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.
Supplementing with soluble corn fiber can help build and retain calcium in bone, according to new research from Purdue University. The study focused on two critical times in a woman’s life adolescence and post-menopause, however the results may be beneficial to all adolescents and adults regardless of age.
“We are looking deeper in the gut to build healthy bone in girls and help older women retain strong bones,” said Connie Weaver, distinguished professor and head of nutrition science. “Soluble corn fiber, a prebiotic, helps the body better utilize calcium during both adolescence and post-menopause. The gut microbiome is the new frontier in health.”
The post-menopause findings are published in the American Journal of Clinical Nutrition, and the adolescent findings are published in Journal of Nutrition. The studies are funded by Tate & Lyle Ingredients America LLC. Weaver serves on the scientific advisory board for Pharmative LLC.
A prebiotic fiber passes through the gut for the microbes in the lower gut to digest. Here is where Weaver found that soluble corn fiber is broken down into short chain fatty acids to aid in bone health.
In the post-menopausal study, calcium retention was measured in 14 women by using an isotope to measure the excretion of 41Ca to measure bone loss. The women consumed 0 grams, 10 grams or 20 grams of this nondigestible carbohydrate each day for 50 days. Bone calcium retention was improved by 4.8 percent and 7 percent for those who consumed 10 grams and 20 grams, respectively. These amounts of soluble corn fiber would be found in supplement form.
“If projected out for a year, this would equal and counter the average rate of bone loss in a post-menopausal woman,” said Weaver, an expert in mineral bioavailability, calcium metabolism, botanicals and bone health.
The calcium 41 technology, an isotope measure to trace calcium deposits through accelerator mass spectrometry in the Purdue Rare Isotope Measurement Laboratory (PRIME Lab), can measure atomic quantities. In the adolescent study, 44Ca and 43Ca were used.
Thirty-one girls either consumed 0 grams, 10 grams or 20 grams of soluble corn fiber carbohydrate each day for three weeks while maintaining their regular diets. Both 10 grams and 20 grams led to improved calcium absorption by 12 percent for female adolescents, which would build 1.8 percent more skeleton a year.
In both studies, gastrointestinal symptoms were minimal and the same for the control groups, as well as in those who consumed soluble corn fiber.
“Most studies looking at benefits from soluble corn fiber are trying to solve digestion problems, and we are the first to determine that this relationship of feeding certain kind of fiber can alter the gut microbiome in ways that can enhance health,” Weaver said. “We found this prebiotic can help healthy people use minerals better to support bone health.”
Calcium is considered a shortfall nutrient, and few people meet the recommended intake of 1,300 milligrams of calcium for healthy bone mass.
“The finding doesn’t mean we should diminish our recommendation to consume calcium and follow a well-balanced diet. This is a strategy to better utilize your minerals,” Weaver said. “Calcium alone suppresses bone loss, but it doesn’t enhance bone formation. These fibers enhance bone formation, so they are doing something more than enhancing calcium absorption.”
Weaver’s team is looking into the mechanisms of how soluble corn fiber boosts calcium absorption and retention, as well as if the prebiotic fiber benefits the body in other ways.
Soluble Corn Fiber can be purchased at many health food stores.
S. A. Jakeman, C. N. Henry, B. R. Martin, G. P. McCabe, L. D. McCabe, G. S. Jackson, M. Peacock, C. M. Weaver. Soluble corn fiber increases bone calcium retention in postmenopausal women in a dose-dependent manner: a randomized crossover trial. American Journal of Clinical Nutrition, 2016; doi: 10.3945/ajcn.116.132761
Corrie M Whisner, Berdine R Martin, Cindy H Nakatsu, Jon A Story, Claire J MacDonald-Clarke, Linda D McCabe, George P McCabe, and Connie M Weaver. Soluble Corn Fiber Increases Calcium Absorption Associated with Shifts in the Gut Microbiome: A Randomized Dose-Response Trial in Free-Living Pubertal Females. J. Nutr. jn227256; 2016; doi: 10.3945/jn.115.227256
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.
In the last 40 years, fructose, a simple carbohydrate derived from fruit and vegetables, has been on the increase in American diets. Because of the addition of high-fructose corn syrup to many soft drinks and processed baked goods, fructose currently accounts for 10 percent of caloric intake for U.S. citizens. Male adolescents are the top fructose consumers, deriving between 15 to 23 percent of their calories from fructose–three to four times more than the maximum levels recommended by the American Heart Association.
A recent study at the Beckman Institute for Advanced Science and Technology at the University of Illinois found that, matched calorie for calorie with the simple sugar glucose, fructose causes significant weight gain, physical inactivity, and body fat deposition.
The paper, “Fructose decreases physical activity and increases body fat without affecting hippocampal neurogenesis and learning relative to an isocaloric glucose diet,” was published in Scientific Reports.
“The link between increases in sugar intake, particularly fructose, and the rising obesity epidemic has been debated for many years with no clear conclusions,” said Catarina Rendeiro, a postdoctoral research affiliate at the Beckman Institute for Advanced Science and Technology and lead author on the study. “The reality is that people are not only consuming more fructose through their diets, but also consuming more calories in general.
“One of the key questions is whether an increase in fructose intake contributes to obesity in the absence of excessive calorie intake.”
The researchers, under the direction of Justin Rhodes of Beckman’s NeuroTech Group and professor of psychology at Illinois, studied two groups of mice for two-and-a-half months: one group was fed a diet in which 18 percent of the calories came from fructose, mimicking the intake of adolescents in the United States, and the other was fed 18 percent from glucose.
“The important thing to note is that animals in both experimental groups had the usual intake of calories for a mouse,” said Rendeiro. “They were not eating more than they should, and both groups had exactly the same amount of calories deriving from sugar, the only difference was the type of sugar, either fructose or glucose.”
The results showed that the fructose-fed mice displayed significantly increased body weight, liver mass, and fat mass in comparison to the glucose-fed mice.
“In previous studies, the increases in fructose consumption were accompanied by increases in overall food intake, so it is difficult to know whether the animals put on weight due to the fructose itself or simply because they were eating more,” Rhodes said.
Remarkably, the researchers also found that not only were the fructose-fed mice gaining weight, they were also less active.
“We don’t know why animals move less when in the fructose diet,” said Rhodes. “However, we estimated that the reduction in physical activity could account for most of the weight gain.”
“Biochemical factors could also come into play in how the mice respond to the high fructose diet,” explained Jonathan Mun, another author on the study. “We know that contrary to glucose, fructose bypasses certain metabolic steps that result in an increase in fat formation, especially in adipose tissue and liver.”
The precise mechanisms are still being investigated, but one thing is certain: high intake of fructose by itself adds pounds.
“We designed this study based on the intake of fructose by adolescents in the United States,” said Rhodes. “Our study suggests that such levels of fructose can indeed play a role in weight gain, favor fat deposition, and also contribute to physical inactivity. Given the dramatic increase in obesity among young people and the severe negative effects that this can have on health throughout one’s life, it is important to consider what foods are providing our calories.”
Fasting as little as eight days a year could help bodies become healthier, according to new research from the University of Southern California.
Fasting two to four days at a time every six months causes stem cells to awake from their normal dormant state, and start regenerating. Researchers discovered this practice eliminated damaged and older cells, and caused new cells to be born, effectively renewing the immune system. This is the first time any natural intervention has ever been shown to trigger this self-renewal.
In mice and humans, white blood cell counts were significantly lowered after long periods without food. These bodies are vital to the human immune system. But, when their numbers decline to a critical point, pathways for hematopoietic stem cells were switched on. These cells manage the immune system and generate new blood.
“When you starve, the system tries to save energy, and one of the things it can do to save energy is to recycle a lot of the immune cells that are not needed, especially those that may be damaged,” Valter Longo of the USC Davis School of Gerontology, said.
Going without food for 48 to 96 hours shifts human bodies to consume stores of fat, glucose (sugar), and ketones (created when fats are broken down for energy). Unhealthy white blood cells are also broken down, so that their components can be reused for the next generation of cells. This process is akin to recycling for the immune system.
After a period of fasting, human immune systems generate new blood cells when nutrients start flowing back into the body. Researchers at USC wanted to know what drives body systems to rebuild the cells.
Protein kinase A, an enzyme known to inhibit cell regeneration, was reduced in the systems of people who are fasting, the study found. Concentrations of a growth-factor hormone called IGF-1 were also lowered in those who have not eaten in days.
Of course most people would not want to fast on only water for two to four days at a time and it is probably not safe except under medical supervision. There are several alternatives that produce some of the same benefits including juice fasting and time restricted eating for people that are healthy enough to do a less extreme form of fasting.
Juice fasting involves drinking raw fruit and vegetable juices usually for one day at a time. Some people juice fast once a week and others once a month. It is important to use at least 50% vegetables to make juice and not overdue the fructose sugars that are concentrated in fruit juice. Typically between 2 and 3 quarts of juice are consumed per day. There are now many brands of pressure pasteurized juices available in health food stores that are raw. High pressure is used to destroy the bacteria instead of heat. Water is not restricted on a juice fast.
Another approach to fasting which has produced beneficial results is time restricted eating. It involves eating with no limit on quantity during an 8 hour consecutive period and then going without food until the next day. Water is available to drink 24 hours each day and not restricted. Some people eat this way every day. A scientific study of time restricted eating which showed impressive results was published in Cell Metablolism.
Reference: Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression. Cell Stem Cell, Volume 14, Issue 6, p810–823, 5 June 2014
Several years ago, researchers at UCLA found that specific regions in the brains of long-term meditators were larger and had more gray matter than the brains of individuals in a control group. This suggested that meditation may indeed be good for all of us since, alas, our brains shrink naturally with age.
Now, a follow-up study suggests that people who meditate also have stronger connections between brain regions and show less age-related brain atrophy. Having stronger connections influences the ability to rapidly relay electrical signals in the brain. And significantly, these effects are evident throughout the entire brain, not just in specific areas.
Eileen Luders, a visiting assistant professor at the UCLA Laboratory of Neuro Imaging, and colleagues used a type of brain imaging known as diffusion tensor imaging, or DTI, a relatively new imaging mode that provides insights into the structural connectivity of the brain. They found that the differences between meditators and controls are not confined to a particular core region of the brain but involve large-scale networks that include the frontal, temporal, parietal and occipital lobes and the anterior corpus callosum, as well as limbic structures and the brain stem.
“Our results suggest that long-term meditators have white-matter fibers that are either more numerous, more dense or more insulated throughout the brain,” Luders said. “We also found that the normal age-related decline of white-matter tissue is considerably reduced in active meditation practitioners.”
The study consisted of 27 active meditation practitioners (average age 52) and 27 control subjects, who were matched by age and sex. The meditation and the control group each consisted of 11 men and 16 women. The number of years of meditation practice ranged from 5 to 46; self-reported meditation styles included Shamatha, Vipassana and Zazen, styles that were practiced by about 55 percent of the meditators, either exclusively or in combination with other styles.
Results showed pronounced structural connectivity in meditators throughout the entire brain’s pathways. The greatest differences between the two groups were seen within the corticospinal tract (a collection of axons that travel between the cerebral cortex of the brain and the spinal cord); the superior longitudinal fasciculus (long bi-directional bundles of neurons connecting the front and the back of the cerebrum); and the uncinate fasciculus (white matter that connects parts of the limbic system, such as the hippocampus and amygdala, with the frontal cortex).
“It is possible that actively meditating, especially over a long period of time, can induce changes on a micro-anatomical level,” said Luders, herself a meditator.
As a consequence, she said, the robustness of fiber connections in meditators may increase and possibly lead to the macroscopic effects seen by DTI.
“Meditation, however, might not only cause changes in brain anatomy by inducing growth but also by preventing reduction,” Luders said. “That is, if practiced regularly and over years, meditation may slow down aging-related brain atrophy, perhaps by positively affecting the immune system.”
But there is a “but.” While it is tempting to assume that the differences between the two groups constitute actual meditation-induced effects, there is still the unanswered question of nature versus nurture.
“It’s possible that meditators might have brains that are fundamentally different to begin with,” Luders said. “For example, a particular brain anatomy may have drawn an individual to meditation or helped maintain an ongoing practice — meaning that the enhanced fiber connectivity in meditators constitutes a predisposition towards meditation, rather than being the consequence of the practice.”
Still, she said, “Meditation appears to be a powerful mental exercise with the potential to change the physical structure of the brain at large. Collecting evidence that active, frequent and regular meditation practices cause alterations of white-matter fiber tracts that are profound and sustainable may become relevant for patient populations suffering from axonal demyelination and white-matter atrophy.”
While the study looked at more traditional meditation there is also evidence from other studies that similar improvements may apply to moving forms such as Tai Chi, Qigong and Shen Zhen.
Reference: Luders E., Clark K., Narr K. L., Toga A. W. (2011). Enhanced brain connectivity in long-term meditation practitioners. Neuroimage 57, 1308–1316. 10.1016/j.neuroimage.2011.05.075
Last year a study showed that sitting continuously for one hour or more was unhealthy. Now a newer and more extensive study of data of over 1 million individuals specifically looked at how much exercise is needed to counter the negative effects of sitting. According to an international team of researchers the health risks associated with sitting for eight or more hours a day whether at work, home or commuting can be eliminated with an hour or more of physical activity a day.
Ever since a study back in 1953 discovered that London bus drivers were at greater risk of heart disease compared to bus conductors, scientists have found increasing evidence that lack of physical activity is a major risk factor for several diseases and for risk of early death. Recent estimates suggest that more than 5 million people die globally each year as a result of failing to meet recommended daily activity levels.
Studies in high-income countries have suggested that adults spend the majority of their waking hours sitting down. A typical day for many people is driving to work, sitting in an office, driving home and watching TV. Current physical activity guidelines recommend that adults do at least 150 minutes of moderate intensity exercise per week. But, is that enough?
In an analysis published today in The Lancet that draws together a number of existing studies, an international team of researchers asked the question: if an individual is active enough, can this reduce, or even eliminate, the increased risk of early death associated with sitting down?
In total the researchers analysed 16 studies, which included data from more than one million men and women. The team grouped individuals into four quartiles depending on their level of moderate intensity physical activity, ranging from less than 5 minutes per day in the bottom group to over 60 minutes in the top. Moderate intensity exercise was defined as equating to walking at 3.5 miles/hour or cycling at 10 miles/hour, for example.
The researchers found that 60 to 75 minutes of moderate intensity exercise per day were sufficient to eliminate the increased risk of early death associated with sitting for over eight hours per day. However, as many as three out of four people in the study failed to reach this level of daily activity.
The greatest risk of early death was for those individuals who were physically inactive, regardless of the amount of time sitting — they were between 28% and 59% more likely to die early compared with those who were in the most active quartile — a similar risk to that associated with smoking and obesity. In other words, lack of physical activity is a greater health risk than prolonged sitting.
“There has been a lot of concern about the health risks associated with today’s more sedentary lifestyles,” says Professor Ulf Ekelund from the Medical Research Council Epidemiology Unit at the University of Cambridge. “Our message is a positive one: it is possible to reduce — or even eliminate — these risks if we are active enough, even without having to take up sports or go to the gym.
“For many people who commute to work and have office-based jobs, there is no way to escape sitting for prolonged periods of time. For these people in particular, we cannot stress enough the importance of getting exercise, whether it’s getting out for a walk at lunchtime, going for a run in the morning or cycling to work. An hour of physical activity per day is the ideal, but if this is unmanageable, then at least doing some exercise each day can help reduce the risk.”
The researchers acknowledge that there are limitations to the data analyzed, which mainly came from participants aged 45 years and older and living in western Europe, the US and Australia. However, they believe that the strengths of the analysis outweigh these limitations. Most importantly, the researchers asked all included studies to reanalyze their data in a harmonized manner, an approach that has never before been adopted for a study of this size and therefore also provides much more robust effect estimates compared with previous studies.
Reference: Ulf Ekelund, Jostein Steene-Johannessen, Wendy J Brown, Morten Wang Fagerland, Neville Owen, Kenneth E Powell, Adrian Bauman, I-Min Lee. Does physical activity attenuate, or even eliminate, the detrimental association of sitting time with mortality? A harmonised meta-analysis of data from more than 1 million men and women. The Lancet, 2016; DOI: 10.1016/S0140-6736(16)30370-1
The ability to reverse aging may reside in a stem cell gene named Nanog.
In a series of experiments at the University at Buffalo, the gene kicked into action dormant cellular processes that are key to maintaining healthy bones, arteries and other telltale signs of growing old.
The findings, published June 29 in the journal Stem Cells, also show promise in counteracting premature aging disorders.
“Our research into Nanog is helping us to better understand the process of aging and ultimately how to reverse it,” says Stelios T. Andreadis, PhD, professor and chair of the Department of Chemical and Biological Engineering at the UB School of Engineering and Applied Sciences, and the study’s lead author.
Additional authors come from UB’s Department of Biomedical Engineering, a joint program between UB’s engineering school and the Jacobs School of Medicine and Biomedical Sciences at UB, and the Department of Biostatistics and Bioinformatics at Roswell Park Cancer Institute in Buffalo.
To battle aging, the human body holds a reservoir of nonspecialized cells that can regenerate organs. These cells are called adult stem cells, and they are located in every tissue of the body and respond rapidly when there is a need.
But as people age, fewer adult stem cells perform their job well, a scenario which leads to age-related disorders. Reversing the effects of aging on adult stem cells, essentially rebooting them, can help overcome this problem.
Andreadis previously showed that the capacity of adult stem cells to form muscle and generate force declines with aging. Specifically, he examined a subcategory of muscle cells called smooth muscle cells which reside in arteries, intestines and other tissues.
In the new study, Panagiotis Mistriotis, a graduate student in Andreadis’ lab and first author of the study, introduced Nanog into aged stem cells. He found that Nanog opens two key cellular pathways: Rho-associated protein kinase (ROCK) and Transforming growth factor beta (TGF-?).
In turn, this jumpstarts dormant proteins (actin) into building cytoskeletons that adult stem cells need to form muscle cells that contract. Force generated by these cells ultimately helps restore the regenerative properties that adult stem cells lose due to aging.
“Not only does Nanog have the capacity to delay aging, it has the potential in some cases to reverse it,” says Andreadis, noting that the embryonic stem cell gene worked in three different models of aging: cells isolated from aged donors, cells aged in culture, and cells isolated from patients with Hutchinson-Gilford progeria syndrome.
Additionally, the researchers showed that Nanog activated the central regulator of muscle formation, serum response factor (SRF), suggesting that the same results may be applicable for skeletal, cardiac and other muscle types.
The researchers are now focusing on identifying drugs that can replace or mimic the effects of NANOG. This will allow them to study whether aspects of aging inside the body can also be reversed. This could have implications in an array of issues to improve quality of life and lifespan.
Reference: Mistriotis, P., Bajpai, V. K., Wang, X., Rong, N., Shahini, A., Asmani, M., Liang, M.-S., Wang, J., Lei, P., Liu, S., Zhao, R. and Andreadis, S. T. (2016), NANOG Reverses the Myogenic Differentiation Potential of Senescent Stem Cells by Restoring ACTIN Filamentous Organization and SRF-Dependent Gene Expression. STEM CELLS. doi: 10.1002/stem.2452
New treatments for osteoporosis or broken bones are on the horizon after scientists discovered they can grow new bone simply by vibrating stem cells.
Currently the only option for patients who suffer complicated breaks is to undergo painful surgery where doctors remove bone from a healthy part of their body and transplant it in the damaged site.
But now Scottish scientists have discovered that stem cells can be coaxed into turning into bone cells – known as osteoblasts – using low frequency vibrations in the lab, a technique dubbed ‘nanokicking.’
Stem cells are thought to be the future of medicine because they can become any cell in the body depending on their environment.
Researchers at the University of West Scotland and the University of Glasgow believe that the 1000Hz frequency mimics conditions experienced by natural bone in the body and induces stem cells to turn into bone in around 28 days, which can then be implanted.
The scientists also hope the same frequency could be used to encourage healing from within the body without the need for a transplant.
“Our bodies are continuously experiencing mechanical stimuli, such as from our walking steps and our heart beat,” said Professor Stuart Reid of the University of West Scotland.
“We know that natural bone has some interesting mechanoelectrical properties, the piezoelectric effect – converting mechanical stress to electricity, which are optimal close to 1000Hz.
“It is also well known that bone can only remain healthy when it is actively being loaded, hence why astronauts lose bone mass when in space. So we believe that we are mimicking something that the cells experience in our bodies, however the exact details are still being untangled.”
Bone is the second most commonly transplanted tissue in the world, behind blood transplants, and is used in many common procedures.
The UK’s aging population means demand is increasing due to conditions such as osteoporosis and hip fractures.
Using a patient’s own stem cells to build new bone would mean there was no risk of rejection. The stem cells could be retrieved from a patient’s bone marrow or even from fat cells from liposuction.
The stem cells are ‘jiggled’ in petri dishes on a specially built vibrating platform called a bioreactor which uses the same technology that astrophysicists use to hunt for gravitational waves – the distortions in space time which occur when black holes collide.
Professor Matt Dalby, of the University of Glasgow said: “The bioreactor we have designed brings together fields of research from different ends of the spectrum: stem cell research on the building blocks of our bodies, to technology used to detect the ripples in space and time caused by the collisions of massive objects.
“It’s amazing that technology developed to look for gravitational waves has a down-to-earth application in revolutionizing bone treatments for cleaner, safer and more effective therapy.”
Prof Reid, added: “The scale of movement that triggers the cells to transform is so small it would be the same as ‘sliding a single sheet of paper in and out from under a football on a table’.”
The team aims to test their lab-grown bone in people within 3 years and that therapy could be available in 10 years.
Further down the line they hope it will be possible to stimulate stem cells directly to heal fractures without surgery.