount of fat compared to the group who exercised after breakfast.

The researchers found that increased fat use is mostly due to lower insulin levels during exercise when a person has fasted overnight. This means that they can use more fat from their fat tissues and the fat found in their muscles as fuel. To test the proof of the principle, the first study involved only men. Future studies will look to translate their findings for different groups of people including women.

While the results did not lead to any differences in weight loss over the six week period, it did show positive and profound effects on the participant’s health. Their bodies were better able to respond to insulin which kept blood sugar levels under control which can potentially lower the risk of heart disease and diabetes.

The team behind the study sought to focus on the impact of the fat stores in muscles for people who either worked out after or before eating and the effect the timing had on insulin response to eating. This study built on emerging evidence that timing of meals in relation to when a person’s exercises can shift how effective exercise is.

The results suggest that by changing the timing of when a person eats in relation to when they choose to exercise, very positive changes to overall health can occur. The group of men who exercised prior to breakfast increased their ability to respond to insulin which is remarkable given that both groups lost a similar amount of weight and both groups gained a similar amount of fitness. The only difference between the groups was the timing of breakfast.

The scientists also found that the muscles from the group of men who exercised prior to breakfast were more responsive to insulin in spite of identical food intake and training sessions. The muscles from this group showed increased key proteins, specifically those which are involved in transporting glucose from the blood stream to muscles.

The study shows that engaging in exercise after an overnight fasted state can increase the health benefits without a change in duration, intensity, or perception of their effort. The team now look to explore the longer term effects of the timing of exercise and eating and whether women will show similar benefits to those found with the men in the study.

To view the original scientific study click below

Lipid metabolism links nutrient-exercise timing to insulin sensitivity in men classified as overweight or obese.

Plastic Teabags and Possible Health Effects

While many people are doing their part in reducing plastic use, there are some tea manufacturers who are actually moving in the opposite direction. Some tea producers are replacing the traditional paper teabags with plastic teabags. A new study has found that those plastic teabags may come with a bit of micro and nano sized plastics which are shed from the bag. What is unknown at this time, is what possible effects on health could come from ingesting these particles

Plastics break down into tiny microplastics and even smaller nanoplastics over time. Nanoplastics are less then 100 nanometers in size which is less than the diameter of a human hair. Scientists have discovered these microscopic particles in aquatic organisms, in the environment and even in the food supply.

Microplastics are found everywhere. Much of our food is wrapped in plastic and often ends up in our food. It also leaches out into the environment. Plastics can end up in things like canned fish, sea salt, honey and chicken.

The study team wondered if these recently introduced plastic teabags could be releasing micro and nanoplastics into the tea during brewing. They also wanted to explore possible effects of the released particles on small aquatic organisms known as water fleas. These are model organisms commonly used in environmental studies.

To conduct the analysis, the team bought four different varieties of commercial teas which were packaged in plastic teabags. They opened the bags, removed the tea leaves then washed the empty bags. They then heated the plastic teabags in containers of water to stimulate the brewing conditions.
To ensure cutting the teabag did not influence the number of particles released, they also used several teabags that had not been emptied or rinsed out.

For each brand tested, three emptied teabags were placed in a clean, single glass vial and then steeped in 10 milliliters of 95 degree Celsius water for a period of five minutes. The teabags were then removed and the water poured into another clean glass container.

By using electron microscopy, the research team took images of the teabags both before and after steeping and their chemical composition analyzed. After brewing, the teabag water was fixed to silicon wafers and dried and Nanoparticle Tracking Analysis was used to count the particles.

They found that the teabags showed significant cracking and degradation after the steeping process. They found that just a single plastic teabag at a brewing temperature of 95 degrees Celsius released about 11.6 billion microplastic and 3.1 billion nanoplastic particles into the brewed water.

These levels are thousands of times higher than those that had been previously reported in other foods. Currently it is estimated that people consume over 74,000 particles of microplastics per year. According to the new study, there is almost 200,000 times that amount in a single cup of plastic teabag tea. The team estimated that a tea drinker would swallow 2.3 million micron sized and 14.7 billion submicron particles in a single cup of tea.

In a different experiment, the team treated water fleas with a variety of doses of the micro and nanoplastics from the teabags. The fleas survived, however they did show some behavioral and anatomical abnormalities.

More research is needed for scientists to determine if drinking tea laced with plastic could lead to negative health effects on people. Very little research has been conducted on human health and the toxicity of microplastics. If these products remain on the shelf, there needs to be a big push do conduct more toxicity tests.

To avoid the possibility, the best bet is to choose paper teabags or loose leaf tea. However, some paper teabags are reinforced with plastic so one needs to do their homework to insure they are purchasing 100% paper teabags.

To view the original scientific study click below

Plastic Teabags Release Billions of Microparticles and Nanoparticles into Tea

Napping for Heart Health

A new study has shown that naps are associated with a lower risk of heart disease. Occasional napping can cut a person’s risk of strokes, heart disease and heart attack by half when compared to those who don’t nap.

The health benefits of napping have been debated for years. Earlier research was inconclusive. Many argue that the studies failed to consider frequency of napping as an important factor.

The research team at the University of California collected data from almost 3,500 randomly selected residents of Lausanne, Switzerland between the ages of 35 and 70. They analyzed the associations between average nap duration and nap frequency effects on the risk of cardiovascular disease over a 5 year period which indicated some interesting trends.

About 58% of the participants did not take naps at all. One in five participants took 1 to 2 occasional naps on a weekly basis and this was associated with a 48% decrease in the risk of a cardiovascular event. One in 5 who were frequent nappers of 3 to 7 naps on a weekly basis, who tended to be male and older, also weighed more, slept longer at night, smoked often, reported more daytime sleepiness and were more likely to have sleep apnea, had a 67% increase in risk of heart disease.

However, when the team took into account lifestyle; cardiovascular risk factors such as age, hours of sleep per night, and disease risks; and sociodemographic, the risk for cardiovascular disease among occasional nappers disappeared.

Initially, frequent napping seemed to increase a person’s risk of heart disease by 67%. That disappeared after taken into account the other factors. This suggests that napping may have a positive impact on cardiovascular disease. Furthermore, no associations with cardiovascular events were found for length of naps – from 5 minutes to 1 hour and more.

The study was observational so it can’t be assumed that napping directly contributed to the decrease risk of heart disease. However, it does contribute to the ongoing debates over health benefits due to napping. Sleep researchers have never completely defined a nap and different cultures look at naps differently. Some sleep researchers say a 20 to 30 minute nap in the early afternoon is the perfect nap.

The study also suggest that might not only be the duration of the naps, but also the frequency that matters. The study of napping is very challenging given it is largely dependent on data. There remains many more questions than answers, however it is time to begin unveiling the power naps may provide for a supercharged heart!

To view the original scientific study click below

Association of napping with incident cardiovascular events in a prospective cohort study.

Humans Have Ability to Regrow Joint Cartilage

Researchers have discovered, contrary to popular belief, that human joint cartilage can repair itself. It does it in a manner similar to that used by creatures such as zebrafish and salamanders. This finding could potentially lead to treatments for osteoarthritis which is the most common disorder of joints in the world.

The research team identified a mechanism for repair of cartilage that seems to be more robust in ankle joints and less so in hips. They believe that further understanding of this salamander like regenerative capacity in humans combined with the critically missing components of this regulatory circuit, might provide a foundation for new approaches for joint tissue repair and even whole human limbs.

The team created a way to determine the age of proteins through internal molecular clocks which are integral to amino acids. These amino acids convert one form to another with predictable regularity.

Proteins which are newly created in tissue have very few or no amino acid conversions. Older proteins actually have many. Through understanding this process, the team was able to use sensitive mass spectrometry to identify when key proteins found in human cartilage, including collagens, were young, middle aged or old.

The team discovered that cartilage age depends largely on where it resides in the body. Cartilage found in the ankles is young, middle aged in the knee and older in the hips. This correlation between the location of cartilage in the body and age aligns with how repair of limbs occurs in certain animals which more readily regenerates at the furthest tips such as the ends of tails and legs.

Additionally, the findings also explain why injuries to the knees and especially the hips, take a long time to heal and often times develop into arthritis. Ankle injuries typically heal much quicker and are less prone to becoming severely arthritic.

The team also learned that molecules which are known as microRNA regulate this process. These microRNAs are much more active in animals that are known for tail, fin or limb repair including zebrafish, salamanders, and African fresh water fish and lizards.

Humans also have these microRNAs…an evolutionary artifact which can provide humans the ability for repair of joint tissue. Similar to animals, microRNA activity is significantly different depending on its location. It is highest in ankles compared to the knees and hips and also higher in the top layer of cartilage as compared to deeper levels of cartilage.

The team explains that the regulators of regeneration in the limbs of salamanders appears to also be the controllers of repair of joint tissue in human limbs. They are calling it the “inner salamander” capacity. They believe microRNAs could be developed as treatments that might prevent, slow or even reverse arthritis.

They believe there is the ability to boost these regulators to fully regenerate cartilage that has degenerated in an arthritic joint. By figuring out what regulators are missing compared with salamanders, they may be able to add the missing components back and then develop a way to regenerate part or even all of an injured human limb. The team believes this is a fundamental mechanism for repair that could be applied not only to cartilage, but also many tissue types.

To view the original scientific study click below

Analysis of “old” proteins unmasks dynamic gradient of cartilage turnover in human limbs.

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