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

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.

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

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

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

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

Blood from world’s oldest woman suggests life limit

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

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

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

New findings about how the aging process works may pave the way to better treatments and revolutionary new medications that could immensely improve human health.

Recent research from USC Viterbi School of Engineering has focused on senescence, the natural process by which cells permanently cease creating new cells. Senescence is one of the major causes of age related declines in health.

Senescent cells are the complete opposite of stem cells. Stem cells have unlimited potential for division or self renewal. Senescent cells can never divide again. They are in a state of cell cycle arrest.

The team discovered that these aging senescent cells ceased producing a class of chemicals known as nucleotides which are DNA building blocks. When the team took these young cells and forced them to cease producing nucleotides, they then became aged or senescent.

This observation means the production of nucleotides is mandatory in keeping cells young. And it additionally means that if cells could be prevented from losing nucleotide synthesis, the cells could age more slowly.

The study team examined cells that were young which were proliferating robustly. They fed them molecules that were labeled with stable isotopes of carbon so that they could trace how the nutrients consumed by the cells were processed into a variety of biochemical pathways.

The team worked with a team to develop 3D imagery of the results. Unexpectedly, the images revealed the senescent cells often contain two nuclei and they do not synthesize DNA.

Previously, senescence had primarily been studied in cells which are known as fibroblasts which are the most common cells which comprise the connective tissue in animals. The team instead focused on how senescence occurs in epithelial cells which are cells that line the surfaces of organs and structures in the body.

The team’s goal was not to completely prevent senescence, however they wanted to find a way to remove senescent cells to promote better function and healthy aging.

The research has applications in the emerging field of senolytics which is the development of medications that might be able to eliminate aging cells. Human clinical trials are in early stages, however studies on mice have indicated that through eliminating senescent cells, mice do age better and have a more productive life span.

They can take mice that are aging and diminishing in function, treat them with senolytic drugs to eliminate the senescent cells and the mice are rejuvenated. The team refers to these drugs as the fountains of youth.

In order for successful senolytic drugs to be developed, it is important to identify exactly what is unique about senescent cells so that developed drugs don’t affect the normal non senescent cells. This is where the research team is at…studying the metabolism of senescent cells and then trying to figure out how senescent cells are unique so that targeted therapeutics around these metabolic pathways can be designed.

To view the original scientific study click below

Inhibition of nucleotide synthesis promotes replicative senescence of human mammary epithelial cells

As we age brain stiffness increases which leads to stem cell dysfunction. New research has demonstrated new ways to reverse this aging process in older stem cells into a younger and healthier state. The results may provide immense implications for understanding the aging process and how new much needed treatments can be developed for brain diseases that are related to aging.

Muscles and joints become stiff as our bodies age which makes movements much more difficult. The study indicates the same is true of the brain. Brain stiffening leads to significant impact on how brain stem cells function.

The multi disciplinary study team which was based at the Wellcome MRC Cambridge Stem Cell Institute, observed both old and young rats to help understand how brain stiffening due to age impacts the function of oligodendrocyte progenitor cells (OPCs). These type of cells are one of the types of brain stem cells which are important to maintaining normal function of the brain. They are also involved in the regeneration of myelin, the fatty sheath which surrounds our nerves and is damaged in multiple sclerosis.

MS affects over 100,000 in the UK, but the affects of age on these cells also declines as healthy people age.

To see whether the function loss in aged OPCs was reversible, the team transplanted older OPCs from the aged rates into the spongy, soft brains of the younger rats. Surprisingly, the older brain cells were rejuvenated and they started to behave similar to the younger, more rigorous cells.

The team them sought to understand how brain stiffness and softness influences the behavior of cells. They investigated Pierzo1 which is a protein found on the surface of the cell and informs the cells whether the environment surrounding it is stiff or soft.

The team was fascinated to see that when they grew young, functioning rat brain stem cells on the stiff material, the cells then became dysfunctional and then lost the ability to regenerate. They actually began to look like older cells. When the older brain cells were grown on the material that was soft they started to function similar to young cells.

When the team removed Piezo1 from the surface of the older brain stem cells, they were able to trick those cells into perceiving a soft surrounding environment even when they were grown on the stiffer material. They were able to delete Piezo1 in the OPCs in the older rat brains which then led the cells to become more rejuvenated and again they were able to assume their normal function of regeneration.

MS is a painful, disabling and relentless disease. Treatments that can prevent or slow the accumulation of disability over time are needed. The study teams research on how brain stem cells age and how the process could be reserved has important implications for treatments in the future.

To view the original scientific study click below

Niche stiffness underlies the ageing of central nervous system progenitor cells.

A new study at the University of Exeter has discovered another good reason to live a healthy lifestyle! The research found that in people with a high genetic risk for developing dementia the risk was 32 percent lower if they followed a healthy lifestyle.

Study participants who had a high genetic risk and led an unhealthy lifestyle were almost three times more likely to develop the disease compared to participants who led a favorable lifestyle and had a low genetic risk of developing dementia.

This study was the first to analyze to what extent a person might offset their genetic risk of developing dementia when living a healthy lifestyle. The findings show that when a person takes action to do their best to offset the risk by living healthy, they can make a difference regardless of the genetic risk.

The study included analyzed data from 196,383 adults aged 60 and older and of European ancestry. The research team identified 1,769 cases of dementia during the follow up period of eight years. The study team grouped all participants into three groups…those with low genetic risk, intermediate genetic risk and high risk.

To assess the genetic risk, the team studied previously published data and then identified known genetic risk factors for Alzheimer’s. Every genetic risk factor was weighted through the strength of its association with this disease.

To assess lifestyles, the team groups all participants into unfavorable, intermediate and favorable categories which were based on self reported physical activity, diet, alcohol consumption and smoking. The team considered regular physical activity, no current smoking, moderate alcohol consumption and healthy diet as healthy behaviors.

The study team discovered that living a healthy lifestyle was linked to a reduced dementia risk across all the genetic risk groups. The team reports that their research delivers a very important message that undermines the fatalistic views of dementia. Many people believe that developing dementia is inevitable due to their genetics. However, because of this new study, it appears people may be able to substantially reduce their risk of development the disease through healthy lifestyle habits.

To view the original scientific study click below

Association of Lifestyle and Genetic Risk With Incidence of Dementia