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 cell’s 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.
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.
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.
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.
Researchers at Mayo Clinic increased normal mouse lifespan by up to 35% by removing senescent cells that accumulate with age and negatively impact health. The results, which appear today in Nature, demonstrate that clearance of senescent cells preserves tissue and organ function and extends lifespan without observed adverse effects.
“Cellular senescence is a biological mechanism that functions as an ‘emergency brake’ used by damaged cells to stop dividing,” says Jan van Deursen, Ph.D., Chair of Biochemistry and Molecular biology at Mayo Clinic, and senior author of the paper. “While halting cell division of these old or damaged cells is important, it has been theorized that once the ‘emergency brake’ has been pulled, these cells are no longer necessary.”
The immune system sweeps out the senescent cells on a regular basis, but over time becomes less effective. Senescent cells produce factors that damage adjacent cells and cause chronic inflammation, which is closely associated with frailty and age-related diseases.
Mayo Clinic researchers used a transgene that allowed for the drug-induced elimination of senescent cells from normal mice. Upon administration of a compound called AP20187, removal of senescent cells delayed the formation of tumors and reduced age-related deterioration of several organs. Median lifespan of treated mice was extended by 17 to 35 percent. They also demonstrated a healthier appearance and a reduced amount of inflammation in fat, muscle and kidney tissue.
“Senescent cells that accumulate with aging are largely bad, do bad things to your organs and tissues, and therefore shorten your life but also the healthy phase of your life,” says Dr. van Deursen. “And since you can eliminate the cells without negative side effects, it seems like therapies that will mimic our findings or our genetic model that we used to eliminate the cells like drugs or other compounds that can eliminate senescent cells would be useful for therapies against age-related disabilities or diseases or conditions.”
Darren Baker, Ph.D., a molecular biologist at Mayo Clinic, and first author on the study is also optimistic about the potential implications of the study for humans.
“The advantage of targeting senescent cells is that clearance of just 60-70 percent can have significant therapeutic effects,” says Dr. Baker. “If translatable, because senescent cells do not proliferate rapidly, a drug could efficiently and quickly eliminate enough of them to have profound impacts on health span and lifespan.”
Darren J. Baker, Bennett G. Childs, Matej Durik, Melinde E. Wijers, Cynthia J. Sieben, Jian Zhong, Rachel A. Saltness, Karthik B. Jeganathan, Grace Casaclang Verzosa, Abdulmohammad Pezeshki, Khashayarsha Khazaie, Jordan D. Miller, Jan M. van Deursen. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature, 2016; DOI: 10.1038/nature16932
One would expect that each time a women carries a baby that the stress and depletion would speed up the aging process and shorten her life. At Simon Fraser University, health sciences professor Pablo Nepomnaschy and postdoctoral researcher Cindy Barha followed a group of 75 Kaqchikel Mayan women over a 13 year period. They discovered just the opposite of what they expected to find. The women who had more children had longer telomeres which is associated with a longer life span and a slower aging process. While it is true that pregnant women receive higher social support and experience an increase in the actions of the gonadal steroid estradiol, which increases during pregnancy those do not seem to offer a sufficient explanation. By combining this study with information that has been discovered from several others we have an interesting answer to the mystery.
An article published in Scientific American during December 2012 holds the key. When a mother is carrying a baby they are connected by the placenta. It acts as a conduit to carry nutrients, oxygen, wastes and other substances between the mother and the fetus. This has been known for a long time. What is new is the discovery that stem cells from the fetus also travel through the placenta passing from the unborn baby back into the mother. They implant in the mother and can live for decades in the brain, lung, thyroid, muscle, liver, heart, kidney, skin and other organs. There is even evidence that if the mother has an internal injury that some of the stem cells from her child may repair the damage. Young stem cells are very powerful for healing and especially appropriate for a mother because half of their genetic material came from her. Not only does a mother carry in her body cells of all her children, but the younger children may carry cells that traveled from the fetus to the mother and then into a different child later on. So oddly enough many women and even some men carry cells in their body that is partly from their children or siblings.
Very young stem cells are powerful and that is basically what a mother is receiving each time she carries a baby. No wonder women who have more children age at a slower rate.
Cindy K. Barha, Courtney W. Hanna, Katrina G. Salvante, Samantha L. Wilson, Wendy P. Robinson, Rachel M. Altman, Pablo A. Nepomnaschy. Number of Children and Telomere Length in Women: A Prospective, Longitudinal Evaluation. PLOS ONE, 2016; 11 (1): e0146424 DOI: 10.1371/journal.pone.0146424
In the United States an increasing number of doctors are already using autologous stem cells in their practice. The stem cells are harvested from the adipose tissue (fat) or blood from bone marrow of the patient and then injected the same day into another part of the body. For instance many doctors inject joints like knees, hips and various parts of the spine. You can learn more about this or locate a physician at www.getprolo.com. The stem cells can also be injected intravenously into the cardiovascular system.
A Japanese researcher, Nobel laureate Shinya Yamanaka, collected genes from mature adult skin tissue and reprogrammed them to become pluripotent, which is a stem cell characteristic that means a cell is able to differentiate into multiple types of cells. This conversion process, referred to as induced pluripotent stem cells (iPSCs), means that we can take adult cells from a person with a particular disease, turn them into iPSCs, and then induce the iPSCs to turn into different types of body cells. Yamanaka’s iPSC findings show how scientists can essentially “make any cell turn into any other type of cell and in effect move through wormholes in developmental time” to produce such things as a pancreas from skin tissue.” As a result, “the petri dish becomes an avatar of the patient” whereby medicines can be identified “that will improve the condition of cells in the patient without having to take cells out of the petri dish and put them back in the patient.”
While harvesting “stem cells” from a patient’s blood from bone marrow or fat from liposuction has great value today neither of these procedures provides pluripotent stem cells needed for diverse tissue differentiation in a laboratory. Rather, these procedures produce mesenchymal cells, which work well for cardiovascular and orthopedic conditions because these tissues are the end organ targets for mesenchymal cells. However, they do not work well for other germ cell layer target organs, such as those produced from endoderm (incl., pancreas, liver, lungs) and ectoderm (incl., nervous system, skin).
Fortunately, there is a lesser known but more viable means for obtaining real pluripotent stem cells that merely involves a blood draw. In 2005, a study published in Minerva Biotechnologica identified stem cells in the blood. In other follow-up studies, scientists showed that such cells could, in fact, be used to regenerate not only heart tissue, but brain, lung, and pancreas as well.
In 2010, a clinical protocol was developed for harvesting, concentrating, reconstituting, and administering pluripotent stem cells obtained from autologous blood. Today the use of stem cells for clinical applications is in its infancy. Physicians still have much to learn about how to more effectively utilize pluripotent stem cells in their practice for the benefit of their patients. Such knowledge includes not only using the most appropriate source for harvesting real stem cells but in improving the means of attracting those stem cells to where they are needed and facilitating their differentiation. As more physicians implement the use of pluripotent stem cells in their practice, such as those obtained from autologous blood, we can begin accumulating the objective data needed to validate stem cells in the present and advance stem cell science into the future.
A hormone that extends lifespan in mice by 40% is produced by specialized cells in the thymus gland, according to a new study by Yale School of Medicine researchers. The team also found that increasing the levels of this hormone, called FGF21, protects against the loss of immune function that comes with age.
Published online in the Proceedings of the National Academy of Sciences on Jan. 11, the study’s findings have future implications for improving immune function in the elderly, for obesity, and for illnesses such as cancer and type-2 diabetes.
When functioning normally, the thymus produces new T cells for the immune system, but with age, the thymus becomes fatty and loses its ability to produce new T cells. This loss of new T cells in the body is one cause of increased risk of infections and certain cancers in the elderly.
Led by Vishwa Deep Dixit, professor of comparative medicine and immunobiology at Yale School of Medicine, the researchers studied transgenic mice with elevated levels of FGF21. The team knocked out the gene’s function and studied the impact of decreasing levels of FGF21 on the immune system. They found that increasing the levels of FGF21 in old mice protected the thymus from age-related fatty degeneration and increased the ability of the thymus to produce new T cells, while FGF21 deficiency accelerated the degeneration of the thymus in old mice.
“We found that FGF21 levels in thymic epithelial cells is several fold higher than in the liver therefore FGF21 acts within the thymus to promote T cell production,” said Dixit.
“Elevating the levels of FGF21 in the elderly or in cancer patients who undergo bone marrow transplantation may be an additional strategy to increase T cell production, and thus bolster immune function,” said Dixit.
Dixit added that FGF21 is produced in the liver as an endocrine hormone. Its levels increase when calories are restricted to allow fats to be burned when glucose levels are low. FGF21 is a metabolic hormone that improves insulin sensitivity and also induces weight loss.
Dixit said further studies will focus on understanding how FGF21 protects the thymus from aging, and whether elevating FGF21 pharmacologically can extend the human healthspan and lower the incidence of disease caused by age-related loss of immune function.
“We will also look to developing a way to mimic calorie restriction to enhance immune function without actually reducing caloric intake.”
Yun-Hee Youm, Tamas L. Horvath, David J. Mangelsdorf, Steven A. Kliewer, Vishwa Deep Dixit. Prolongevity hormone FGF21 protects against immune senescence by delaying age-related thymic involution. Proceedings of the National Academy of Sciences, 2016; 201514511 DOI: 10.1073/pnas.1514511113
Liver-derived metabolic hormone fibroblast growth factor 21 (FGF21) improves insulin sensitivity and extends lifespan in mice. Aging also compromises the adaptive immune system by reducing T-cell production from the thymus. In this paper, we describe a new immunological function of FGF21 as a regulator of T-cell production from thymus in aging. The overexpression of FGF21 prevents thymic lipoatrophy, which protects the mice from age-induced loss of naïve T cells. FGF21 expression in thymic epithelial cells and signaling in thymic stromal cells support thymic function in aging. Loss of FGF21 in mice increases lethality postirradiation and delays the reconstitution of thymus. Hence, we highlight FGF21 as an immunometabolic regulator that can be harnessed to delay immune senescence.
Age-related thymic degeneration is associated with loss of naïve T cells, restriction of peripheral T-cell diversity, and reduced healthspan due to lower immune competence. The mechanistic basis of age-related thymic demise is unclear, but prior evidence suggests that caloric restriction (CR) can slow thymic aging by maintaining thymic epithelial cell integrity and reducing the generation of intrathymic lipid. Here we show that the prolongevity ketogenic hormone fibroblast growth factor 21 (FGF21), a member of the endocrine FGF subfamily, is expressed in thymic stromal cells along with FGF receptors and its obligate coreceptor, ?Klotho. We found that FGF21 expression in thymus declines with age and is induced by CR. Genetic gain of FGF21 function in mice protects against age-related thymic involution with an increase in earliest thymocyte progenitors and cortical thymic epithelial cells. Importantly, FGF21 overexpression reduced intrathymic lipid, increased perithymic brown adipose tissue, and elevated thymic T-cell export and naïve T-cell frequencies in old mice. Conversely, loss of FGF21 function in middle-aged mice accelerated thymic aging, increased lethality, and delayed T-cell reconstitution postirradiation and hematopoietic stem cell transplantation (HSCT). Collectively, FGF21 integrates metabolic and immune systems to prevent thymic injury.
Valuing your time more than the pursuit of money is linked to greater happiness, according to new research published by the Society for Personality and Social Psychology.
In six studies with more than 4,600 participants, researchers found an almost even split between people who tended to value their time or money, and that choice was a fairly consistent trait both for daily interactions and major life events.
“It appears that people have a stable preference for valuing their time over making more money, and prioritizing time is associated with greater happiness,” said lead researcher Ashley Whillans, a doctoral student in social psychology at the University of British Columbia. The findings were published online in the journal Social Psychological and Personality Science.
The researchers found an almost even split with slightly more than half of the participants stating they prioritized their time more than money. Older people also were more likely to say they valued their time compared to younger people.
“As people age, they often want to spend time in more meaningful ways than just making money,” Whillans said.
The researchers conducted separate surveys with a nationally representative sample of Americans, students at the University of British Columbia, and adult visitors of a science museum in Vancouver. Some of the studies used real-world examples, such as asking a participant whether he would prefer a more expensive apartment with a short commute or a less expensive apartment with a long commute. A participant also could choose between a graduate program that would lead to a job with long hours and a higher starting salary or a program that would result in a job with a lower salary but fewer hours.
A participant’s gender or income didn’t affect whether they were more likely to value time or money, although the study didn’t include participants living at the poverty level who may have to prioritize money to survive.
If people want to focus more on their time and less on money in their lives, they could take some actions to help shift their perspective, such as working slightly fewer hours, paying someone to do disliked chores like cleaning the house, or volunteering with a charity. While some options might be available only for people with disposable income, even small changes could make a big difference, Whillans said.
“Having more free time is likely more important for happiness than having more money,” she said. “Even giving up a few hours of a paycheck to volunteer at a food bank may have more bang for your buck in making you feel happier.”
1.Whillans, A., Weidman, A., and Dunn, E. Valuing Time Over Money Is Associated with Greater Happiness. Social Psychological and Personality Science, January 2016 DOI: 10.1177/1948550615623842
How do the trade-offs that we make about two of our most valuable resources—time and money—shape happiness? While past research has documented the immediate consequences of thinking about time and money, research has not yet examined whether people’s general orientations to prioritize time over money are associated with greater happiness. In the current research, we develop the Resource Orientation Measure (ROM) to assess people’s stable preferences to prioritize time over money. Next, using data from students, adults recruited from the community, and a representative sample of employed Americans, we show that the ROM is associated with greater well-being. These findings could not be explained by materialism, material striving, current feelings of time or material affluence, or demographic characteristics such as income or marital status. Across six studies (N = 4,690), we provide the first empirical evidence that prioritizing time over money is a stable preference related to greater subjective well-being.
Acoustics experts have created a new class of sound wave — the first in more than half a century in a breakthrough they hope could lead to a revolution in stem cell therapy.
The team at RMIT University in Melbourne, Australia, combined two different types of acoustic sound waves called bulk waves and surface waves to create a new hybrid: “surface reflected bulk waves.”
The first new class of sound wave discovered in decades, the powerful waves are gentle enough to use in biomedical devices to manipulate highly fragile stem cells without causing damage or affecting their integrity, opening new possibilities in stem cell treatment.
Dr Amgad Rezk, from RMIT’s Micro/Nano Research Laboratory, said the team was already using the discovery to dramatically improve the efficiency of an innovative new “nebuliser” that could deliver vaccines and other drugs directly to the lung.
“We have used the new sound waves to slash the time required for inhaling vaccines through the nebuliser device, from 30 minutes to as little as 30 seconds,” Rezk said.
“But our work also opens up the possibility of using stem cells more efficiently for treating lung disease, enabling us to nebulise stem cells straight into a specific site within the lung to repair damaged tissue.
“This is a real game changer for stem cell treatment in the lungs.”
The researchers are using the “surface reflected bulk waves” in a breakthrough device, dubbed HYDRA, which converts electricity passing through a piezoelectric chip into mechanical vibration, or sound waves, which in turn break liquid into a spray.
“It’s basically ‘yelling’ at the liquid so it vibrates, breaking it down into vapour,” Rezk said.
Bulk sound waves operate similar to a carpet being held at one end and shaken, resulting in the whole substrate vibrating as one entity. Surface sound waves on the other hand operate more like ocean waves rolling above a swimmer’s head.
“The combination of surface and bulk wave means they work in harmony and produce a much more powerful wave,” said Rezk, who co-authored the study with PhD researcher James Tan.
“As a result, instead of administering or nebulising medicine at around 0.2ml per minute, we did up to 5ml per minute. That’s a huge difference.”
The breakthrough HYDRA device is improving the effectiveness of a revolutionary new type of nebuliser developed at RMIT called Respite. Cheap, lightweight and portable, the advanced Respite nebuliser can deliver everything from precise drug doses to patients with asthma and cystic fibrosis, to insulin for diabetes patients, and needle-free vaccinations to infants.
In a study published Monday in the Proceedings of the National Academy of Sciences, the scientists tracked 1,000 people born in 1972-73 in the coastal city of Dunedin in New Zealand and calculated their “biological age” after their 38th birthdays based on a wide range of biomarkers. The measurements included:
•Kidneys, liver, lungs, metabolic and immune systems
•HDL cholesterol, cardiorespiratory fitness, lung function
•Length of the telomeres (protective caps at the end of chromosomes that have been found to shorten with age)
•Dental health like the condition of the gums
•Condition of the tiny blood vessels at the back of the eyes, (which are a proxy for the brain’s blood vessels)
They looked at the volunteers at age 26, 32 and 38 and found that while most of them aged at a normal pace — one year’s worth of physiological changes for each chronological year — some of them aged surprisingly slower or faster.
In fact, researchers calculated, the “biological ages” of the 38-year-olds ranged from 30 to nearly 60 years. From the report:
The fastest-aging study participants experienced two to three years of changes with the passage of a single calendar year. They tended to have worse balance and motor coordination and were physically weaker. Belsky and his colleagues said that these volunteers reported having more trouble with basic tasks like climbing stairs or carrying groceries.
Moreover, those who were aging fast also showed evidence of cognitive decline. Their IQ scores, which according to previous studies have been shown to remain relatively constant throughout a person’s life, were lower by age 38.
One particularly interesting finding of the study was that the people who were physiologically older looked older, at least according to Duke undergraduates who were asked to guess their ages from their pictures.
The study, which was funded in part by the National Institute on Aging, is significant because it looked at young adults. Most previous aging research is focused on the second half of the average person’s life, in the 50s, 60s, and 70s.
“Our findings indicate that aging processes can be quantified in people still young enough for prevention of age-related disease, opening a new door for antiaging therapies,” the researchers wrote. “The science of healthspan extension may be focused on the wrong end of the lifespan; rather than only studying old humans, geroscience should also study the young.”
Belsky said that in the future a person’s biological age could serve as a simple measure of a person’s health that may help patients better understand the battery of numbers they get from their doctors today.
“A single number would be much easier to process,” Belsky said.
He said the measurement could also help with assessing the health of a community. Right now we look at things like disease end points, new diagnoses, hospitalizations and death, but all are imperfect because they don’t give us a picture of the health of a whole person.