Dr Mercola Interviews Dr Villeponteau the Formulator of Stem Cell 100

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

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

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

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

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

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

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

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

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

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

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

Click here for more information about Stem Cell 100

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

Aging Reversed / ABC News

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

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

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

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

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

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

Stem Cells Secret’s of 115 Year Old Woman

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

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

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

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

Blood from world’s oldest woman suggests life limit

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

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

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

Diabetes Prevention with Intermittent Fasting

Scientists at the German Institute of Human Nutrition have found through research on mice that have been put on intermittent fasting, have exhibited lower pancreatic fat. Pancreatic fat has been shown to contribute to the development of type 2 Diabetes. This type of fasting is known to improve the sensitivity to the glucose lowering hormone insulin and can also protect against fatty liver.

Fatty liver has been previously investigated and is known as a frequently occurring disease. However, very little has been known in regards to excess weight induced accumulation of fat in the pancreas and its effects on the onset of type 2 diabetes.

The team has now discovered that mice who are overweight and prone to diabetes have a high accumulation of fat cells in their pancreas. Mice that are resistant to diabetes because of their genetic make up and despite their excessive weight, had hardly any fat cells in their pancreas. Instead they had fat deposits in their liver. Accumulations of fat outside the fat tissue in the muscles, liver and even bones, have a negative effect on those organs and the whole body. What impact fat cells might have within the pancreas has not been previously clear.

The research team divided the animals that were overweight and prone to diabetes into two groups. The first group of mice were allowed to eat as much they wanted and whenever they wanted. The second group of mice underwent a regime of intermittent fasting. One day they were given unlimited chow and the following day they were not fed at all.

After five weeks, the team noted differences in the pancreas of the mice. An accumulation of fat cells were found in the first group. In the second group however, there were hardly any deposits of fat in the pancreas.

To find out how fat cells could impair pancreas function, the team isolated adipocyte (a cell specialized for the storage of fat and found in connective tissue) precursor cells taken from the mice’ pancreas for the first time and then allowed them to differentiate into mature fat cells. If these mature fat cells were then cultivated together with the Langerhans islets of the pancreas, the islets beta cells increasingly secreted insulin. The team suspects that an increase secretion of insulin causes the Langerhans islets of animals prone to diabetes to deplete more quickly and cease functioning completely after time.

The islets of Langerhans are islet like accumulations of hormone producing cells within the pancreas. A healthy adult has approximately one million Langerhans islets. Beta cells produce the blood glucose lowering hormone known as insulin and they make up about 75 to 80% of the islet cells. When blood glucose levels are elevated, these beta cells secrete insulin into the blood steam to normalize levels.

The most current data suggests that not only should liver fat be reduced to help prevent the onset of type 2 diabetes, but under certain genetic conditions, an accumulation of fat in the pancreas might also play a decisive role in the development of this disease.

Intermittent fasting just might be a very promising therapeutic approach. Intermittent fasting is easy to integrate into daily life, does not require drugs and is non invasive. Intermittent fasting simply involves not eating during certain times of the day. However, black coffee, water and unsweetened tea can be consumed around the clock. Fasting can last between 16 and 24 hours or alternatively a maximum of 500 to 600 calories can be consumed on two days within a week.

One of best forms of intermittent fasting is the 16 and 8 method. This method involves eating only within an eight hour window during a day then fasting for the other 16 hours. One meal which is typically breakfast is omitted.

To view the original scientific study click below

Pancreatic adipocytes mediate hypersecretion of insulin in diabetes-susceptible mice

Enhance Brain Function with Just a Short Bout of Exercise

Short bouts of exercise has been found to directly boost gene function which increases the connections between neurons in the hippocampus. This part of the brain is associated with memory and learning. Not only is exercise good for health, but according to recent research it can also help make you smarter!

Neuroscientists at Oregon Health & Science University designed research using mice that specifically measured their brain’s response to just single bouts of exercise. Mice that were normally sedentary were placed on running wheels for short periods. They ran a few kilometers in a two hour time period.

The results of the study found that short term bouts of exercise similar to the human equivalent of 4,000 steps or a weekly game of basketball, promoted synapses increases in the hippocampus. The team made the discovery through analyzing genes that increased in single neurons which were activated during exercise.

A particular gene stood out, the Mtss 1L gene. This gene has been ignored in previous studies of the brain. This gene encodes a protein which causes the cell membrane to bend. When this gene is activated through short bursts of exercise, it will promote small neuron growths known as dendritic spines which is the site where synapses form.

The study has shown that an acute burst of exercise can prime the brain for learning. For the next stage of their research, the scientists plan to pair acute bursts of exercise with learning tasks to more fully understand the impact on memory and learning.

To view the original scientific study click below

Exercise-induced enhancement of synaptic function triggered by the inverse BAR protein, Mtss1L