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.

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

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

lroot on April 16th, 2018

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.

lroot on April 14th, 2018

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.

lroot on April 11th, 2018

Adult Stem Cells

Researchers at Duke NUS Medical School headed by Gedas Greicius and Professor David Virshup, Director of the Programme in Cancer and Stem Cell Biology, have identified how the stem cell neighborhood, or niche, keep stem cells alive in the gut.

Stem cells have the ability to differentiate or develop into many different cell types in the body. They also serve as a repair system to replace damaged or aged cells. With the ability to regenerate, stem cells offer enormous potential to improve health, quality of life and lifespan.

Stem cells in our adult tissues live in very specific locations called stem cell niches where they provide an ideal and specialized neighborhood for stem cells. The stem cells in the niche are undifferentiated which means they have not changed into mature cells. This stem cell niche regulates how stem cells participate in tissue maintenance, regeneration and repair. The niche prevents stem cells from being depleted while also protecting the body from an over production of the stem cells. This understanding of stem cell niches is important in the field of stem cell therapeutics.

To understand the role of the niche, the researchers needed to identify the key cell types that regulate the numerous processes that take place within the cell niche. The key regulators in the intestinal cell niche are hormones called R-spondins and Wnts which are frequently expressed together. It has been unclear what type of niche cells make the R-spondins and Wnts.

The team studied the source and functional role of RSPO3, a R-spondin, and Wnts. RSPO3 is by far the most abundant R-spondin produced in the small intestine of a mouse. Using a mouse model, they identified the specific cell called a subepithelial myofibroblast as an essential source of both RSPO3 and Wnts. If these niche cells cannot make Wnts, mice will not develop adult intestines, and if they cannot make RSPO3 mice cannot repair the intestine after injury.

The work demonstrates the close interaction between epithelial stem cells and the niche that regulates them. The research provides new insights into the structure of the stem cell niche after injury and in health.

Reference: Gediminas Greicius, Zahra Kabiri, Kristmundur Sigmundsson, Chao Liang, Ralph Bunte, Manvendra K. Singh, David M. Virshup. PDGFRa pericryptal stromal cells are the critical source of Wnts and RSPO3 for murine intestinal stem cells in vivo. Proceedings of the National Academy of Sciences, 2018; 115 (14): E3173 DOI: 10.1073/pnas.1713510115

lroot on April 5th, 2018

Intestinal Function

A new research study conducted by the students and faculty at Binghamton University, State University at New York, has revealed that food packaging could be negatively affecting the way in which our digestive tract operates. Zinc Oxide (ZnO) nanoparticles at doses that are relevant to what might be normally eaten in a meal or in a day, change the way our intestines absorb nutrients or your intestinal cell gene and protein expression.

ZnO nanoparticles are present in the lining of certain canned goods for their antimicrobial properties and to help prevent staining of sulfur-producing foods. In this study, canned tuna, corn, asparagus and chicken were studied using mass spectrometry to estimate how many particles might be transferred to the food. The findings revealed the food contained 100 times the daily dietary allowance of zinc. The researchers then looked at the effect the particles had on the digestive tract.

The researchers looked at how an animal model (chickens) respond to nanoparticle ingestion. The cell culture results are similar to results found in animals and that the gut microbial populations are affected. The effects of nanoparticles on intestinal cells have been looked at before, but the research tended to work with really high doses and looked for obvious toxicity like cell death. The current study looked at cell function which is a more subtle effect and looked at nonparticle doses which are closer to what might people might really be exposed to.

The nanoparticles tend to settle onto the cells representing the gastrointestinal tract and cause loss or remodeling of the microvilli which are tiny projections on the surface of the intestinal absorptive cells that assist in increasing the surface area available for absorption. Loss of surface area tends to result in a decrease in nutrient absorption. Also, some of the nanoparticles cause pro-inflammatory signaling at high doses which can increase the permeability of the intestinal model. An increase in intestinal permeability means that compounds that are not supposed to pass through into the bloodstream might be able to.

The researchers note that it is difficult to forecast what the long-term effects of nanoparticle ingestion are on human health, especially based on results from a cell culture model. The model does show that the nanoparticles do have effects on the in vitro model, and understanding their effect on the gut function is an important area of study for consumer safety. Future studies will focus on the food additive-gut microbiome interactions.

Journal Reference:
1. Fabiola Moreno-Olivas, Elad Tako, Gretchen J. Mahler. ZnO nanoparticles affect intestinal function in an in vitro model. Food & Function, 2018; 9 (3): 1475 DOI: 10.1039/C7FO02038D

Brain Cells

Researchers show for the first time that healthy older men and women can generate just as many new brain cells as younger people.

There has been controversy over whether adult humans grow new neurons, and some research has previously suggested that the adult brain was hard-wired and that adults did not grow new neurons. This study, to appear in the journal Cell Stem Cell on April 5, counters that notion. Lead author Maura Boldrini, associate professor of neurobiology at Columbia University, says the findings may suggest that many senior citizens remain more cognitively and emotionally intact than commonly believed.

“We found that older people have similar ability to make thousands of hippocampal new neurons from progenitor cells as younger people do,” Boldrini says. “We also found equivalent volumes of the hippocampus (a brain structure used for emotion and cognition) across ages. Nevertheless, older individuals had less vascularization and maybe less ability of new neurons to make connections.”

The researchers tested hippocampi from 28 previously healthy individuals aged 14-79. This is the first time researchers looked at newly formed neurons and the state of blood vessels within the entire human hippocampus. The researchers had determined that study subjects were not cognitively impaired and had not suffered from depression or taken antidepressants, which Boldrini and colleagues had previously found could impact the production of new brain cells.

In rodents and primates, the ability to generate new hippocampal cells declines with age. Waning production of neurons and an overall shrinking of the dentate gyrus, part of the hippocampus thought to help form new episodic memories, was believed to occur in aging humans as well.

The researchers from Columbia University and New York State Psychiatric Institute found that even the oldest brains they studied produced new brain cells. “We found similar numbers of intermediate neural progenitors and thousands of immature neurons,” they wrote. Nevertheless, older individuals form fewer new blood vessels within brain structures and possess a smaller pool of progenitor cells descendants of stem cells that are more constrained in their capacity to differentiate and self-renew.

Boldrini surmised that reduced cognitive-emotional resilience in old age may be caused by this smaller pool of neural stem cells, the decline in vascularization, and reduced cell-to-cell connectivity within the hippocampus. “It is possible that ongoing hippocampal neurogenesis sustains human-specific cognitive function throughout life and that declines may be linked to compromised cognitive-emotional resilience,” she says.

Boldrini says that future research on the aging brain will continue to explore how neural cell proliferation, maturation, and survival are regulated by hormones, transcription factors, and other inter-cellular pathways.

Reference: Maura Boldrini, Camille A. Fulmore, Alexandria N. Tartt, Laika R. Simeon, Ina Pavlova, Verica Poposka, Gorazd B. Rosoklija, Aleksandar Stankov, Victoria Arango, Andrew J. Dwork, René Hen, J. John Mann. Human Hippocampal Neurogenesis Persists throughout Aging. Cell Stem Cell, 2018; 22 (4): 589 DOI: 10.1016/j.stem.2018.03.015

lroot on March 30th, 2018

Biological Age

A study published in Nature Genetics and led by scientists at Van Andel Research Institute (VARI) and Cedars Sinai, have developed a new computational, straightforward method to measure cellular age. The findings may lead to simpler, better screening and a way to measure the success of anti-aging therapies.

The findings reveal a measurable, progressive loss of specific chemical tags that regulate gene activity and can be detected at the earliest stays of development. These changes will continue throughout a person’s life and will correlate with cellular rather than chronological age.

The study builds on a 2011 long time collaboration and discovery by Benjamin Berman, Ph. D. of Cedars-Sinai and Peter Laird, Ph.D. and Hui Shen, Ph.D. of VARI. The 2011 discovery first determined loss of these DNA marks (called methyl groups) occurs in specific areas of the genome. However, at the time the techniques used could not detect this process occurring in normal cells. Our cellular clock begins ticking the moment our cells start dividing. This method allowed the researchers to track the history of the past divisions and measure age-related changes to the genetic code that may contribute to both dysfunction and normal aging.

Every cell in the nearly 40 trillion cells in the human body can trace its lineage back to a single, fertilized egg cell which contains the original copy of a person’s DNA. Throughout a person’s lifetime, the cells divide and replace damaged or old cells at different rates based on factors such as their function in the body, would healing and environmental insults.

Even though undergoing elaborate biological quality control checks, each cell division chips away at the genome’s integrity which leaves behind an accumulating number of changes. Principal among these is a dramatic shift in the location and number of methyl groups on the genome which is part of a process that begins during fetal development and continues through a lifetime.

What the researchers found striking about the results from their new method is that they push back the start of that process to the earliest stages of in utero development. Until recently mechanisms behind loss of DNA methyl groups (known as hypomethylation) have largely been unknown. It appears to be more profound in tissues with a high turnover rate such as skin and the epithelium. Typically, tissues with high turnover rates are more susceptible because there are more chances for errors to accumulate. What is being seen is a normal process of cellular aging.

The research project encompassed more than 200 mouse datasets and 340 human datasets the most in-depth study of its kind. The study would not have been possible without massive swaths of accessible data from large-scale sequencing projects.

Reference: Wanding Zhou, Huy Q. Dinh, Zachary Ramjan, Daniel J. Weisenberger, Charles M. Nicolet, Hui Shen, Peter W. Laird, Benjamin P. Berman. DNA methylation loss in late-replicating domains is linked to mitotic cell division. Nature Genetics, 2018; DOI: 10.1038/s41588-018-0073-4

lroot on March 23rd, 2018

New Human Organ

Researchers have identified a previously unknown feature of human anatomy with implications for the function of all organs, most tissues and the mechanisms of most major diseases.

Published March 27 in Scientific Reports, a new study co-led by an NYU School of Medicine pathologist reveals that layers of the body long thought to be dense, connective tissues below the skin’s surface, lining the digestive tract, lungs and urinary systems, and surrounding arteries, veins, and the fascia between muscles are instead interconnected, fluid-filled compartments.

This series of spaces, supported by a meshwork of strong (collagen) and flexible (elastin) connective tissue proteins, may act like shock absorbers that keep tissues from tearing as organs, muscles, and vessels squeeze, pump, and pulse as part of daily function.

Importantly, the finding that this layer is a highway of moving fluid may explain why cancer that invades it becomes much more likely to spread. Draining into the lymphatic system, the newfound network is the source of lymph, the fluid vital to the functioning of immune cells that generate inflammation. Furthermore, the cells that reside in the space, and collagen bundles they line, change with age, and may contribute to the wrinkling of skin, the stiffening of limbs, and the progression of fibrotic, sclerotic and inflammatory diseases.

The field has long known that more than half the fluid in the body resides within cells, and about a seventh inside the heart, blood vessels, lymph nodes, and lymph vessels. The remaining fluid is “interstitial,” and the current study is the first to define the interstitium as an organ in its own right, and as one of the largest of the body, say the authors.

The researchers say that no one saw these spaces before because of the medical field’s dependence on the examination of fixed tissue on microscope slides, believed to offer the most accurate view of biological reality. Scientists prepare tissue this examination by treating it with chemicals, slicing it thinly, and dying it to highlight key features. The “fixing” process makes vivid details of cells and structures, but drains away any fluid. The current research team found that the removal of fluid as slides are made causes the connective protein meshwork surrounding once fluid-filled compartments to pancake, like the floors of a collapsed building.

“This fixation artifact of collapse has made a fluid-filled tissue type throughout the body appear solid in biopsy slides for decades, and our results correct for this to expand the anatomy of most tissues,” says co-senior author Neil Theise, MD, professor in the Department of Pathology at NYU Langone Health. “This finding has potential to drive dramatic advances in medicine, including the possibility that the direct sampling of interstitial fluid may become a powerful diagnostic tool.”

The study findings are based on newer technology called probe-based confocal laser endomicroscopy, which combines the slender camera-toting probe traditionally snaked down the throat to view the insides of organs (an endoscope) with a laser that lights up tissues, and sensors that analyze the reflected fluorescent patterns. It offers a microscopic view of living tissues instead of fixed ones.

Using this technology in the fall of 2015 at Beth Israel Medical Center, endoscopists and study co-authors David Carr-Locke, MD, and Petros Benias, MD, saw something strange while probing a patient’s bile duct for cancer spread. It was a series of interconnected cavities in this submucosal tissue level that not match any known anatomy.

Faced with a mystery, the endoscopists walked the images into the office of their partnering pathologist in Theise. Strangely, when Theise made biopsy slides out of the same tissue, the reticular pattern found by endomicroscopy disappeared. The team would later confirm that very thin spaces seen in biopsy slides, traditionally dismissed as tears in the tissue, were instead the remnants of collapsed, previously fluid-filled compartments.

For the current study, the team collected tissue specimens of bile ducts during twelve cancer surgeries that were removing the pancreas and the bile duct. Minutes prior to clamping off blood flow to the target tissue, patients underwent confocal microscopy for live tissue imaging.

Once the team recognized this new space in images of bile ducts, they quickly recognized it throughout the body, wherever tissues moved or were compressed by force. The cells lining the space are also unusual, perhaps responsible for creating the supporting collagen bundles around them, say the authors. The cells may also be mesenchymal stem cells, says Theise, which are known to be capable of contributing to the formation of scar tissue seen in inflammatory diseases. Lastly, the protein bundles seen in the space are likely to generate electrical current as they bend with the movements of organs and muscles, and may play a role in techniques like acupuncture, he says.

Reference: Petros C. Benias, Rebecca G. Wells, Bridget Sackey-Aboagye, Heather Klavan, Jason Reidy, Darren Buonocore, Markus Miranda, Susan Kornacki, Michael Wayne, David L. Carr-Locke, Neil D. Theise. Structure and Distribution of an Unrecognized Interstitium in Human Tissues. Scientific Reports, 2018; 8 (1) DOI: 10.1038/s41598-018-23062-6

lroot on March 21st, 2018

Mesenchymal Stem Cells

Ever notice how a cut inside the mouth heals much faster than a cut to the skin? Gum tissue repairs itself roughly twice as fast as skin and with reduced scar formation. One reason might be because of the characteristics of gingival mesenchymal stem cells, or GMSCs, which can give rise to a variety of cell types. Mesenchymal stem cells are also found in bone marrow and adipose (fat) tissue.

“This study represents the convergence of a few different paths we’ve been exploring,” says Songtao Shi, chair and professor of Penn Dental Medicine’s Department of Anatomy and Cell Biology and the senior author on the study. “First, we know as dentists that the healing process is different in the mouth; it’s much faster than in the skin. Second, we discovered in 2009 that the gingiva contains mesenchymal stem cells and that they can do a lot of good therapeutically. And, third, we know that mesenchymal stem cells release a lot of proteins. So here we asked, How are the gingival mesenchymal stem cells releasing all of these materials, and are they accelerating wound healing in the mucosal tissues?”

Xiaoxing Kou, a visiting scholar at Penn Dental Medicine, was the first author on the work. Shi and Kou collaborated with colleagues Chider Chen and Anh Le from Penn Dental Medicine as well as Yanheng Zhou from Peking University, Xingtian Xu from the University of Southern California, Los Angeles, Claudio Giraudo and Maria L. Sanmillan from the Children’s Hospital of Philadelphia, and Tao Cai from the National Institute of Dental and Craniofacial Research.

From earlier work by Shi’s group and others, it was clear that mesenchymal stem cells perform many of their functions by releasing signaling molecules in extracellular vesicles. So to understand what distinguishes mesenchymal stem cells in the gingiva from those in the skin, the Penn-led team began by comparing these extracellular vesicles between the two types. They found that the GMSCs contained more proteins overall, including the inflammation-dampening IL-1RA, which blocks a proinflammatory cytokine. IL-1RA also happens to be used as a therapy to treat rheumatoid arthrisits, an inflammatory condition.

Next the team zoomed in to look at what might be controlling the release of IL-1RA and other cytokines. They had a suspect in the protein Fas, which they had earlier connected to immune regulation. They found that in gingival MSCs had more Fas than skin MSCs, and that mice deficient in Fas had reduced IL-1RA as well as reduced secretion of IL-1RA.

Further molecular probing revealed that Fas formed a protein complex with Fap-1 and Cav-1 to trigger the release of small extracellular vesicles. To identify the connection with wound healing, they examined wound tissue and found that IL-1RA was increased in GMSCs around the margins of wounds. Mice lacking IL-1RA or in which the protein was inhibited took longer to heal gingival wounds.

In contrast, when the researchers isolated IL-1RA that had been secreted from GMSCs and injected it into wounds, it significantly accelerated wound healing.

“We found that mesenchymal stem cells, and especially gingival mesenchymal stem cells, release large amount of cytokines through an extracellular vesicle,” says Kou.

These findings may have special significance for people with diabetes, a major complication of which is delayed wound healing. In the study, the researchers found that GMSCs in mice with diabetes were less able to secrete extracellular vesicles compared to GMSCs in healthy mice, and their GMSCs also had less IL-1RA secretion. Introducing extracellular vesicles secreted from the GMSCs of healthy mice reduced wound healing time in diabetic mice.

“Our paper is just part of the mechanism of how these stem cells affect wound healing,” Kou says, “but I think we can build on this and use these cells or the extracellular vesicles to target a lot of different diseases, including the delayed wound healing seen in diabetic patients.” Moving forward, Shi, Kou and colleagues want to move their work into the clinic.

“We are targeting translational therapies,” says Shi. “These cells are easy to harvest from the gingiva, and that makes them a beautiful cell for clinical use. We have a lot of work ahead of us, but I can see using these cells to reduce scar formation, improve wound healing, and even treat many inflammatory and autoimmune diseases.”

Reference: Xiaoxing Kou, Xingtian Xu, Chider Chen, Maria Laura Sanmillan, Tao Cai, Yanheng Zhou, Claudio Giraudo, Anh Le, Songtao Shi. The Fas/Fap-1/Cav-1 complex regulates IL-1RA secretion in mesenchymal stem cells to accelerate wound healing. Science Translational Medicine, 2018; 10 (432): eaai8524 DOI: 10.1126/scitranslmed.aai8524

Group Exercise

Working out in groups and with friends can be a big bonus. One of the benefits researchers discovered was that it lowered stress in a study by 26 percent and significantly improved the quality of life! Dayna Yorks, lead researcher for the study conducted by the University of New England College of Osteopathic Medicine, says the communal benefits of friends and colleagues coming together and working out together pays dividends beyond exercising alone. Doing something difficult while encouraging one another, supports the concept of a physical, emotional and mental approach to health that is important to reducing stress.

The study involved 69 medical students a group known for a self-reported low quality of life and with high levels of stress. The students were allowed to self select a twelve week exercise program either as individuals or within a group setting. A control group was included which abstained from exercise other than biking or walking for transportation purposes. Every four weeks the study completed a survey which asked them to rate their levels of quality of life and perceived stress in three categories including mental, emotional and physical.

The participants who worked out in a group spent at least 30 minutes at least once a week in CXWORX, a core strengthening and functional fitness training program. At the end of the twelve week study period, the mean monthly survey scores showed significant improvements in all three quality of life categories mental (12.6% increase), physical (24.8% increase) and emotional (26% increase). The students also reported a 26.2% reduction in perceived stress levels.

The individual fitness participants were allowed to engage in any exercise regimen they preferred which could include weight lifting and running but they had to work out alone or with no more than two partners. The individual exercisers worked out twice as long, but saw no significant changes in any category except mental (11% increase). The control group also saw no significant changes in quality of life or perceived stress.

Dr. York suggests that given the findings, not only should medical schools consider adding group fitness opportunities to their students, but anyone should think about engaging in more group exercise programs. This type of exercise regimen is an excellent outlet to manage stress and feel better mentally, physically and emotionally!

Reference: Dayna M. Yorks, Christopher A. Frothingham, Mark D. Schuenke. Effects of Group Fitness Classes on Stress and Quality of Life of Medical Students. The Journal of the American Osteopathic Association, 2017; 117 (11): e17 DOI: 10.7556/jaoa.2017.140