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

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.

Low Fat Milk Linked to Less Aging in Adults

A study conducted at Brigham Young University by exercise scientists has found that people who consume low fat milk experience several years less biological aging when compared to those who drink high fat milk, both 2% and whole milk. This supports existing dietary guidelines which do not recommend high fat milk as part of a healthy diet.

The study assessed 5,834 adults and included data from the National Health and Nutrition Examination Survey as well as questionnaires for the participants. They looked at the relationship between telomere length along with milk intake frequency (daily drinkers vs. weekly drinkers or less) and the milk fat content that was consumed (whole vs. 2% vs. 1% vs. skim).

Telomeres are the end caps of human chromosomes and act like biological clocks. They are correlated with age. As people get older, their telomeres get shorter. People who consumed more high fat milk showed telomeres that were significantly shorter.

For every 1% increase in milk fat consumed (drinking 2% vs. 1% milk), telomeres were 69 base pairs shorter in the adults in the study. This translates into more than four years in biological aging. In the very extreme milk drinkers, the adults who drank whole milk had telomeres that were a striking 145 base pairs shorter.

Half of the adult participants in the study consumed milk on a daily basis with another quarter consuming milk at least weekly. Less than a third of the adults consumed full fat milk and an additional 30% reported drinking 2% milk. Approximately 10% consumed 1% milk and another 17% consumed non fat milk. 13% did not drink any cow milk.

Surprisingly, the study found that people who did not consume milk at all had shorter telomeres than adults who drank low fat milk meaning they aged quicker than skimmed milk drinkers. This suggests that there may be some anti aging benefits to consuming milk, but there is sweet spot to be found.

The study suggests that the milk fat and subsequent link with cellular aging was most likely due at least in part to increases inflammation and oxidative stress caused by the increase in saturated fat consumption. The team believes that this saturated fat in high fat milk is the culprit that causes the damage and contributes to the death of tissues in the human body.

Milk is one of the most controversial foods in the U. S. Current dietary guidelines for Americans encourage adults to consume low fat milk, both 1% and non-fat, and avoid high fat milk altogether. It isn’t necessarily a bad thing to drink milk, but according to the study, the type of milk matters.

To view the original scientific study click below

Milk Fat Intake and Telomere Length in U.S. Women and Men: The Role of the Milk Fat Fraction

New Discovery May Extend Healthy Lifespan by 50%

Scientists have identified pathways that could enable humans to live for well over 100 healthy years according to one of the scientists who participated in the research. The synergistic cellular pathways for longevity that increase the lifespan five fold were discovered in C. elegans which are a nematode worm used as models in aging research. This translates to extending human lifespan by about 50%.

C. elegans are popular models for aging research because they share many of its genes with humans and due to its short lifespan of three to four weeks, scientists can quickly assess the effects of genetic and environmental interventions for extending healthy lifespan.

The discovery of two major pathways governing aging in C. elegans has created intensive research. These pathways are conserved which means they have been passed down to humans through the evolutionary process. A variety of drugs that can extend healthy lifespan through altering these pathways are currently under development. The discovery of the synergistic effect has opened the door to more effective therapies aimed at anti aging.

The recent research used a double mutant in which the insulin signaling IIS and TOR pathways were genetically altered. Because an alteration of the IIS pathways will yield a 100% increase in lifespan and an alteration of the TOR pathway yields a 30% increase, the double mutant would be expected to live 130% longer. However, its lifespan was amplified by 500%.

Despite this discovery in C. elegans of cellular pathways that govern aging, it wasn’t clear how these pathways interact with each other. Through helping to characterize these interactions, the research team is paving the way for needed therapies to increase healthy lifespan for the rapidly aging population.

The synergistic extension is something the team calls “wild”. The effect wasn’t one plus one equals two. It was one plus one equals five. The findings demonstrate that nothing throughout nature exists in a vacuum. To develop the most effective treatments for anti aging, longevity networks rather than individual pathways needs to be looked at.

This discovery of the synergistic interaction might lead to the use of combination therapies with each affecting a different pathway to extending human healthy lifespan. The synergistic interaction might also explain why researchers have not be able to identify a single gene that is responsible for the ability of some humans to live to very old ages free of major diseases.

To view the original scientific study click below

Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity.

High Levels of Exercise and Slower Cellular Aging

New research has revealed how a high level of exercise can slow one type of aging. This is the kind of aging that occurs within our cells. We just have to be willing to put in some sweat equity!

Researchers at Brigham Young University have found that people who consistently perform physical activity at a high level have significantly longer telomeres when compared to those have live a sedentary lifestyle as well as those who are moderately active.

Telomeres are protein end caps on our chromosomes. The are like our biological clock and are strongly tied to aging. Every time a cell replicates, it loses a tiny bit of the end caps. As a result, the process of aging gradually shrinks or shortens our telomeres.

The team analyzed data from 5,823 adults who participated in the CDC’s National Health and Nutrition Examination Survey. This survey is one of the few indexes that includes telomere length values for the study participants. The index also includes data for 62 activities participants may have participated in over a 30 day period. This data was analyzed to calculate the participant’s levels of physical activity.

The research found that adults with high physical activity levels have telomeres with a biological aging boost of nine years when compared to those who live comparably idle lifestyles. They also have a 7 year advantage compared to those who engage in moderate levels of physical activity.

In order to be considered to be a highly active person, men must engage in 40 minutes of jogging 5 days per week and women must engage in 30 minutes of jogging 5 days per week. To see a significant difference in slowing biological aging, a little exercise won’t make it. People have to work out regularly and at high levels.

The study showed that the shortest telomeres came from people who were considered sedentary. They had 140 base pairs of DNA less at the endpoints of their telomeres compared to the highly active participants. Surprisingly, the study showed that there was no significant or meaningful difference in telomere length between the participants who were sedentary and those who engaged in low or moderate physical activity.

The exact mechanism responsible for how exercise preserves the telomeres is unknown. The team believes the mechanism may be tied to the combination of oxidative stress and inflammation. Earlier studies have determined telomere length is closely tied to those two factors. And it is well known that physical activity can suppress both these factors over time.

It is well known that regular physical activity can help reduce mortality and prolong life. Now it is known that part of that advantage might be related to the preservation of telomeres that occurs with high physical activity.

To view the original scientific study click below

Physical activity and telomere length in U.S. men and women: An NHANES investigation.

New Research into Tendon Stem Cells for Recovery

Due to the buildup of scar tissue from a variety of tendon injuries such as jumper’s knee and rotator cuffs, secondary tendon ruptures along with painful and challenging recoveries can occur. New research has shown that the existence of stem cells in tendons can potentially be harnessed to not only improve the healing of tendons but also even avoid surgery.

Tendons are the connective tissue that tethers our muscles to our bones. These tendons improve not only our stability but also facilitate the transfer of force which allows us to move. However, they are particularly susceptible to damage and injury.

Once tendons are injured they rarely fully recover. This can result in mobility limitations and often times requires long term pain management and even surgery. The problem is the fibrous scars which disrupt the tissue structure of the tendons.

The research which was conducted at the Carnegie Institution for Science, revealed all of the cell types which are found to be present in the Patellar Tendon which is found below the kneecap. This included previously undefined tendon stem cells.

Because injuries to the tendons rarely heal completely, it has been thought that tendon stem cells did not even exist. Many researchers have searched for them but to no avail until the recent work which defined them for the first time.

Stem cells are blank cells which are associated with nearly even tissue type which have not fully differentiated into a specific function. They can self renew which creates a pool from which newly differentiated types of cells can form to support a particular tissue’s function. Muscle stem cells for example differentiate into muscle cells.

The research team showed that both tendon stem cells and fibrous scar tissue cells originate in the identical space which is the protection cells that surround our tendons. Additionally, the tendon stem cells are part of a competitive system with precursors of fibrous scars. This explains why healing of injured tendons is so challenging.

The researchers demonstrated that both scar tissue precursor cells and tendon stem cells are stimulated into action by a protein known as platelet derived growth factor A. When tendon stem cells become altered so they do not respond to this particular growth factor, then only scar tissue and no new tendon cells form following an injury.

Tendon stem cells must outcompete scar tissue precursors so they can prevent the formation of difficult fibrous scars. Discovering a therapeutic way to block these scar forming cells and instead enhance the tendon stem cells could be a huge game changer for treating tendon injuries.

To view the original scientific study click below

A Tppp3+Pdgfra+ tendon stem cell population contributes to regeneration and reveals a shared role for PDGF signalling in regeneration and fibrosis.

Does Elderberry Really Minimize Flu Symptoms?

A new study by researchers at the University of Sydney’s Faculty of Engineering and IT have found that compounds contained in elderberries can directly inhibit the flu virus’s entry and also replication in human cells. These compounds can additionally help strengthen the immune response to this virus. While modern scientists have struggled to explain the medicinal benefits of herbal products and folk medicine, these methods have been used for millennia to help combat a variety of ailments.

Although the flu fighting properties of the elderberry fruit have been previously observed, the team sought to perform a more comprehensive examination of the mechanisms through which phytochemicals found in elderberries can help combat the flu virus.

The study involved the use of commercially farmed elderberries which were made into a juice serum. This serum was applied to cells at all stages after they had been infected with the flu virus…before, during and after. The phytochemicals from the juice were shown to be effective at stopping the flu virus infecting the cells.

And surprisingly to the research team, they were even more effective at inhibiting viral propagation at the later stages of the flu cycle when the cells had been infected with the virus. The study showed that this common fruit has a direct and potent antiviral effect against the flu. It inhibits the initial sages of the infection by blocking key viral proteins that are responsible for viral attachment and entry into host cells.

In addition, the team identified that the solution from the elderberry also stimulated the cells to release certain cytokines. These are chemical messengers which the immune system uses for communication between different cells types in an effort to coordinate a better response against invading pathogens.

They also found that the antiviral activity of the elderberry can be attributed to its anthocyanidin compounds. These are phytonutrients which are responsible for the vivid purple coloring of the fruit.

The elderberry which is also known as sambucus nigra, is an antioxidant rich fruit most common to North America and Europe. It is commonly consumed as wine or jam. For the medicinal benefits, elderberry extract is available in table or syrup form.

The flu virus is one of the leading cause of worldwide mortality. It affects almost 10% of the world’s population and contributes to one million deaths on an annual basis.

To view the original scientific study click here: Anti-influenza activity of elderberry.

Can Intermittent Fasting Help you Live Longer?

Typically for many people a New Year is the perfect time to adopt new habits both in the gym and at the grocery store. People can be eager to try out new diets, but does scientific evidence actually support claims made for these diets?

Mark Mattson, Ph. D., a neuroscientist at John Hopkins Medicine, has studied intermittent fasting for 25 years and adopted it himself about 20 years ago. He concludes that intermittent fasting does live up to the claims that it can be a part of a healthy lifestyle.

Generally, intermittent fasting diets fall into two categories: 5:2 intermittent fasting in which people will limit themselves to one moderate sized meal two days each week, and daily time restricted eating which narrows eating times to 6 to 8 hours per day.

A variety of animal and human studies have shown that alternating between eating and fasting supports cellular health. The thought is that most likely this happens by triggering an age old adaptation to periods of food scarcity referred to as metabolic switching. This switch occurs when cells use up stores of rapidly accessible sugar based fuel and begin converting fat into energy which occurs in a slower metabolic process.

Studies have shown that this metabolic switch improves the regulation of blood sugar, suppresses inflammation, and increases the resistance to stress. Most Americans consume three meals in addition to snacks every day so they do not experience the switch and the suggested benefits.

Mattson also notes that four different studies in both people and animals found intermittent fasting also decreases blood pressure, resting heart rates, and blood lipid levels. There is also mounting evidence that this type of fasting can modify risk factors which that are associated with diabetes and obesity.

Two studies conducted at the University Hospital of South Manchester NHS Foundation Trust which involved 100 overweight women showed that the women on the 5:2 intermittent fasting diet lost the same amount of weight as women who restricted their calories. Additionally they did better with insulin sensitivity and reduced belly fat when compared to those in the reduced calorie group.

Recently, Mattson says preliminary studies have suggested that intermittent fasting could also benefit brain health. A multi center clinical trial at the University of Toronto found that 220 healthy and non obese adults who maintained a calorie restricted diet for a period of two years showed evidence of improved memory in a variety of cognitive tests. If further studies show the proof that fasting can improve learning and memory, interventions may be developed that can stave off dementia and neurodegeneration.

Mattson believes we are at a point where medical school curricula alongside advice and healthy diets and exercise may be developed. Although he recognizes that researchers do not completely understand the specific mechanisms of metabolic switching and that there are some people who or unwilling or unable to adhere to a fasting program.

With guidance and patience, most people are able to incorporate fasting regimes into their lives. It does take the body some time to adjust to intermittent fasting and to get past some of the initial hunger pangs and irritability that can accompany it. These symptoms typically pass after two weeks to a month as the brain and body become accustomed to this new habit.

To manage that hurdle, Mattson suggests that health care professionals advise patients to gradually increase the frequency and duration of the fasting periods over the course of several months, instead of going cold turkey.

To view the original scientific study click below

Effects of Intermittent Fasting on Health, Aging, and Disease.

Caffeine may Offset some of Negative Effects of High Fat & Sugar in Diet

Researchers from the University of Illinois have conducted a new study on rats that suggests caffeine may offset some of the health risks associated with diets high in sugar and fat. What they found was that rats who consumed caffeine which was extracted from mate tea gained 16% less weight and accumulated 22% less body fat compared to rats who consumed decaffeinated mate tea.

Mate tea is an herbal beverage high in flavonoids, phytochemicals, and amino acids. It is consumed as a stimulant by people living in southeastern Latin American countries. The amount of caffeine in a serving of mate tea ranges from 65 to 130 milligrams. The caffeine in coffee ranges from 30 to 300 milligrams per one cup.

The rats in the study ate a diet that contained 40% fat, 15% protein and 45% carbohydrates for four weeks. They also consumed one of the forms of caffeine equivalent to someone who drinks four cups of coffee daily.

At the end of the study period, the percentage of lean body mass in the different groups of the rats differed significantly. The rats that consumed caffeine from the mate tea, coffee, or synthetic sources accumulated less body fat compared to the rats in the other groups.

The accumulation of lipids in the adipocytes in the rats was significantly associated with increased body fat and greater body weight gain. To understand the mechanism of this action, the team performed cell culture studies where they exposed adipose cells from mice to synthetic caffeine or the mate or coffee extracts.

They discovered that regardless of the source, caffeine decreased the accumulation of lipids in adipose cells by 20% to 41%. The team also tracked the expression of a variety of genes that are associated with obesity and lipid metabolism. This included the fatty acid synthase gene (Fasn) which is an enzyme compound involved in the synthesis of fatty acids from glucose, and also the lipoprotein lipase gene (Lpl) which codes for an enzyme which breaks down triglycerides.

All caffeine treatments regardless of the origin significantly down regulated the expression of both Fasn and Lpl. Within the cell cultures, Fasn expression diminished by 31% to 39% and the Lpl expression diminished by 51% to 69% among cells that had been treated with synthetic caffeine or the caffeine derived from coffee or mate tea.

In the rats that were given the mate tea caffeine, expression of Fasn decreased by 39% in their fat tissue and decreased by 37% in their livers. Additionally, the decreased expression of the Fasn gene and two other genes in the liver evoked a lower production of low density lipoprotein cholesterol and triglycerides in the liver.

The study adds to a growing body of research which suggests mate tea might help fight obesity. It also provides other beneficial health effects associated with the vitamins, flavonoids, and phenolic compounds it contains.

Based on the studies findings, caffeine can be considered an anti obesity agent. The consumption of caffeine from mate and other sources alleviates the negative impact of a high sucrose and high fat diet on body composition due to the modulation of certain lipogenic enzymes in the liver and adipose tissue. The diminished expression of Lpl and Fasn brought about the lower synthesis and accumulation of triglycerides in the andipose tissue.

The findings of the study could be scaled to people to understand the roles of caffeine and mate tea as possible strategies in preventing overweight and obesity in addition to subsequent metabolic disorders which are associated with these conditions.

To view the original scientific study click below

Caffeine, but not other phytochemicals, in mate tea (Ilex paraguariensis St. Hilaire) attenuates high-fat-high-sucrose-diet-driven lipogenesis and body fat accumulation.