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 an 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:

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

lroot on January 16th, 2019

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.

lroot on January 14th, 2019

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

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.

lroot on January 11th, 2019

noise pollution

Results from a study conducted by the Barcelona Institute for Global Health have shown that people who are exposed to the highest levels of traffic noise are at an increased risk of becoming obese. Even just a 10 dB increase in mean noise levels was shown to be associated with a 17% increase in developing obesity.

The study began when the researchers wanted to confirm whether results from earlier studies demonstrated a correlation between several markers for obesity and traffic noise. The study involved 3796 adult participants in the population based Swiss SAPADIA cohort study and had also attended a minimum of two follow-up visits between years 2001 and 2011.

The study was based on objective measures including participants height, weight, waist circumference, body mass index and abdominal fat. The data was then analyzed along with estimates of exposure to traffic noise which was developed in the context of the Swiss SiRENE project.

The researchers also analyzed exposure to noise generated from railway traffic and aircraft. They did not find any significant correlation except in long term exposure to the railway noise which was not associated with obesity but was associated with an increased risk of overweight.

The design and methodology of the study were selected to allow the team to review all data from two different perspectives. Cross sectional analysis was used to examine more objective measures and to study the participant population at a specific time.

The other study, a longitudinal design, allowed the team to evaluate how the increased risk of obesity evolved over the time frame of the study. The correlations with traffic noise pollution were consistent in both studies. Overweight only correlated with exposure to noise from traffic in the cross section study. The team did not find any correlation between body mass index and noise exposure which was measured continuously throughout the longitudinal study.

This study adds additional evidence to further support the hypothesis that obesity is affected by traffic related noise. The results of this study which were obtained in a different population from earlier studies were similar. However, the team indicates that additional longitudinal studies are needed to further confirm correlation and to examine some inconsistencies with the data which prevented the team from formulating an explanation that would be accepted by the scientific community.

Repeated exposure to noise pollution is a widespread public health problem. Noise is a stress factor that contributes to communication, rest and sleep. A variety of studies have shown that noise contributes to a risk of a variety of diseases and it alters our sleep and generates stress. Hormone levels can be altered and sleep disturbances deregulate glucose metabolism and will also alter appetite. When sleep patterns are disturbed, the immune system functions can be affected along with control of appetite and expenditure of energy.

Several epidemiological and experimental studies have shown a correlation between sleep deprivation and increased risk of obesity and overweight. A potential link between long term exposure to noise and the increased risk of obesity may contribute to stress and sleep quality.

The research has shown some indication that reducing traffic related exposure to noise may be a way to combat obesity. For instance noise reducing foam can be installed in corners of rooms to absorb and decrease sound levels.

To view the original scientific study click here: Long-term exposure to road traffic noise may increase the risk of obesity.


One huge question that fitness experts and scientists are curious about is whether nutrition or exercise has the most positive impact on bone strength. Researchers at the University of Michigan set out to answer that question by looking at mineral supplementation and exercise in mice.

The research team discovered surprising results. They found that nutrition had a greater impact on strength and bone mass over exercise. Even when the exercise training was discontinued, the mice retained gains in bone strength as long as they remained on a mineral supplemented diet.

The long term mineral supplementation diet not only led to increased strength and bone mass, but the ability to maintain the increase even after training was discontinued. Although the test was conducted on mice, in regards to the progression to humans diet is much easier for people to carry on as they age and are not able to do as much exercise or any at all.

Another important finding was that diet alone has benefits on bone even without the exercise. This is another surprise as the team expected that exercise with a normal diet would result in greater gains in bone strength but that wasn’t the case. However, combining the two amplifies the gains.

The team looked at increased calcium and phosphorus and found benefits to increasing both of their supplements. This doesn’t mean that people should start buying and consuming these two supplements. The findings don’t translate directly from the mice to humans. However, it does give the researchers a conceptual place to begin.

Humans achieve peak bone mass in their early twenties with declines after that. The question now is how to maximize the amount of bone mass while young so that when the declines do begin, people are at a better place.

The team also preformed a battery of mechanical assessments on bone. Bone doesn’t always predict or scale with the mechanical quality of the bone tissue. The mice were tested after eight weeks of training plus a supplemented diet or a normal diet and then after eight weeks of no training.

Calcium is one of the major building blocks of our bone tissue, however there are many other minerals and nutrients also needed including magnesium, silicon, manganese, boron, vitamin K2, vitamin D3 and vitamin C. Some of the best bone building foods are green leafy vegetables such as kale, swiss chard, and collard greens which contain many of these nutrients.

To view the original scientific study click here: Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice

lroot on December 21st, 2018


Lutein is a potent antioxidant that offers a wide range of health benefits. It is best known for protecting the eyes and spinach along with other dark leafy vegetables contain the highest levels. Interestingly, a new study from Linkoping University, Sweden, has found that how you prepare fresh spinach and other dark green leafy vegetables can maximize lutein. Of course there are many other nutrients in natural foods that are also better preserved and absorbed using the same approach.

This study allowed the team to see what influence the level of lutein in the blood would have by increasing dietary intake of this antioxidant. The research group studied which method of spinach preparation allowed the greatest benefit of lutein maximization. Spinach was chosen as the vegetable of choice for the study because it contains comparatively high levels of lutein and is also consumed by many people.

Preparation methods that are typically used at home were used in the study. The researchers compared several temperatures and heating times along with cold preparations such as spinach in salads and in smoothies.

The research team used baby spinach from a supermarket in their study. The spinach samples which were prepared in cooked fashion were fried, steamed, and boiled for up to 90 minutes and the lutein content was measured at different times. The team also compared different heating times. Lutein like other nutrients degrades with heat.

The results shows that heating time was important when spinach is boiled. The longer the spinach is boiled the less lutein is retained. When spinach is fried at a high temperature, a large amount of lutein was degraded after just two minutes. And more lutein was lost when spinach was baked in the oven at a higher temperature than when it is cooked in a soup or stew.

The study did show that reheating spinach in the microwave actually compensated for some loss of lutein. More lutein was released from the spinach as the plant structure was further broken down by microwaving.

The best way to maximize lutein from spinach is to not heat it at all. Eating it raw in a salad or adding it to a smoothie gains the most benefits. And when spinach is chopped into small pieces and then a fat added such as a dairy product in a smoothie, more lutein is released and the fat actually increases the solubility of the lutein in the fluid.

Spinach is just one of the great sources of lutein. Other sources include kale, brussel sprouts, parsley, broccoli and peas along with orange juice, kiwi, red peppers, squash and grapes. As concluded in the above study, consuming any of the sources in their raw form gains the most benefits from lutein.

To view the original scientific study click here: Liberation of lutein from spinach: Effects of heating time, microwave-reheating and liquefaction.

lroot on December 20th, 2018

pothos ivy

Pothos Ivy just got a remake and will now remove benzene and chloroform from the air around it! Researchers at the University of Washington genetically modified this common houseplant and the resulting plant can clean these two pollutants which are hazardous compounds that are too small to be trapped in HEPA air filters.

Benzene which is a component of gasoline can build up in homes when we store lawn mowers and cars in attached garages. Even burning candles produce this compound. Chloroform is present in small amounts in chlorinated water and can be released when we take showers or boil water. Both compounds have been found to be linked to cancer. They aren’t commonly talked about because previously nothing could be done about them in our homes.

The modified Pothos Ivy plants express a protein called 2E1 which will transform these compounds into molecules which the plants will then use to support their growth. The process took 2 years and while other lab plants might only take a few months to achieve the intended results, the team chose the pothos because it is a robust houseplant that grows very well under a variety of conditions.

The researchers used a protein called cytochrome P450 2E1 or 2E1 for short, which is present in all mammals including humans. This protein turns chloroform into carbon dioxide and chloride ions and turns benzene into a chemical called phenol. However, 2E1 is located in our livers and is actually turned on when we consume alcohol. It is not available to us to help us process any pollutants in the air.

The team decided to have this reaction occur outside the body in a plant which they call an example of the “green liver” concept. The p450 2E1 cytochorme was taken from rabbits. It was then introduced into the pothos ivy so that each cell would express the protein. Pothos ivy does not flower in temperate climates so the genetically modified plants would not be able to spread via pollen.

They then tested how well the modified plants could remove the two pollutants from air compared to how well normal pothos ivy would preform. Both types of plants were put in glass tubes and then either chloroform gas or benzene was added. Over the following 11 days the team tracked how the concentration of each pollutant changed in the tubes.

The concentration of chloroform gas did not change over time in the unmodified plants. But the concentration of chloroform dropped by 82 percent after three days in the modified plants. And by the sixth day was almost undetectable. The benzene concentration also decreased in the modified plants, however more slowly. By the eighth day though the benzene concentration dropped by almost 75 percent. Normal pothos ivy only broke down less than 10 percent in the first week.

The team did use much higher pollutant concentrations that would typically be found in homes so they could detect changes. They anticipate that the levels of the two pollutants would drop similarly in homes and perhaps even faster over the same time frame.

If used in the home, the plants would need to be inside an enclosure with something to move the air past the leaves such as a fan. A plant sitting in a corner will have some effect on that particular room, but without airflow it would take a longer time for a molecule on another side of the room to reach the plant. And the transgenic plant also produces a green fluorescent protein that glows under UV light. This was added to make the plant more appealing and also to make it easy to spot!

The research team is now working on increasing the plants capabilities by adding a protein which can break down another hazardous molecule found in homes which is formaldehyde. This compound is present in some wood products such as laminate flooring and cabinets and in tobacco smoke.

All these hazardous compounds are very hard to get rid of. Without proteins to break down the molecules, high energy processes would have to be used. It makes more sense, is simpler and more sustainable to put the proteins all together in a common houseplant. And 2E1 is beneficial to the plant since they use chloride ions and carbon dioxide to make their food, and they use phenol to help make components of their cell walls.

The plant may soon be available in Canada where it does not grow outside. However it does grow in southern Florida so to get approval in the United States the research team has to show that the genetically modified pothos plant is no more likely to cause problems as a weed than regular pothos. Until it is available spider plants remove many pollutants so can be used in homes to help purify the air.

To view the original scientific study click here: Greatly Enhanced Removal of Volatile Organic Carcinogens by a Genetically Modified Houseplant, Pothos Ivy (Epipremnum aureum) Expressing the Mammalian Cytochrome P450 2e1 Gene. Environmental Science & Technology, 2018; DOI: 10.1021/acs.est.8b04811

lroot on December 11th, 2018

waking up

A study conducted by Raphael Vallat, Ph.D. at The University of California, Berkeley, has shown why people have a hard time waking up in the morning. Sleep Inertia or brain fog is real and makes it difficult for some people to drag themselves out of bed in the morning.

Early risers might deny it but as evidenced by the study, brain fog can take quite a while to dissipate and prior to the current study, researchers weren’t sure why it existed. Dr. Vallat asserts that even though the body is awake and moving in the morning, the brain can be asleep in some capacity following the wake up time.

When a person wakes up from sleeping, the brain doesn’t immediately switch from that sleeping state to a fully awakened state. Instead it goes through a transition period called sleep inertia which can last even up to 30 minutes after awakening. During this particular period, the brain will progressively switch from sleep to a normal wakefulness and our mental & cognitive performance does also.
To test this transitional period and prove how real it is, the team had 34 participants take 45 minute naps during which time they entered two periods of a deep sleep which are known as N2 and N3. The participants did not however enter REM (Rapid Eye Movement) sleep which is the deepest type of sleep. Upon awakening, Dr. Vallat tested the participants alertness using two subtraction tests which was one five minutes after awakening and one 25 minutes after awakening.

Similar to anyone who has experienced brain fog, the participants tended to make more mistakes after awakening, and their brain scans revealed why this happened. When a person is awake, the brain switches between two different modes which occur in two separate circuits. One is the task active mode such as when we are being productive or reading, and the second one is non focused task negative mode which is mind wandering. When we are awake we oscillate between the two modes and when the task active mode is functioning, there will usually be a decrease in activity with the task negative circuit.

What causes the sleep inertia to be different is the brain struggling to switch fluidly between the two circuits. It seems the brain is not really able to switch between these two different modes during sleep inertia resulting in lower performance with a mental calculation task.

The research team’s results indicate that during the period of sleep inertia the brain will slowly regain its ability to switch between the two modes divided by functional segregation. They believe it will take about 30 minutes to ultimately achieve this.

Unfortunately, they know there isn’t much a person can do to speed up their wake up process. Even a caffeine boost is not a true solution. There were some results that indicated caffeine increased the functional segregation between the two modes (task active and task negative networks) resulting in an enhancement of the brain’s ability to switch between the two modes. But it seems it does not actually work rapidly enough to cut through sleep inertia.

Caffeine takes about 30 to 60 minutes to reach peak level. Sleep inertia dissipates in about 30 minutes which is before the caffeine would even begin to work on the body. Instead of trying to caffeinate through slow brain functioning, Dr. Vallat suggests the only real fix for sleep inertia is time. Waiting a few minutes before making important decisions or hitting the road running is the best tonic especially if waking up from a very deep slumber.

lroot on December 10th, 2018


In an effort to assist people with muscle disorders, researchers at The University of Texas Health Science Center at Houston have engineered a new line of stem cells to study how they may be converted into muscle.

Muscle disorders which affect over 50,000 people in the United States cause muscles to deteriorate and weaken. And in very severe cases, they can involve respiratory and cardiac muscles which can lead to death. Currently there are no cures for these types of disorders.

The team engineered a new human stem cell line just for skeletal muscle. By tagging the muscle genes which are known as PAX7 and MYF5 with two fluorescent proteins, they were able to ensure the purity of the muscle stem cells. They screened several bioactive compounds in order to improve formation of muscle from stem cells. They also used color tags to observe muscle stem cell activity.

In the lab which was at the Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases at UT, the researchers used CRISPR/Cas9, a gene editing method, to add the fluorescent color tags to the genes.

The stem cells which were generated from the patient’s stem cells were used to generate muscle. The team’s current research provided a step by step road map to make these stem cells into muscle stem cells.

Within a culture of human tissue, the stem cells that had been modified showed promising results. Additionally they showed promise in a mouse model of Duchenne muscular dystrophy. Compared to previous studies, the new strategy allowed more efficient and faster generation of muscle stem cells and with superior engraftment in the mice.

The team believes these muscle stem cells will be used by researchers initially to study the pathophysiology of muscular diseases and to create disease models that researchers are able to use to test promising treatments or to evaluate gene correction efficiency.

It is hoped that the cells can someday be used as a form of stem cell therapy. Our bodies our constantly replacing our skeletal muscle cells. However, muscle disorders make it difficult to replenish muscle because of the exhaustion and failure of muscle stem cells.

To view the original scientific study click here: A Myogenic Double-Reporter Human Pluripotent Stem Cell Line Allows Prospective Isolation of Skeletal Muscle Progenitors

lroot on December 3rd, 2018

back pain

Degeneration of the intervertebral disc is a very common problem which afflicts a large group of our population. Both neck and back pain are very often the result of progressive damage of the discs which separate our spinal vertebrae.

Healthy intervertebral discs work by absorbing stress which has occurred on the spine during movement. They then adjust our posture so we can move freely. If the discs wear out, pain develops in a variety of areas in a person’s neck and/or back.

Currently treatments for this disc degeneration have included replacing the damaged discs with new artificial ones or spinal fusion surgery. These approaches unfortunately have limited benefits because they cannot replace the full function of the discs they replace.

Now a research team at the University of Pennsylvania’s Perelman School of Medicine, School of Veterinary Medicine and the School of Engineering and Applied Science are aiming to solve this problem. They are working on developing bioengineered intervertebral discs which are harvested and made out of a person’s own stem cells. Because stem cells are undifferentiated cells which have the ability to transform into specialized cells, they are the focus of a variety of medical research studies.

For the past 15 years the team at the University of Pennsylvania has been working on these new disc models beginning with lab studies, then progressing to studies on small animals, and now recently studies on large animals.

Previously the team tested the new discs which they call disc like angle ply structures (DAPS) for 5 weeks in rat tails. In the next study, the research team further developed the engineered discs. The new model called endplate modified DAPS (eDAPS)were tested in the rats once again for up to 20 weeks. The new structure allowed the disc to retain its shape better and was more easily integrated in the surrounding tissue.

Several tests were run which included MRI scans and a variety of in depth tissue and mechanical analysis. The team discovered that in the rat model the eDAPS effectively restored the original disc function and structure.

With this success, the team was motivated to study eDAPS in goats. They proceeded to implant the device within the cervical spines of some of the goats. Goats were chosen for the study because the cervical spine discs of these animals have similar dimensions of those in humans. Goats also have semi upright stature which allowed the team to bring this study one step closer to conducting human trials.

The teams tests on goats proved to be successful. The eDAPS integrated quite well with the surrounding tissue. Additionally, the mechanic function of the discs either matched or surpassed that of the original cervical discs of the goats.

The next step will involve conducting more extensive trials on goats which will help the scientists to better understand how well eDAPS works. The team then plans to test eDAPS in human models of intervertebral disc degeneration which hopefully gets them one step closer to conducting clinical trials.

Implanting a device made of a person’s own cells is highly desirable. Using a true tissue engineered motion preserving replacement device in arthroplasty is something that has not been done yet in orthopedics. It would certainly be a large shift in treating spinal diseases and how surgeons approach motion sparing reconstruction of joints.

To view the original scientific study click here: watch-these-tissue-engineered-spinal-disks-mimic-real-thing