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 February 7th, 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 February 5th, 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 February 4th, 2019


The worldwide population of people age 60 and over is growing faster than all of the younger age groups. The result is a growing occurrence of chronic disease and lower quality of life which is challenging healthcare and economic systems. Scientists from Gero and MIPT have collaborated with researchers from the University of Edinburgh, PolyOmica and other institutions to analyze medical histories and genetic data of more than 300,000 people aged 37 to 73 which was made available by UK Biobank.

The study which has been published in Communications Biology, shows that the most prevalent chronic diseases share the common underlying mechanism which is the process of aging which is a mortality law known as Gompertz. The risk of death from all causes increases exponentially after age 40 and doubles at about every 8 years. Through analyzing the dynamics of the incidence of disease in the clinical data provided, the researchers observed that this dynamic was compatible with the Gompertz Mortality Law.

Health span can be used as a natural proxy for investigating the genetic factors which control the rate of aging which is called the holy grail target for interventions for anti aging. The researchers studied the genomes of the study group to help them understand genetic factors that are associated with human health span.

12 genetic loci (a fixed position on a chromosome) affecting a healthy life expectancy were discovered. A minimum of three genetic loci were found to be associated with the risk of a variety of diseases and health span at the same time and could therefore form the genetic signature for aging. Other genes were also found to be associated with disease and also with parental early survival. Other genetic variants predict death and are also involved in earlier onset of macular degeneration. Another chromosome locus was not seen to be associated with any incidence of disease at its full genome level, however it was affecting the health span of some of the studied individuals.

The team also found a number of genes associated with a number of complex traits of the skin such as the color of skin, eyes and hair, tanning and freckles and a variety of other diseases. Strong genetic correlations were also found between a variety of disease and health span including smoking, education level and parental age at death.

Studying longevity genetics is complicated due to limited availability of data sets containing clinical data of individuals who have been genotyped and have already reached their end of lifespan. Health span as a target phenotype offers a promising way to interrogate human longevity genetics by tapping research potential of large groups of living individuals with important clinical information.

To view the original scientific study click here: Identification of 12 genetic loci associated with human healthspan

lroot on February 2nd, 2019


Results from a new study have suggested that social jet lag may play an important role in circadian markers for health outcomes. Social jet lag occurs when a person goes to bed and wakes up later on weekends than they normally do during the week. Findings suggest this can be associated with worse mood, poorer health and increased fatigue and sleepiness.

Like normal jet lag, social jet lag is a consequence of our bodies being forced between two time zones. One is dictated by work and our social obligations, the other by our circadian clock. Like anyone who has experienced jet lag, social jet lag leads to trouble sleeping. Our bodies take a while to adapt to a new time zone or different sleep patterns at different times during the week.

Almost all of the bodies hormones are on some sort of circadian rhythm and when they are shifting with different sleep times, the entire system will not work as efficiently as it should.

The research team at the Sleep and Health Research Program at the University of Arizona, Tucson, shows that each hour of social jet lag is associated with an 11 percent increase in the likelihood of diseases of the heart. These outcomes are independent of insomnia symptoms and sleep duration which are both related to health and social jet lag.

The study reveals how important sleep regularity, beyond the length of sleep time alone, plays a significant role in the health of a person. This suggests that sleeping at regular times may be a simple, effective and inexpensive prevention for hearth disease and other health issues.

The study involved analyzing survey responses from 984 adults aged 22 to 60 years which was provided by the community based Sleep and Healthy Activity, Diet, Environmental, and Socialization study.

Social jet lag was analyzed using the Sleep Timing Questionnaire and was figured by subtracting weekday from weekend sleep midpoint. Overall health was self reported via a standardized scale. Questions were also used to asses sleep duration, cardiovascular disease, insomnia, sleepiness and fatigue.

Another study discovered that adults with higher levels of social jet lag had a higher likelihood of being overweight or obese and suffer from metabolic syndrome compared to those who have more regular sleep patterns. This study found that just one hour of social jet lag resulted in an accumulation of about 2 additional kilograms of fat mass on average by the age of 39.

The American Academy of Sleep Medicine has recommended that adults should get 7 or more hours of sleep per night which should occur on a regular basis for promoting optimal health. In addition to the amount of time spent sleeping, healthy sleep also requires appropriate timing and regularity and good quality.

To view the original scientific study click here: Sociodemographics, Poor Overall Health, Cardiovascular Disease, Depression, Fatigue, and Daytime Sleepiness Associated with Social Jetlag Independent of Sleep Duration and Insomnia

lroot on February 1st, 2019

girl meditating

Researchers have discovered a distinct link between meditation and how people who practice it respond to feedback. The University of Surrey conducted a study that has shown that meditation adapts the brain to respond better to feedback.

The study included experienced, novice and non-meditators. All were trained to choose images associated with rewards with each pair of images containing varying probabilities of rewards. Some images resulted in a reward 80% of the time while others resulted in a reward just 20% of the time. Study participants eventually learned to choose the pairing that had the higher outcome.

The participants who meditated were much more successful in choosing the high probability pairings which indicated a tendency to learn from positive outcomes. The non-meditators who learned the pattern via low probability pairings suggested a tendency to learn from negative outcomes.

The study participants were connected to an EEG during the study. Results from the EEG showed that all three groups responded similarly to positive feedback. However, the neurological response to negative feedback was the highest in the non-meditation group which was followed by the novice group and lastly by the mediation group. The results indicate that the brains of meditators are less affected by negative feedback which may be attributed to the altered levels of dopamine resulting from meditation.

Dopamine is integral to how we learn and process information. The current study indicates that meditation may be a way to affect the levels of dopamine in the brain and how humans deal with negative and positive feedback.

Humans have been meditating for over 2000 years, however the neural mechanisms of meditation are still relatively unknown. The findings from the current study demonstrate that on a deep level people who meditate respond to feedback in a more even handed way that those who do not meditate.

Meditation can improve immune function and reduce stress. With the current study, the researchers have found that it can also impact how we receive feedback…that is if we quickly learn from mistakes or if we need to keep making them before finding the right answer. This can impact how people perform in the classroom and workplace.

To view the original scientific study click here: Meditation experience predicts negative reinforcement learning and is associated with attenuated FRN amplitude.

lroot on January 24th, 2019


Want to ramp up your metabolism and help reverse some signs of aging? New research has uncovered previous unknown effects of fasting which include increased metabolic activity and newly identified anti-aging benefits.

A study conducted by scientists at the Okinawa Institute of Science and Technology Graduate University and Kyoto University suggests that putting the body in “starvation mode” via fasting, leads to fuel substitution, increased mitochondrial activation and altered signal transduction, and anti oxidation.  The research team identified 30 previously unreported substances which increase with fasting.

The study presented an analysis of whole human blood, red blood cells and plasma which was drawn from the four individuals who were fasting for the study. Fasting induced metabolic activation. The scientists observed changing levels of metabolites which are substances that are formed during the chemical processes that give organisms energy which allows them to grow.

The team’s results showed the discovery of 44 metabolites which included 30 which had not previously been identified. These metabolites increased among the subjects between 1.5 and 60 fold within 58 hours of fasting.

In previous studies, various metabolites had been identified whose quantities declined with age. These included three metabolites known as isoleucine, leucine, and ophthalmic acid. With fasting, these metabolites increased in levels which suggested a mechanism that could help increase longevity in fasting individuals. These are important metabolites for maintenance of muscle and antioxidant activity respectively. These results suggest there could be a possibility of a rejuvenating effect realized by fasting.

The human body utilizes carbohydrates for immediate energy when they are available. When the body is starved of carbs, it will begin looting its other energy stores. This act of energy substitution leaves a trail of metabolites known as carnitines, butyrates and branched chain amino acids. These metabolites have been shown to accumulate during fasting.

Fasting appears to elicit additional effects beyond the energy substitution. From their analysis of human blood, the scientists have noted both established fasting markers and many more. They found a global increase in substances which are produced by the citric acid cycle which is a process where organisms release energy that is stored in the chemical bonds of proteins, carbohydrates and lipids. The marked increase suggests that these tiny powerhouses running every cell are thrown into overdrive during fasting.

It appears fasting also enhances the metabolism of pyrimidine and purine which are chemical substances that play key roles in protein synthesis and gene expression. This finding suggests that fasting might reprogram which protein cells build at what time which alters their function. This change might promote homeostasis in cells or edit their gene expression as a response to environmental influences.

When these two substances are metabolized, they also boost the production of antioxidants. Several antioxidants were found to significantly increase over the 58 hour study period. Antioxidants help protect cells from free radicals which are produced during metabolism. Products of a metabolic pathway referred to as pentose phosphate pathway, also stay the harmful effects of oxidation and were seen to increase during fasting however only in plasma.

The researchers believe these antioxidant effects may serve as the body’s principal response to fasting. Starvation can foster a dangerously oxidative internal environment. This study shows the first evidence of antioxidants as a fasting marker. The study introduces the novel thought that fasting may boost production of a variety of age related metabolites which are abundant in youth but depleted with aging.

A variety of studies show that caloric restriction and fasting have a prolonged effect on lifespan in model animals but the detailed mechanism is still a mystery. The researchers believe it might be possible to verify effects of anti-aging from a variety of viewpoints by developing drugs or exercise programs which would be capable of causing a metabolic reaction which would be similar to fasting.

The next step would be to replicate the results in a larger study and investigate how the metabolic changes might be triggered by other methods. It is hoped that by understanding these changes greater wisdom will be attained about fasting for maintaining health and longer lifespan.

To view the original scientific study click here: Diverse metabolic reactions activated during 58-hr fasting are revealed by non-targeted metabolomic analysis of human blood.

lroot on January 22nd, 2019

man and woman

According to research from the Netherlands Cohort Study (NLCS), men’s and women’s lifespans differ. Weight and body size may influence the lifespan of women more than it does the lifespan of men. The thought is factors such as genes, hormones and/or lifestyle are how the two different sexes are influenced.

Physical activity is linked to longer lifespans in both men and women, however it seems that the more time men spend physically active every day the greater their chances are for reaching old age. However per the findings, 60 minutes per day was associated with the best chances of women reaching old age.

The average life expectancy has increased over the past few decades, however recently there is the start of a plateau in some developed nations. Increasing levels of physical inactivity and obesity are thought to be responsible for the trend.

Early research has studied the associations between weight (body mass index or BMI), physical activity and reaching old age, however most studies have combined both men and women or focused just on men.

To research the differences, the current study by NLCS analyzed data from more than 120,000 women and men between the ages of 55 and 69 when it started in 1986. The goal was to see if there were links between weight, height, physical activity, leisure time and the likelihood of the participants reaching 90 and if there were differences between women and men.

Approximately 4161 women and 3646 men between the ages of 68 and 70 provided detailed information in 1986 about their current height, weight, weight when 20 years old and their leisure time and physical activity. This included activities such as dog walking, home improvements, gardening, cycling, walking and recreational sports. The physical activity was grouped in daily quotas of less than 30 minutes, 30 to 60 minutes and 90 minutes or more.

The participants were monitored until age 90 or death, whichever came first. The research team considered potentially influential factors such as smokers, former smokes, educational levels and their usual energy intake.

Approximately 944 women and 433 men lived to age 90. Women who survived to this age were on the average taller, had weighed less at the beginning of the study and had put on less weight since they were 20 than those who were heavier and shorter. Additionally, women who were more than 5’ 9” in height were 31% more likely to reach the age of 90 than women who were less than 5’3”. No similar associations were seen among the male participants.

When physical activity was analyzed, men who were over 90 minutes active per day were 39% more likely to reach the age of 90 over those men who did less than 30 minutes of daily physical activity. Every additional 30 minutes of physical activity per day was associated with a 5% increase in their chances of reaching age 90.

This was not the case for the women. Those who were physically active 30-60 minutes per day were 21% more likely to reach the age of 90 than those whose physical activity was less than 30 minutes per day. However, there was an optimal threshold for the women. About 60 minutes of physical activity per day was associated with the best chance of them reaching the age of 90.

Although this was an observational study and actual cause can’t be established, the findings based on the large number of participants all of whom were of similar age, strengthens the results. This study is just one of a few to differentiate factors of lifestyle which could be associated with longer lifespan between women and men.

The researchers point out that there may be an association between body size and reaching old age in men, however behavior and illness history did appear to influence the correlations found and also there were differences between non-smokers and smokers.

To view the original scientific study click here: Body size, non-occupational physical activity and the chance of reaching longevity in men and women: findings from the Netherlands Cohort Study. Journal of Epidemiology & Community Health, 2019 DOI: 10.1136/jech-2018-211410

lroot on January 21st, 2019


Emulsifiers which are common ingredients found in a variety of foods have come under scrutiny for their negative impact on health. Manufacturers use emulsifiers which are chemicals to extend the shelf life of certain foods and to alter a food’s texture. They have generated quite a bit of attention lately, and studies in mice have shown they can produce both behavioral and physiological changes.

Previous studies have shown that emulsifiers have the ability to alter the microbiome of mice which causes low grade inflammation and the increased risk of metabolic disorders and obesity. A study in humans also concluded that gut bacteria are directly impacted by these common food additives which subsequently leads to intestinal inflammation.

A group of researchers at Georgia State University in Atlanta took these findings to a new level. They set out to investigate whether two of the most common emulsifiers, carboxymethylcelluose (CMC) and polysorbate-80 (P80) might also have an influence on mental well being.

Scientists have shown that there is a clear, two way connection between the gut and the brain. Gut health and the health of gut bacteria have a significant influence on mental health. A study from 2011 discovered that treating mice with Lactobacillus rhamnosus which is a type of good bacteria, led to measurable changes in the brain and reduced anxiety related behaviors.

Another study conducted on mice that had no gut bacteria, showed higher levels of anxiety type behaviors when compared with controls. A recent study showed that mice given antibiotics early in life significantly alter the microbiome, social behavior and anxiety levels in the mice long term.

The most recent study using CMC and P80 investigated whether these two emulsifiers might alter the mental state of the mice. The researchers added CMC and P80 to the drinking water of the mice for a period of 12 weeks. They then measured their behavior, any changes in their microbiome and a variety of physiological parameters. They found that the emulsifiers effects on general systemic inflammation could be extended to the brain and also to behavior.

Interestingly, they found that the two emulsifiers did impact gut bacteria but in different ways between female and male mice. And they showed the changes in behavior were also different between the two sexes.

They saw an increase in anxious behavior more prominently in the male mice. In the female mice there was reduced social behavior. It is somewhat of a mystery why the differences occur, however the scientists know there are certain differences in the way the female and male immune systems work so this might offer some answers.

The next step for the researchers is to move from the mouse model to larger animals. How the results in mice are relevant to humans is inherently difficult particularly with behavioral disorders. In recent years it has been observed that there is a rise in anxiety in Western society. At the same time, there has been a marked increase in inflammatory bowel disease which leads researchers wondering if food additives might be playing a role in these shifts.

The scientists are now investigating the mechanisms behind dietary emulsifiers impacting the intestinal microbiota in addition to the relevance to humans. Science does show that our microbiome play a significant part in our health and there is a very strong need to assess food additives on food safety.

To view the original scientific study click here: Dietary emulsifiers consumption alters anxiety-like and social-related behaviors in mice in a sex-dependent manner.

lroot on January 14th, 2019

skin aging

Dermal fibroblasts which are specialized cells that reside deep in the skin indicate how skin ages based on a study by the University of California San Diego School of Medicine. The team has discovered how our skin loses its ability to form fat during aging.

Dermal fibroblasts can convert into fat cells under the dermis which gives skin a youthful look and also produces peptides that will help fight infections. If the fibroblasts lose their ability to convert into fat, the skin is not able to fight infection effectively and the skin loses its more plump and youthful appearance.

A protein called transforming growth factor beta or TFG-B which controls many cellular functions within our body, stops dermal fibroblasts from their conversion into fat cells. It also prevents the cells from being able to produce the antimicrobial peptide cathelicidin which helps protect the skin from bacterial infections.

Babies have quite a bit of this type of fat under their skin which makes their skin very good at fighting some types of infections. With aging, dermal fibroblasts lose this ability to form fat under the skin. Skin that has this layer of fat looks more youthful. With the aging process, the appearance of the skin has a lot to do with this loss of fat.

Researchers used chemical blocks to inhibit the TGF-B pathway in mice. This caused the skin to revert back to a younger function which allowed dermal fibroblasts to convert into fat cells. If they turned off the pathway in mice through genetic techniques, they had the same result.

Understanding the biological process which leads to age related loss of the specialized fat cells could be used to help our skin fight infections such as Staphylococcus aureas. This pathogenic bacteria is the main cause of infections of the heart and skin and a significant factor in worsening diseases. When this particular infection becomes antibiotic resistant it then is known as methicillin resistant Staphylococcus aureas which is the leading cause of infection deaths in the U.S.

The team notes that eating a high fat diet is not the path to converting the dermal fibroblasts into fat cells. Obesity will also interfere with the ability to fight infections.

The next step for the researchers is to begin studying the infant’s immune system to obtain a firmer grasp of fibroblast development. They hope the results may also help them understand what goes wrong with other diseases.

To view the original scientific study click here:
Age-Related Loss of Innate Immune Antimicrobial Function of Dermal Fat Is Mediated by Transforming Growth Factor Beta