Dr Mercola Interviews Dr Villeponteau the Formulator of Stem Cell 100

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

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

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

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

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

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

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

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

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

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

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

Click here for more information about Stem Cell 100

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

Aging Reversed / ABC News

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

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

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

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

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

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

Stem Cell Secret’s of 115 Year Old Woman

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

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

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

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

Blood from world’s oldest woman suggests life limit

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

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

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.

Exercise Protein May Improve Physical Activity, Performance and Fitness

A recent study from the USC Leonard Davis School of Gerontology has shown that during exercise people express a strong hormone and that hormone when given to mice improves their physical capacity, performance and fitness. The research team’s findings have indicated new potential for addressing physical decline in humans during the aging process.

The study has revealed a detailed observation of how mitochondrial genome will encode instructions for regulating performance, physical capacity and metabolism that occurs with aging and may have the ability to increase a healthy lifespan.

Mitochondria are the energy source for cells. They also serve as the hub that coordinates and fine tunes metabolism through active communication throughout the body. As people age, this communication network appears to deteriorate. However, the recent research has suggested that it is possible to restore that communication network or refresh older mice so that they becomes just as fit as mice that are younger.

The team set out to look at the MOTS-c role. MOTS-c is one of a variety of newly identified hormones which mimic the results of exercise. This particular hormone is unique because rather than being encoded in the larger genome in the nucleus of a cell, it is encoded in the mitochondria’s small genome. This provides a brand new genome for targeting new interventions.

For the study, the team tested the affects of injecting MOTS-c in affected mice of a variety of ages through measuring physical performance and capacity in middle-aged mice (12 months of age), young mice (2 months of age) and older mice (22 months of age). The mice were given physical challenges which included running on a treadmill that accelerated and keeping their balance on a rod that rotated. All mice receiving the MOTS-c treatment and of all ages showed significant results of the challenges, scoring better than mice that were untreated and of all ages.

Interestingly, even the mice that were given a high-fat diet indicated significant physical improvements following MOTS-c injection and also showed less gain in weight that the untreated mice. The findings are similar to previous studies of MOTS-c injections in mice which also showed reversed age and diet dependent resistance to insulin and obesity due to an induced diet.

The team also saw significant physical improvements in MOTS-c treated older mice who were near the end of their life. The later life treatment showed improved gait, grip strength and physical performance which were all assessed through a walking test since a running test wasn’t possible for these older mice.

The mice who were older were equivalent to 65 years of age and older in humans. Once they were treated, their capacity on the treadmill was doubled and were also able to outperform the untreated, middle-aged cohorts.

In order to measure what effects exercise has on MOTS-c levels in humans, the team collected plasma and muscle tissue from the skeletons of young, healthy male participants who were instructed to exercise on stationary bicycles. The test samples were collected previous to the exercise, during the exercise period and following the exercise in addition to samples collected after a 4 hour resting period.

Levels of MOTS-c in muscle cells showed significant increases almost 12-fold following exercise and stayed partially elevated following the four hour resting period. Additionally, levels of MOTS-c in the blood plasma increased by about 50% both after and during exercise returning to baseline following the 4 hour rest. These results indicate that exercise in and of itself was the factor which prompted the expression of mitochondrial encoded managed peptides.

As a result of the studies in mice and the MOTS-c expression during exercise in people, there is support of the idea that the aging process is regulated by genes in nuclear and mitochondrial genomes. Although additional research is needed in regard to MOTS-c, the current data has indicated that treatments with MOTS-c might increase healthy lifespans in humans and additionally address a variety of age related diseases and conditions such as frailty.

The team has indicated that their findings from the MOTS-c injections in mice are quite promising for eventual translation into people. This is especially promising given the findings were the result of treatments in the mice beginning at an older age.

Reduced walking capacity and reduced stride length are indicators of declines in human physical performance and are greatly associated with morbidity and mortality in humans. Interventions that can target age related frailty and decline which can be applied in later life could be more feasible when compared to treatments for a lifetime.

To view the original scientific study click below

MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis.

Energy Drinks Can Have Adverse Effects on Heart

A study led by researchers at Texas A&M University has shown that some energy drinks have harmful effects on the muscle cells of the heart. The team observed that cardiomyocytes which are human heart cells that have been grown in a lab, when exposed to some energy beverages showed an increased heartbeat rate and a variety of other factors that affect cardiac function.

When these results are placed in the context of the human body, drinking these beverages has been linked to irregular beating of the heart, increased blood pressure, cardiomyopathy which is a disease of the heart muscle making it difficult to pump blood, and other conditions affecting the heart.

Global sales of energy beverages is estimated at $53 billion in 2018 and is rapidly growing. It has become important to understand any potential negative and unintended health problems associated with these drinks.

The consumption of energy beverages is not regulated and they are widely and easily accessible to all age groups over the counter. The consumption of them has been linked to a wide range of negative health effects in people and many of these effect the heart.

The team evaluated 17 widely available drinks which are sold over the counter. They then treated each drink with cardiomyocytes. They additionally studied the composition of each drink using novel methods. They then compared the effects and the differing ingredient concentrations of each drink and were able to conclude which ingredients might be contributing more to the adverse effects on the treated cardiomyocytes.

Through using mathematical models, they will able to determine that the possible presence of adenine, theophylline, and azelate are all substances that can result in negative effects on the heart. Very little is known in regards to these ingredients that could contribute to the negative effects of the energy drinks on the heart.

The evidence for the cardiovascular effects from these beverages on humans does remain inconclusive since the controlled clinical trials were mainly limited in the number of participants. The only tested a limited number of energy beverage types and were difficult to compare directly due to the fact that they employ different methods to evaluate the function of the cardiovascular system.

Additional research on the ingredients which were identified in this study is warranted to ensure the safety of consuming them, especially with consumers who have pre-existing health conditions.

However, the current study does show that some of the tested energy beverages have effects on human cardiomyocytes and the data does corroborate other studies on humans. The hope is that consumers will carefully consider the performance enhancing benefits of these particular beverages versus the emerging data which has suggested that they may have real adverse effects.

The team also hopes that the FDA will take a closer look at whether these drinks may need to be carefully reviewed in regards to possible labeling of their possible adverse health effects, and also whether certain age groups and susceptible sub-populations should be advised against drinking them.

To view the original scientific study click below

Relationships between constituents of energy drinks and beating parameters in human induced pluripotent stem cell (iPSC)-Derived cardiomyocytes

Combat Chronic Inflammation with Muscle Exercises

A team of biomedical engineers from Duke University have shown that human muscle possesses the natural ability to fend off some of the damage caused by chronic inflammation through exercise. Their discovery was manifested when they used engineered, grown in the lab human muscle.

There are a variety of processes that take place throughout the body through exercise. It can be somewhat difficult to differentiate which cells and systems are performing what inside the body of an active human. The team can mix and match a variety of cell types and tissue components from their engineered muscle platform and in the recent study, their discovery showed the muscle cells were able to take on anti-inflammatory measures on their own.

Inflammation can be good or bad. When a person injures their body, the first response is a low level inflammation reaction that will clear out debris and help in the rebuilding of tissue. As a response in other times, the body’s immune system will overreact and begins creating an inflammatory response that leads to damage. This is often the case in some COVID-19 situations where a deadly cytokine storm occurs. Additionally, there are a variety of diseases that also bring on chronic inflammation such as sarcopenia and rheumatoid arthritis which can lead to the wasting away of muscle and weakening its capability to contract.

There are a large variety of molecules which can lead to inflammation. Interferon gamma is a molecule that is pro-inflammatory and has been linked to a variety of muscle dysfunction and wasting. Earlier research in both animals and humans has exhibited that in general, exercising can assist in mitigating some of the results of inflammation. However, it has been challenging to differentiate what particular role these cells might play and also how they can be interacting with particular offending molecules for example, interferon gamma.

It is well known that diseases that are chronically inflammatory encourage muscles to atrophy. The team set out to see if the identical thing would occur in their engineered human muscle that was grown in the lab in a Petri dish. They not only confirmed that interferon gamma mostly works via a specific signaling pathway, they also were able to show that through exercising the muscle cells they were able to directly counter the pro-inflammatory signaling pathway separate from the presence of other tissues and cell types.

The team then set out to show proof that muscle by itself is able to block the destructive effects of interferon gamma. They used an engineered muscle platform which the lab had been developing over the previous decade. They initially grew functional, contracting human skeletal muscle in the lab and then began improving their processes by adding reservoirs of stem cells and immune cells to the mix.

The team involved in the recent study, utilized the lab-grown, fully functional muscles and overwhelmed them with high levels of interferon gamma for a period of seven days in order to copy the effects caused by long lasting periods of chronic inflammation. As the team expected, the muscle lost a large amount of its strength and it also became smaller.

They then reapplied the interferon gamma, however this time they also used a pair of electrodes to simulate an exercise regime on the muscle. They discovered that this procedure just about completely prevented the results of chronic inflammation. They also demonstrated that the simulated exercise on the muscle inhibited a particular molecular pathway contained in the muscle cells. They also showed that two particular medications that are used to treat rheumatoid arthritis also blocked the same pathway which resulted in the identical anti-inflammatory effects.

When the muscle cells were exercised, the muscles specifically were directly rivaling the pro-inflammatory signal that was being induced by interferon gamma quite to the surprise of the team. The results indicate how beneficial human muscles that are grown in the lab could be in the discovery of novel mechanisms that occur in disease and ultimately finding possible treatments. There certainly are thoughts that regimes and optimal levels of exercise could be a tool in fighting chronic inflammation while at the same time deterring over stressing cells. The hope is by using the lab engineered muscle, researchers will be able to find out if their notions could be true.

To view the original scientific study click below

Exercise Mimetics and JAK Inhibition Attenuate IFN-induced Wasting in Engineered Human Skeletal Muscle

Links Between Diet, Illnesses and Gut Microbes

Research has shown that diets which are rich in plant based and healthy foods encourage gut microbes which are associated with a lower risk of a variety of common illnesses and also heart disease. Now a new study conducted by researchers at Harvard T. H. Chan School of Public Health, King’s College London, the University of Trento, Italy, Massachusetts General Hospital and start-up company ZOE has revealed the link between diet, illnesses and gut microbes.

The study using blood chemical profiling and metagenomics revealed a panel of 15 different gut microbes that are linked to reduced risks of type 2 diabetes, obesity and a variety of common illnesses.

The Personalized Responses to Dietary Composition Trial 1 (PREDICT 1) was used to analyze very detailed data in regards to the gut microbiomes of the participants in addition to their cardiometabolic blood biomarkers, and their eating habits. The data indicated strong associations between the participant’s diet, their microbiome and their health.

The team was able to identify microbes that negatively or positively correspond to bad and good to a person’s risk of particular illnesses such as heart disease, diabetes and obesity. Interestingly, the microbiome show a greater link to these particular markers instead of other factors one of which is genetics. Some of the microbes were shown to be novel and haven’t even been named yet.

The healthy type diet was defined as a diet which would contain a variety of foods that are associated with a reduced risk of diseases that are considered chronic. The team discovered that trial participants who consumed this type of diet or one that is plant rich, had a higher likelihood of having levels that are high in specific gut microbes that are good and linked to a lower risk of some of the common health condition. They also found biomarkers that are microbiome based for obesity in addition to markers for impaired tolerance of glucose and cardiovascular disease which are also factors for COVID risk. Their findings could be utilized for help in creating personalized diet plans that are designed for the specific goal of improving a person’s health.

The team’s research may help in modifying personalized composition of each person’s individual microbiome in an effort to optimize their health through selecting the foods that are best suited for each person’s unique and individual biology.

As an example, the team’s discoveries have revealed that a person having a microbiome that is rich in Blastocysitis species and Prevotella copri was linked to a person being able to maintain a blood level that is favorable following a meal. Some of the other species were associated to reduced post-meal blood fat levels and inflammation markers.

As noted by the team, when we are eating we’re not only nourishing our body, but also feeding trillions of the microbes that reside in our gut.

The team was surprised to see such clear and large groups of what is informally called bad and good microbes that emerged from their analysis. And they were additionally excited about the discovery that very little is known to microbiologists about the microbes that haven’t been named. This has become a large area of research that could open future new insights into how the gut microbiome could be used as a target that is modifiable in improving human health and metabolism.

To view the original scientific study click below

Microbiome connections with host metabolism and habitual diet from 1,098 deeply phenotyped individuals.

Mental Well Being and Link to Cardiovascular and Overall Health

The National Institute of Mental Health in 2019 showed data that indicated that almost 51.5 million adults living in the U.S. were experiencing some kind of mental health challenge. And with the COVID-19 pandemic that has affected so many in the U.S., it is now estimated that 40% of adults are experiencing a mental health challenge or a substance abuse disorder. The AHA has now published information that relates to the link between cardiovascular health and overall health, and psychological wellness.

The authors of the information started their work by studying negative psychological health and the connection it may have to cardiovascular disease. Their work included studying research into traumatic and chronic stress, anxiety, pessimism, anger, hostility, and depression.

The author’s analysis of the overall data indicated increases in blood pressure readings, reduced blood flow to the heart, heart rate irregularities, and inflammatory markers which are all linked to the above mentioned mental conditions or traits.

People who have negative conditions or similar traits that affect their mental health are more likely to experience type 2 diabetes, high cholesterol, cardiovascular disease, weight issues and high blood pressure. The team also discovered that these particular people had a higher likelihood of engaging in a variety of behaviors which will negatively affect their health such as being inactive, smoking, not taking prescribed medications and unhealthy diets.

The team also looked at a variety of studies in regards to how cardiovascular health is affected by positive psychological characteristics. Participants in the studies who indicated sense of purpose, greater optimism, mindfulness, emotional vitality, life satisfaction, resilience, gratitude, and well being had a much lesser likelihood of having cardiovascular disease or stroke and they also had reduced mortality risk.

People who indicate a positive status in regards to their mental health were more likely to show better glucose control, lower cholesterol, lower blood pressure and less inflammation. The people who reported a healthy mental status had a higher likelihood of engaging in behaviors that are beneficial such as adhering to prescribed medications, not smoking, engaging in high levels of physical activity, visiting their healthcare professional on a regular basis, and engaging in eating habits that are heart healthy.

Analysts also looked at how interventions that center around psychological symptoms or conditions might impact cardiovascular and overall outcomes of health. The research included interventions such as promoting coping skills, reducing stress, and cultivating a positive state of well-being.

They discovered that these particular studies showed that engagement in body/mind programs and psychological therapy led to greater cardiovascular health and wellness in general. Effective programs that emphasize psychological health include psychotherapy, therapies for stress reduction, meditation, and collaborative approaches in care management.

When it comes to people who are at risk or have heart disease, healthcare providers should address the patient’s mental health wellness in combination with all physical conditions that affect their body such as cholesterol levels, blood pressure, chest pains and more.

And while there is volumes of research data which does reflect a link between negative psychological health and the risk of cardiovascular diseases, the team believes there is plenty of evidence that shows a tangible link between the body, the heart and the mind.

To view the original scientific study click below

Psychological Health, Well-Being, and the Mind-Heart-Body Connection: A Scientific Statement From the American Heart Association

Stretching Better than Walking for Lower Blood Pressure

A recent study from the University of Saskatchewan (USask) has shown that stretching is more effective and superior to brisk walks for reducing blood pressure in people who have high blood pressure or could be at risk of developing high blood pressure. The team found that just 30 minutes of stretching for 5 days each week resulted in better improvements in blood pressure over a 30 minute walk for 5 days of the week.

The CDC reports that about 45% of adults in the U.S. which equates to about 108 million people have hypertension. In 2018, hypertension was either a contributing cause or a primary cause of almost half a million deaths. And according to the National Heart, Lung and Blood Institute, uncontrolled or undiagnosed hypertension can result in a variety of diseases including chronic kidney disease, cardiovascular disease, vascular dementia and eye damage.

Health care professionals will typically recommend aerobic exercise to lower blood pressure. However, earlier research has shown that stretching might lower blood pressure due to improved blood flow and reduced stiffness of arteries. Stretching is not just about stretching muscles. When you stretch you are also stretching the blood vessels that feed into muscle, including all arteries. By reducing stiffness of arteries, there is less resistance to the flow of blood. Resistance to blood flow will increase blood pressure.

The current study by USask researchers is the first to test walking against stretching in a head-to-head comparison in the identical group of participants. The team randomly assigned 40 females and males with a mean age of 61 to two groups for an eight week study period. One group participated in a whole body stretching routine for 30 minutes each day for 5 days per week. The other group participated in brisk walks for the same amount of time and frequency. Every participant had elevated blood pressure or had stage 1 hypertension at the beginning of the study.

The stretching routine consisted of 21 stretching exercises with each participant performing each stretch two times while holding each stretch for 30 seconds and with a 15 second rest period between stretches.

The participants in the walking routine were asked to monitor their pulse and increase their pace if their pulse fell short of 50-65% of the maximum heart rate for their age.

All participant’s blood pressure was measured at both the beginning and at the end of the 8-week program utilizing three different techniques – one with a sphygmomanometer while the person sat down, one using the same meter while the person was lying down, and one with an automatic ambulatory blood pressure monitor which was set to take readings in 20 minutes intervals during waking time and in 45 minute intervals during sleep.

When compared to brisk walking, stretching resulted in greater reductions in blood pressure across all three types of the measurements. The study did show that the walkers lost more body fat from their waist over the 8 week period. The two different groups did not differ in their overall levels of activity outside their 30 minute daily routines. This indicates that the group participants did not compensate by adjusting or changing their usual levels of activity.

People who walk for help in reducing their blood pressure should continue to do so, but think about adding in some sessions of stretching. People should not come away from the research thinking they should not be participating in some kind of aerobic activity such as biking, walking, etc. All these activities have positive effects on blood sugar, cholesterol levels and body fat.

While the research protocol had the participants stretching for 30 minutes each time, the team suspects people can still benefit the same from shorter routines that emphasize the larger groups of muscles in the legs, in particular the hamstrings and the quadriceps. Yoga has been shown to product similar reductions in blood pressure.

The advantage to stretching is that it can be easily incorporated into a person’s daily routine, it doesn’t put people at the mercy of the weather, it is easy on the joints, and does not require a big commitment of time.

The team is currently seeking funding to engage in a larger study that would include more participants. Their goal is to expand the scope beyond measurements of blood pressure to explore possible physiological reasons behind why stretching results in reduced blood pressure – such as changes in the body’s nervous system and arterial stiffness.

To view the original scientific study click below:
Stretching is Superior to Brisk Walking for Reducing Blood Pressure in People With High–Normal Blood Pressure or Stage I Hypertension.

Simple Knee Injection Could Halt Osteoarthritis

A team of scientists have recently found a method for a simple knee injection that could possibly halt the effects of this disease. The team was able to show that by targeting in mice a specific protein pathway then follow with putting it in overdrive, they could halt the degeneration of cartilage over time.

The team then built on this finding by illustrating that by treating mice who had surgically induced knee cartilage degeneration, through the identical pathway through state of the art nano-medicine, they could reduce the knee pain and degeneration of cartilage quite dramatically.

The team’s lab is just one of the few studying EGFR (epidermal growth factor receptor) signaling in cartilage. From their beginning, they have discovered that EGFR inactivation or deficiency speeds up the progression of osteoarthritis in mice. Therefore, they proposed that its activation might be utilized for osteoarthritis treatment. They have proven that over-activating it within the knee will block the progression of the disease.

Although the tests from a variety of other labs that also work with EGFR have shown controversial and confusing results, the current labs work has consistently shown ties between EGFR deficiencies and osteoarthritis which has formed the foundation of this team’s hypothesis.

The team compared regular mice with mice that contained a molecule that will bind to EGFR which is known as a ligand, that had been over-expressed in chondrocytes which are cartilage building blocks. The over-expression will drive the over-activation EGFR signaling that occurs in knee cartilage.

When the team examined the mice, they found that the mice with over-expressed EGFR ligand consistently had enlarged cartilage. This meant that the cartilage wasn’t deteriorating like the mice that had the normal EGFR activity. Additionally, as these mice entered adulthood, their cartilage was shown to be resistant to degeneration and a variety of other osteoarthritis hallmarks. This occurred even when the meniscus of their knee showed damage.

The team then went further to prove that the mice over-activated EGFR was the cause for the resiliency in these mice. They found that treatments called gefitnib which have been designed to block function of EFGR, removed the protection against degeneration of the cartilage.

Using all this knowledge, the team looked toward possible clinical treatments. Using a new variety of tests, they then created nano-therapeutics using a potent EGFR ligand to transform growth factor-alpha onto nano-particles in synthetic form, to inject into the mice who previously had damage to their knee’s cartilage.

EGFR ligands which are free only have a very short half-life and therefore can’t be retained inside a joint capsule because of their small size. Nanoparticles will help restrict them in the joint, offer protection from degradation, lessen off-target toxicity, and send them deep within dense cartilage in order to reach chondrocytes.

When the mice were given an injection of the nano-therapeutics, the team noted that they slowed down the degeneration of the cartilage and hardening of bone in addition to easing knee pain. They also noted there were no significant side effects experienced in the mice that were treated.

Although there are a lot of technical aspects the team’s application will need to be worked out, the ability to slow down or even stop the direction of osteoarthritis through an injection instead of surgery, would quite dramatically alter how we function and feel after injury and as we age.

Treatments are most likely in the distant future for humans, however the nano-particles that were used have been tested in the clinic and considered safe. This paves the way for quick translation to clinical use.

To view the original scientific study click below

Targeting cartilage EGFR pathway for osteoarthritis treatment.