Dr Mercola Interviews Dr Villeponteau the Formulator of Stem Cell 100

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

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

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

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

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

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

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

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

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

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

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

Click here for more information about Stem Cell 100

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

Aging Reversed / ABC News

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

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

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

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

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

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

Stem Cells Secret’s of 115 Year Old Woman

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

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

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

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

Blood from world’s oldest woman suggests life limit

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

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

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

Regenerating Neurons in the Brain and Eye

The death of neurons whether in the eye or in the brain can result in a variety of human neurodegenerative diseases that range from blindness to Parkinson’s disease. Treatments currently available for these type of disorders only slow the progression of the illness. This is because once a neuron dies it cannot be replaced.

A study conducted by researchers from the University of Notre Dame, Johns Hopkins University, Ohio State University and the University of Florida have identified networks of genes that regulate the process which is responsible for determining if neurons will regenerate in certain animals such as zebrafish.

The study is proof of principle indicating that it is possible to regenerate neurons in the retina. The team also believes the process for regenerating neurons located in the brain will be similar.

For the research, the team mapped genes of animals that have the ability to regenerate neurons in the retina. One example is found in zebrafish. When their retina is damaged, cells known as Muller glia go through a reprogramming process. During this process, the Muller glia cells change their gene expression and become like progenitor cells or cells that are used during early organism development. These now progenitor cells can become any cell that is necessary to fix the retina that has become damaged.

People also have Muller glia cells. However, when a human retina is damaged, the Muller glia cells respond with gliosis which is a process that will not allow them to reprogram.

After the team determined the different animal processes for retina damage recovery, they had to decipher if the process for gliosis and reprogramming were similar. They wondered if the Muller glia follow the identical path in non-regenerating and regenerating animals or would the paths be totally different. This knowledge would be important so they would be able to use Muller glia cells to regenerate neurons in the retina in humans. Understanding whether it would be a matter of redirecting the current Muller glia path or if an entirely different process would be required.

They found that the regeneration process only needed the organism to turn back on its early processes of development. They were also able to illustrate that during zebrafish regeneration Muller glia also go through gliosis. This means that organisms that have the ability to regenerate retinal neurons do follow a similar path to animals that cannot.

The network of genes in zebrafish are able to move Muller glia cells from gliosis into the reprogrammed state, however the network of genes in mice models blocked the Muller glia from reprogramming. From here, the team was able to modify zebrafish Muller glia cells into a similar state that blocked the reprogramming while also having mice models regenerate some neurons in the retina.

The next step for the researchers is to try and identify the number of gene regulatory networks that are responsible for neuronal regeneration and exactly which genes within the network are the ones responsible for regulating regeneration.

To view the original scientific study click below

Gene regulatory networks controlling vertebrate retinal regeneration

Coffee After Breakfast for Metabolic Control

Research from the Centre for Nutrition, Exercise and Metabolism at the University of Bath (UK) looked at the combined effects of caffeine and disrupted sleep on our metabolism and found surprising results. They found that a strong, black cup of coffee to wake you up following a bad night’s sleep might impair control of blood sugar levels.

The team showed that while one night of poor sleep has limited impact on a person’s metabolism, drinking coffee to perk up from a slumber can have a negative effect on blood sugar control. Due to the importance of keeping our blood sugar levels in a safe range to reduce the risk of conditions such as heart disease and diabetes, the team’s results could have far reaching implications on health. This is especially important considering the worldwide popularity of coffee.

For the study the physiologists at the University of Bath had 29 healthy women and men undergo three different overnight experiments which were in a random order. In one, these participants had a normal night’s sleep and were then asked to consume a sugary beverage on waking in the morning.

In another experiment, the participants experienced a disrupted night’s sleep (the researchers woke them up every hour for a five minute period), and then on waking were given the identical sugary beverage as the first group.

For the third experiment, the participants experienced the same disrupted sleep as the second group but in this group they were given a strong, black cup of coffee 30 minutes prior to drinking the sugary beverage.

Blood samples were taken from all participants in each of the tests. They were taken after consuming the sugary beverage which in energy calories mirrored what might typically be consumed for breakfast.

The team’s findings highlight that one night of disrupted sleep did not result in any worsening of the participant’s blood glucose/insulin responses at breakfast when compared to a normal night’s sleep. Earlier research has suggested that losing many hours of sleep over one night and/or multiple nights might have negative effects on metabolism. Based on the new research, a single night of fragmented sleep which could be due to noise disturbance, insomnia or other disruptions, does not have the same effect.

However, a cup of strong, black coffee before breakfast substantially increased the blood glucose response to breakfast by about 50%. Population based surveys have indicated that coffee may be associated with good health although past research has demonstrated that caffeine has the ability to cause insulin resistance.

The new study reveals that the remedy of consuming coffee following a bad night’s sleep may solve the problem of feeling sleepy, however could lead to limiting the body’s ability to tolerate sugar consumed with breakfast.

The team notes that nearly half of us will wake up in the morning and prior to doing anything else will reach for a cup of coffee. Intuitively, the more tired we are the stronger the coffee we will consume. This new study is important and shows far reaching health implications as until now we have had limited knowledge in regards to what this may be doing to our bodies and in particular to our blood sugar and metabolic control.

The study shows that consuming coffee first thing in the morning and particularly after a bad night’s sleep, impairs our blood sugar control. We may be able to improve this by eating breakfast first and consuming coffee later if we feel we need it.

The results have indicated that one night of disrupted sleep did not worsen the participant’s blood glucose/insulin response to the sugary beverage compared to a normal night’s sleep which can be reassuring to many of us. However, beginning the day following a poor night’s sleep with a strong cup of coffee did have a negative effect of about 50% on glucose metabolism.

People should try to balance the potentially stimulating benefits of caffeinated coffee in the morning with the potentially higher blood glucose levels. It may be better to drink coffee after breakfast rather than before.

There is still a lot more to be learned about the effects of sleep on our metabolism. Questions remain as to how much sleep disruption is required to impair our metabolism and what longer term implications of this might be. Also, can exercise for instance help to counter some of this.

To view the original scientific study click below

Glucose control upon waking is unaffected by hourly sleep fragmentation during the night, but is impaired by morning caffeinated coffee

Fructose and Inflammatory Bowel Disease

A new study conducted on mice has suggested that a diet that is high in the sugar fructose exacerbates inflammatory bowel disease (IBD). It appears that changes in gut bacteria mediate the effect.

IBD is an overall term for a variety of conditions that feature chronic inflammation of the digestive system. The two most common types are Crohn’s Disease and ulcerative colitis. Symptoms of IBD include stomach pain, persistent diarrhea, bloody stools or rectal bleeding, fatigue and unexplained weight loss.

The CDC reports that the number of adults who receive an IBD diagnosis every year in the U. S. has increased from 2 million in the year 1999 to 3 million in 2015.

Earlier research in animals found that a diet which is high in fructose can damage the colon and also lead to inflammation. This suggests that a higher intake of fructose may be a reason for the increased incidence of IBD in recent years.

Population studies have not always indicated a link between refined sugar intake and IBD. One large study did not find an association between any specific dietary pattern and IBD although the results did show that a diet which is high in soft drinks and sugar did increase the risk of a person developing ulcerative colitis in cases where intake of vegetables was low.

High fructose corn syrup is added to candy, baked goods, sodas and other processed foods by manufacturers of these products. Consumption of fructose has increased by nearly one-third in the U.S. over the last 30 years according to estimates. The increase in IBD parallels the higher levels of the consumption of fructose not only in the U. S. but other countries as well.

The team involved in the recent study set out to investigate whether fructose exacerbates inflammation in mouse models with IBD. They additionally tested the idea that changes in the microbiota in the gut mediate the inflammatory effects of consuming fructose.

The team’s findings have provided evidence of a direct association between IBD and dietary fructose which support the idea that the high consumption of fructose could exacerbate the disease in people who have IBD. This is especially relevant because the potential exists in providing people with IBD guidance on diet choices.

The team performed a variety of experiments with the goal of investigating which effects a diet high in fructose could have on three different mouse models with IBD.

The first model which used a chemical known as dextran sodium sulfate which provokes the type of inflammatory response which will occur in IBD, showed that the a high fructose diet did increase the severity of this inflammation. However in contrast, a high glucose diet did not increase this inflammation.

The team also noted that giving antibiotics to the mice reduced the damaging effects of a diet high in fructose on the colon. This suggests that bacteria found in the gut were mediating the harmful effects.

In contract, transplants of fecal material obtained from mice that had been fed the high fructose diet increased inflammation in the mice who had received them. This shows additional evidence of the role gut bacteria play in IBD.

When the team looked more closely at the mucus layer which protects the cells that line the colon, they discovered that the diet high in fructose reduced the thickness by almost one-fifth. Bacteria infiltrated the mucus and became in direct contact with the cells.

They also found that the diet changed the prevalence of a variety of species of bacteria that live in the gut. It boosted the population of a species known as Akkermansia muciniphila. In earlier studies, researchers have shown that this particular species has the ability to degrade mucus and that it is associated with inflammation in the colon.

The second model of IBD used in the experiments involved infecting the mice with a bacterium known as Citrobacter rodentium which also provokes the inflammation found in IBD. These mice were fed high amounts of fructose which worsened the inflammation and also promoted the growth of the bacteria.

The team confirmed the association between IBD and fructose in a genetic model of this disease. This particular model recreates a type of immune response that has the ability to make some people with IBD more likely to develop inflammation in the colon. Once again, consumption of high amounts of fructose increased the inflammation of the colon in these mice.

Researchers say the next step is to conduct more studies on whether people with IBD are at an increased risk of developing colon cancer due to a lifetime of chronic inflammation of the gut. They also plan on developing interventions to help prevent the pro-inflammatory effects dietary fructose.

To view the original scientific study click below

Dietary Fructose Alters the Composition, Localization and Metabolism of Gut Microbiota in Association with Worsening Colitis

Cognitive Decline Offset by Lifestyle Changes

According to the CDC at least 5 million people living in the U.S. live with Alzheimer’s Disease and related dementias. As the population ages, experts believe this number will increase quite significantly. A new study of older adults has shown that how increasing physical activity and changing diet can reduce the risk of dementia related diseases even if the person already has a cognitive decline diagnosis.

Dementia is a group of disorders that are characterized by difficulties in remembering, thinking and reasoning. Alzheimer’s is the most common type of cognitive decline. Even though scientists do not know the exact biological cause of Alzheimer’s, they do know that a variety of lifestyle factors does increase a person’s risk of developing dementia.

Lifestyle changes that affect this risk include alcohol consumption, smoking, physical activity and diet. One study has estimated that close to half of all cases of Alzheimer’s disease worldwide could have links to certain lifestyle factors.

A recent study led by The Australian National University in Canberra, conducted trials of a series of lifestyle interventions in people who were already experiencing cognitive decline. The goal was to see whether these changes might improve a person’s cognitive state and potentially reduce the risk of developing dementia.

The research team discovered that people who actively changed certain aspects of their lifestyle choices, were able to experience significant improvements in their cognition. This suggests that by making certain lifestyle changes, the course of cognitive decline could be altered and could also reduce a person’s risk of developing Alzheimer’s.

The study involved 119 participants aged 65 or older who had either subjective cognitive decline (SCD) which is the self reported experience of memory loss of confusion, or had mild cognitive impairment (MCI) which is a clinically diagnosed form of cognitive decline. Medical professionals consider both forms of cognitive decline as early onset symptoms of dementia, although not everyone with MCI or SCD will develop dementia.

The study which is a part of the Body, Brain, Life for Cognitive Decline trial, set out to determine whether activity levels and diet can reduce the risk of dementia in people diagnosed with cognitive decline.

The participants were split roughly into two groups. Over an eight week period, the active control group completed online modules on the risk of dementia including information on dementia, lifestyle factors, Mediterranean diet, physical activity and cognitive engagement. These participants were instructed to implement this information into their own lifestyles.

The intervention group of participants received the identical online information in addition to active components to assist with implementing their information into their lifestyles. These included an exercise physiologist session, dietitian sessions, and online brain training.

At the end of the study, the intervention group’s cognition levels were significantly higher than the other group. Over the six months of follow-up, researchers noted that these participants were able to improve their lifestyle choices and had higher cognition scores. They measured this using a variety of tools including the Alzheimer’s Disease Assessment Scale Cognitive Subscale.

The team also assessed exposure to lifestyle risk factors for developing Alzheimer’s and showed that the intervention group was also significantly lower at the 3 month follow-up. However, at the six month follow-up this was not the case. This suggests that people need to maintain their diet and activity improvements to see continued benefits.

The study shows that people who are already experiencing cognitive declines, can reduce their risk for developing dementia later in life. With the right interventions, they may retain sufficient neuroplasticity of their brain to bounce back from decline. The fact that people can achieve this by adapting cost effective and relatively simple lifestyle changes, is very promising.

The research team notes that a follow-up trial with more participants than the original 119 and over a longer period will be important to confirm their findings and additionally demonstrate sustained cognitive improvements. They also note that participants who did not maintain a reduced risk of Alzheimer’s by the end of the study, suggests that some people may require “booster” sessions to ensure continuation of benefits.

To view the original scientific study click below

Lifestyle Risk Factors and Cognitive Outcomes from the Multidomain Dementia Risk Reduction Randomized Controlled Trial, Body Brain Life for Cognitive Decline (BBL?CD)

New Breakthrough for Regenerative Dentistry

Researchers at the Karolinska Institutet have recently revealed new knowledge on the cellular makeup and growth of teeth that can expedite new developments in regenerative dentistry and treatments for tooth sensitivity. Regenerative dentistry is a biological therapy for damaged teeth.

Teeth develop via a complex process where soft tissue along with connective tissues, blood vessels and nerves are bonded with three different types of hard tissue into a functional body part. Scientists often use the mouse incisor as an explanatory models for the process. The mouse incisor grows continuously and is renewed during the animal’s life.

Although the mouse incisor has been well studied in a developmental context, a variety of fundamental questions in regards to the various tooth cells, stem cells and their cellular dynamics and differentiation still remain unanswered.

By using a single-cell RNA sequencing method along with genetic tracing, the research team have now identified and characterized all populations of cells in mouse teeth and additionally in the young growing and adult human teeth.

From stem cells to completely differentiated adult cells they were able to decipher the differentiation pathways of odontoblasts which give rise to dentine (the hard tissue closest to the pulp) and ameloblasts which give rise to the enamel. They also discovered new types of cells and cell layers in teeth that can play a part in tooth sensitivity.

Some of the team’s findings can also explain certain characteristics of the immune system in teeth. Other findings have shed new light on the formation of tooth enamel which is the hardest tissue in the human body.

The team hopes and believes their work can form the basis for new approaches to dentistry in the future. They hope it can help expedite the fast expanding field of regenerative dentistry. Their results have been released publicly in the form of searchable interactive and user friendly atlases of human and mouse teeth. They believe they will prove a useful resource not only for dental biologists but additionally for researchers who are interested in development and regenerative biology in general.

To view the original scientific study click below

Dental cell type atlas reveals stem and differentiated cell types in mouse and human teeth

Immune System Affects Body and Mind

A study from the Washington University School of Medicine has shown that a molecule which is produced by the immune system acts on the brains of mice to change behavior. The evidence illuminates a surprising body-mind connection.

The research team found that in mice, immune cells surrounding the brain produce a molecule that is then absorbed by brain neurons where it seems to be necessary for normal behavior. The findings indicate that elements of the immune system affect both body and mind and that the immune molecule known as IL-17 may be the link between the two.

The team notes that the brain and the body are not as separate as many people think. What they found is that the immune molecule IL-17 is produced by immune cells that reside in areas around the brain. These molecules could affect brain function through interactions with neurons to influence anxiety-like behaviors in mice. The team is now looking at whether too little or too much of IL-17 could be tied to anxiety in people.

IL-17 is a cytokine which is a signaling molecule that assists in orchestrating the immune response to infection through activating and directing immune cells. It has also be tied to autism in animal studies and also depression in people.

However, it is something of a mystery how the IL-17 molecule might influence brain disorders. Much of an immune system in the brain and a few immune cells that reside there do not produce IL-17. The tissues surrounding the brain are teeming with immune cells and among them a small population known as gamma-delta T cells that produce the immune molecule IL-17.

The research team set out to determine if gamma-delta T cells near the brain have an impact on behavior. Using mice, the team discovered that the meninges are rich in gamma-delta T cells and these cells under normal conditions continually produce IL-17, filling the tissues around the brain with IL-17.

To determine if gamma-delta T cells or IL-17 affect behavior, the team put the study mice through established tests of social behavior, memory, anxiety and foraging. The mice that lacked gamma-delta T cells or IL-17 were indistinguishable from mice who had normal immune systems on all measures except anxiety.

In the wild, open fields keep mice exposed to predators such as hawks and owls. They have therefore evolved a fear of open spaces. The team conducted two separate tests which involved giving mice the option of entering exposed areas. The mice with normal amounts of IL-17 and gamma-delta T cells kept mostly to the enclosed and more protective edges during the tests. The mice without IL-17 and gamma-delta T cells ventured into the open spaces. The team interpreted this lapse of vigilance as decreased anxiety.

Additionally, the team discovered that neurons in the brain have receptors on their surfaces that will respond to IL-17. When these receptors were removed so that the neurons could not detect the presence of IL-17, the mice indicated less vigilance. The team says these findings suggest that behavioral changes are not a byproduct but instead an important and integral part of neuro-immune communication.

The team did not expose the study mice to viruses or bacteria to study the effects of infection directly. They did however, inject the animals with lipopolysaccharide which is a bacteria product that elicits a strong response from the immune system. Gamma-delta T cells in the tissues surrounding the mice’s brains produced more IL-17 in response to the injection. However, when the animals were then treated with an antibiotic the amount of IL-17 was decreased. This suggests the gamma-delta T cells could detect the presence of normal bacteria such as those found in the gut microbiome as well as invading bacterial species, and appropriately respond to regulate behavior.

The team suggests that the link between the immune system and the brain may have evolved in a multi-pronged survival strategy. Increased vigilance and alertness could help rodents survive an infection through discouraging behaviors that increase the risk of predation or further infection while in a weakened state.

They believe the immune system and the brain have most likely evolved together. Selecting special molecules such as IL-17 to protect us behaviorally and immunologically, is a smart way to protect against infection. This is a great example of how cytokines which have evolved to fight against pathogens are also acting on the brain and modulating behavior.

The research team is now studying how gamma-delta T cells in the meninges detect bacterial signals that come from other parts of the body. They are also investigating how IL-17 signaling in neurons translates into changes in behavior.

To view the original scientific study click below

T cells regulate anxiety-like behavior via IL-17a signaling in neurons. Nature Immunology, 2020; DOI: 10.1038/s41590-020-0776-4

Laughter and Smiling Act as Stress Buffers

Researchers at the University of Basel has reported that people who laugh frequently throughout their everyday lives may be better equipped to handle stressful events. And it is the frequency rather than the intensity of a person’s laughter that makes the biggest difference.

It is estimated that people laugh about 18 times per day and this is typically interactions with other people and depending on the amount of pleasure they experience with those interactions. Researchers have reported differences related to age, gender and time of day. For example, it is known that women will smile more than men on average.

Now, the team at the Division of Clinical Psychology and Epidemiology of the Department of Psychology at the University of Basel, have conducted a study in regards to the relationship between stressful events and laughter in relation to perceived stress in everyday life.

For the intensive longitudinal study, an acoustic signal from a mobile phone app was used to prompt the study’s participants to answer questions eight times per day at irregular intervals for a time period of 14 days. The study’s questions related to the intensity and frequency of laughter and also the reason for the laughing in addition to any stressful events or stress symptoms they experienced during the time since the previous signal.

Through this method, the research team was able to study the relationships between stressful events, laughter, and psychological and physical symptoms of stress such as “I felt restless” or “I had a headache” as part of everyday life. The study was based on data from 41 psychology students who were an average age of just under 22 and of whom 33 were women.

The first result of the observational study was expected based on the specialist literature that is, in phases in which the participants laughed frequently, stressful events were linked to more minor symptoms of subjective stress. However, the next finding was unexpected. In regards to the interplay between stressful events and the intensity of laughter which was noted as weak, medium or strong, there was no statistical correlation with symptoms of stress. This may be because people are better at estimating the frequency of their own laughter rather than its intensity.

To view the original scientific study click below

Does laughing have a stress-buffering effect in daily life? An intensive longitudinal study.

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