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.

Dangers of Eating Carmelized Red Meat

The world’s best chefs have taught us to grill, pan fry and barbecue a steak to perfection! And while we may be seeking that extra flavor that cooking with these methods provides, new research has found that consuming red and processed meats through high-heat caramelization increased a protein compound that may increase the risk of stroke, heart disease and complications in diabetes.

The research from the University of South Australia provides important insights into diet for people who are at risk for degenerative diseases. When red meat is seared at high temperatures through roasting, grilling or frying, it produces compounds called advanced glycation end products (AGEs). When these compounds are consumed, they accumulate in the body and interfere with normal functions of the cells.

The consumption of high-AGE foods can increase our total daily AGE intake by 25%. Higher levels contribute to vascular and myocardial stiffening, oxidative stress, and inflammation which are all symptoms of degenerative diseases.

The study tested the impacts of two different diets. One was high in red meat and processed grains. The other was high in whole grains, legumes, nuts, and white meat that was cooked either by boiling, stewing, steaming or poaching.

The research has shown that the diet high in red meat significantly increased AGE levels in the blood which suggests they may contribute to the progression of diseases. Largely preventable, cardiovascular disease is the number cause of death worldwide. In Australia it is responsible for one in five of all deaths.

While there are still questions about how dietary AGEs are actually linked to chronic disease, the current research shows that eating red meat will alter AGE levels.

If we want to reduce the risk of heart disease, we need to cut back on how much red meat we consume and also be more considerate about how to cook it. Grilling, searing, and frying may be the preferred cooking methods, but these methods may not be the best choice for people looking to reduce their risk of disease. Slow cooked meats are a better option for long-term health.

To view the original scientific study click below

Differential Effects of Dietary Patterns on Advanced Glycation end Products: A Randomized Crossover Study

Biological Aging Linked to Consumption of Ultra-Processed Foods

A new study from researchers at the University of Navarra in Pamplona, Spain has shown that ultra-processed foods (UPFs) are linked to the shortening of the body’s telomeres. Shorter telomeres are a marker of accelerated biological aging.

The research indicates that telomeres were twice as likely to be short in people who consumed more than 3 servings per day of UPFs. Having multiple servings daily of junk food such of chips, cookies, fast-food and other processed meals, doubles the chances that certain strands of telomeres would be shorter than those who ate healthier.

Globally, the consumption of fresh food is decreasing while the consumption of UPFs is on the rise. UPFs are manufactured food products made up of the building blocks of naturally occurring foods – sugars, oils, fats and protein isolates. And while their components are often extracted from natural sources, unfortunately they ultimately contain very little or even in no in the way of whole foods. The ingredients and processes used in the manufacturing of UPFs makes them highly convenient, almost imperishable and ready-to-consume which are all attractive to consumers.

They are typically high profit for manufacturers because of the low cost ingredients and long shelf-life. However, these properties result in these products being nutritionally unbalanced or poor and liable to being over consumed often at the expense of more nutritious alternatives and less processed choices.

Often companies that produce UPFs add emulsifiers and flavorings for taste in addition to colorings and other cosmetic additives to achieve a more desired appearance.

The research team analyzed health data of 886 people aged 55 or older (the average age was 67.7 years) who gave saliva samples for DNA in 2008. The participants also self-reported their daily food consumption and checked back with the team every 2 years. The study included 645 men and 241 women.

The participants were then sorted into four groups of equal size based on UPF servings they consumed daily. The low group consumed less than 2 servings per day, the medium-low group 2 to 2.5 servings per day, the medium-high group 2.5 to 3 servings per day, and the high group more than 3 servings per day.

The likelihood of shortened telomeres increased dramatically with the number of servings of UPFs beginning with the medium-low group. This group was 29% more likely to exhibit reduced telomere length while the medium-high group was 40% more likely to do so. The participants in the high group were 82% more likely to have shortened telomeres.

The team also noted that the participants in the high group were more likely to have family history of cardiovascular disease, diabetes and abnormal blood fats and snacked more often in between meals. They also consumed more saturated fats, polyunsaturated fats, cholesterol, sodium, sugar sweetened beverages, fast food, and processed meats and consumed less carbohydrates, fruit, fiber, vegetables, protein, olive oil and other micronutrients.

Previous research has not conclusively established a link between telomere length and UPFs. However, the new research has noted associations between telomere length and the consumption of sugar sweetened beverages, alcohol, processed meats, and foods that are high in sugar and saturated fats. Other research has shown a UPF connection to a variety of serious conditions such as hypertension, obesity, metabolic syndrome, depression, type 2 diabetes and some types of cancer. However, these particular conditions also tend to be age related and therefore difficult to link definitively to the consumption of UPFs.

Finally, the team’s findings did link the consumption of UPFs to excessive body weight, all-cause mortality, and hypertension.

To view the original scientific study click below

Ultra-processed food consumption and the risk of short telomeres in an elderly population of the Seguimiento Universidad de Navarra (SUN) Project

Antibody that Sets Gluten Sensitivity Apart from Celiac Disease

A recent study at Columbia University Vagelos College of Physicians and Surgeons, has shown that antibodies which are produced by people who are sensitive to gluten are different from those produced by people with celiac disease. The discovery could help doctors diagnose gluten sensitivity.

Currently, a large amount of doctors will often dismiss complaints from people who claim to be affected by foods that contain gluten but do not have celiac disease. Celiac disease is a well documented autoimmune disease that is started by exposing a person to the dietary protein that is in barley, rye and wheat.

This belief has changed based partly on studies that have delved into the biological basis for gluten sensitivity that is not the same as celiac disease. However, many conditions of non-celiac gluten sensitivity consisting of how to diagnose it and what causes it is still poorly understood.

This study has shown that people who do suffer from non-celiac gluten sensitivity like people with celiac disease, produce an elevated level of anti-gluten antibodies. However, the two conditions are different in the antibody types produced and the subsequent inflammatory responses these antibodies trigger.

The research team analyzed blood samples obtained from 40 participants who had celiac disease, 80 participants with non-celiac gluten sensitivity, and 40 healthy controls. All participants ate an unrestricted, gluten-containing diet.

They discovered that the B cells found in celiac disease produced a subclass profile of lgG antibodies with high probability of inflammation that is linked to autoimmune activity and also intestinal cell damage. In contrast, the people with non-celiac gluten sensitivity produced lgG antibodies that are linked to a more subdued inflammatory response.

Those antibodies can possibly be used at later dates to provide doctors more easily diagnose people with non-celiac gluten sensitivity which is hard to diagnose. The profiles of the different antibodies also suggest the rise of new therapies for celiac disease. This disease is currently only treated through diet.

The team’s data suggests that celiac patients generate a strong B-cell inflammatory response every time they eat gluten. However, the immune system in person’s with non-celiac gluten sensitivity adheres from its previous encounters with gluten and generates a lower amount of inflammatory responses to the antigen in concurrent interactions.

The team believes that if they can drive specific cells of celiac patients toward less inflammatory states, they would be able to reduce or prevent the degree of the immunologic reaction to gluten.

To view the original scientific study click below

Subclass Profile of IgG Antibody Response to Gluten Differentiates Non-Celiac Gluten Sensitivity from Celiac Disease.

Help Retain Muscle Mass in Over 50’s with Vitamin C

Recent research has shown that Vitamin C could help people over 50 retain muscle mass in later life. The study shows that people who are older and eat plenty of Vitamin C which is found in berries, vegetables, potatoes and citrus fruits, have the best skeletal muscle mass.

The findings are especially important because people tend to lose skeletal muscle mass as they age. This can lead to frailty, a reduced quality of life, and even sarcopenia which is a condition characterized by loss of skeletal function and muscle mass. Muscle mass loss is an important condition to prevent during aging to minimize both societal and personal costs.

People who do not consume enough Vitamin C in their diet are at risk of Vitamin C deficiency which can cause tiredness, weakness and fragile bones. In extreme cases, it can lead to scurvy. About two-thirds of our body’s total Vitamin C is found in the skeletal muscles. It is used for making carnitine which is a critical substance that provides energy for muscles to function properly and also collagen which is an essential structural component of muscle.

As we age, we lose strength and skeletal muscle mass. People over 50 lose up to 1% of their skeletal muscle mass every year. This loss is believed to affect more than 50 million people globally. It is a big problem due to the fact that it lead to a variety of poor outcomes that can lead to physically disability, type 2 diabetes, a reduced quality of life and even death.

Vitamin C consumption is linked with skeletal muscle mass. It helps defend the tissues and cells that make up our body from potentially harmful free radicals. If these free radicals are unopposed, they can contribute to the destruction of muscle which speeds up age related declines.

Until recently, few studies have researched the importance of Vitamin C intake for older adults. The team who conducted the recent study set to find out whether people who consumed more Vitamin C had more muscle mass than other people.

The team studied data from more than 13,000 people between the ages of 42 and 82 who are taking part in the EPIC (European Prospective Investigative into Cancer and Nutrition) Norfolk Study. They calculated the participant’s skeletal muscle mass and analyzed their Vitamin C intakes taken from their 7-day food diary. The team also examined the amount of Vitamin C in their blood which provides results less susceptible to possible error in reporting diet.

The statistical analysis also took into consideration other important factors such as a participant’s physical activity and energy and protein intake which can also have effects on skeletal muscle mass.

The team studied a large sample of older Norfolk residents and discovered that people with the highest amounts of Vitamin C in their blood or diet had the greatest estimated skeletal muscle mass which compared to those with the lowest amounts. They found that nearly 50% of women and nearly 60% of men were not consuming as much Vitamin C as they should. Women in the highest category of Vitamin C consumption had muscle mass 3% greater than those in the lowest category.

This study complements findings from earlier work in young and older women. In this study the team found that women who ate more Vitamin C foods not only had more muscle mass but also had much better leg function meaning they were stronger.

The findings suggest that dietary Vitamin C is important for muscle health in older women and men and may be useful in preventing age related loss of muscle. This is significant because Vitamin C is readily available in vegetables, fruits and supplements so improving the intake of this vitamin is very straightforward.

The findings promote the concept that optimal nutrition may help reduce muscle decline and further encourages and emphasizes that people of all ages follow healthy eating guidelines which includes eating a wide variety of fruits and vegetables every day.

People do not need to take mega doses of Vitamin C to get benefits. Eating a citrus fruit such as an orange every day and consuming a vegetable side as part of a meal can be sufficient for most people. And for people with dietary concerns, supplements can provide a suitable alternative.

To view the original scientific study click below

Lower Dietary and Circulating Vitamin C in Middle- and Older-Aged Men and Women Are Associated with Lower Estimated Skeletal Muscle Mass.

How Fructose Consumption Affects The Liver

A new study has found that the excessive consumption of fructose which is a sweetener common in the American diet, can lead to non-alcoholic fatty liver disease (NAFLD) which is comparably abundant in the U.S. However, contrary to previous thought, researchers are now reporting that fructose only adversely affects the liver after it has reached the intestines. Here the sugar disrupts the epithelial barrier which protects the internal organs from bacterial toxins in the gut.

NAFLD is the most common cause of chronic liver disease throughout the world and it can progress to more serious conditions. The new findings point to an approach that could prevent damage to the liver in the first place.

Consumption of fructose in the U.S. has been skyrocketing since the 1970s with the introduction of high fructose corn syrup (HFCS). This is a cheaper sugar substitute that is commonly and broadly used in packaged and processed foods such as cereals, baked goods and soft drinks.

Multiple studies in humans and animals have linked increased HFCS consumption to some of the nation’s numerous inflammatory conditions such as heart disease, cancer and diabetes, and also the nation’s obesity epidemic. Currently the U.S. FDA regulates it similar to other sweeteners such as honey or sucrose and advises only moderate intake.

The new study defines a specific role and risk for HFCS in the development of fatty liver disease. Interestingly, the ability of fructose which is plentiful in dates and dried figs to induce fatty liver was known to the ancient Egyptians who fed geese and ducks dried fruit to make their version of foie gras.

With the advent of metabolic analysis and modern biochemistry, it has become obvious that fructose is two to three times more potent than glucose in increasing liver fat which is a condition that triggers NAFLD. The increased consumption of soft drinks that contain HFCS is linked to the explosive increase in NAFLD incidences.

Fructose is broken down in the digestive tract by an enzyme known as fructokinase which is produced both by the gut and the liver. By using mouse models, researchers discovered that excessive fructose metabolism in intestinal cells reduces the production of proteins that maintain the gut barrier. This is a layer of tightly packed epithelial cells that are covered with mucus to prevent bacteria and microbial products such as endotoxins from leaking out of the intestines and into the blood.

Through deteriorating the barrier and increasing its permeability, excessive fructose consumption can lead to a chronic inflammatory condition called endotoxemia which has been shown in both experimental animals and pediatric NAFLD patients.

The researchers in the current study found that leaked endotoxins that reach the liver provoke increased production of inflammatory cytokines and stimulated the conversion of fructose and glucose into fatty acid deposits. It is very clear to the team that fructose does its harm in the intestine and if intestinal barrier deterioration is prevented, the fructose does little harm to the liver.

The team has noted that feeding mice with high amounts of fructose and fat will result in particularly severe adverse health effects. This is a condition that mimics the 95th percentile of relative fructose intake by American adolescents who get close to 21.5 percent of their daily calories from fructose. And this is often in combination with calorie dense foods such as french fries and hamburgers.

The team did find that when fructose intake was reduced below a certain threshold, no adverse effects were noted in mice. This suggests that only excessive and long-term consumption of fructose represents a health risk. Moderate fructose intake by normal consumption of fruits appears to be well tolerated.

Unfortunately, there are many processed foods that contain HFCS and most people are unable to estimate how much fructose they are actually consuming. Increased awareness and education are the best solutions to this problem, however for those people who have progressed to the severe form of NAFLD known as nonalcoholic steatohepatitis, these findings offer some ray of hope of a future therapy based on the restoration of gut barrier.

To view the original scientific study click below

Fructose stimulated de novo lipogenesis is promoted by inflammation.

Vitamin & Mineral Supplements Linked to Shorter and Less Severe Illness Symptoms

The results of a 12 week study conducted by Oregon State University has shown that older adults who took a daily mineral and multivitamin supplement containing Zinc and high amounts of Vitamin C experienced less severe symptoms and shorter periods of sickness when compared to those in a control group who received a placebo.

The research group included 42 healthy adults aged 55 to 75 and was set-up to measure the supplement’s effects on certain immune system indicators. The research team also looked at bloodstream levels of Vitamin C, Vitamin D and Zinc while the participants took the supplement. These particular micronutrients are important for proper immune function. The immune indicators which included white blood cells’ ability to kill incoming pathogensm were unaltered in the group receiving the supplement.

The group who received the multivitamin showed improved Zinc and Vitamin C status in their blood. Interestingly, illness symptoms that were reported by this group were less severe and were shorter lasting than those who were in the placebo group.

The same percentage of participants in both groups reported symptoms, but the number of days in the group who received the supplement averaged fewer than three compared to more than six for the participants in the placebo group.

The team notes that the observed illness differences were striking. And though the study was limited to self-reporting of illness data and the study was not designed to answer this question, the observed differences have suggested that additional larger studies that would be designed for these outcomes are warranted and as the team also notes, long overdue.

As people age, the risk of mineral and vitamin deficiencies that contribute to age related immune system deficiencies increases. Throughout the United States, Europe and Canada, research has suggested that more than one-third of older adults are deficient in at least one micronutrient and often times more than one.

These deficiencies contribute to a decline in a person’s immune system and are most often characterized by increased levels of inflammation in addition to reduced innate immune functions and reduced T-cell function. Because multiple nutrients support the function of the immune system, older adults often benefit from taking mineral and multivitamin supplements. These supplements are readily available, inexpensive and generally regarded as safe.

The multivitamin supplement that was used in this study focused on minerals and vitamins typically believed to help with immunity. It contained 700 micrograms of Vitamin A, 400 international units of Vitamin D, 45 milligrams of Vitamin E, 6.6 milligrams of Vitamin B6, 400 micrograms of folate,
9.6 micrograms of Vitamin B12, 1,000 milligrams of Vitamin C, 5 milligrams of Iron, 0.9 milligrams of Copper, 10 milligrams of Zinc, and 110 micrograms of Selenium.

Supplementation was associated with significant increased circulating levels of both Vitamin C and Zinc and with illness symptoms that were shorter lasting and less severe. These findings support other findings that go back decades, even to the days of Linus Pauling’s research with Vitamin C. The current results from this study suggest more and better designed research studies are needed to further explore the positive role mineral and multivitamin supplementation might play in bolstering the immune system in older adults.

To view the original scientific study click below

The Effect of a Multivitamin and Mineral Supplement on Immune Function in Healthy Older Adults: A Double-Blind, Randomized, Controlled Trial.

How To Combat Immune Aging

As we age, the human immune system becomes less effective at fighting infections and less responsive to vaccinations. The aging immune system is also associated with chronic inflammation which increases the risk of almost all conditions and diseases linked to old age.

The good news is that by adopting the right diet and exercising, a person can go a long ways towards maintaining healthy immunity into older age. We now live in a time of high average life expectancies and our long evolutionary history has adapted us for a variety of lifestyles and these have drastically changed.

Immunity, as a result, weakens in older age and also becomes imbalanced. Two branches of the immune system are affected – the innate immunity and the adaptive immunity. Innate immunity is our first line of defense against infections and will fail to resolve after the initial threat has passed which in turn causes chronic systemic inflammation.

Adaptive immunity is responsible for remembering and attacking particular pathogens and will steadily lose its ability to defend the body against bacteria, viruses, and fungi. The loss of adaptive immunity which comes with older age causes people to become more susceptible to infections and can also reactivate dormant pathogens that had been previously suppressed. The weaker adaptive immunity associated with older adults means their bodies will respond less strongly to vaccines.

Researchers have labeled the persistent low level inflammation that is related to almost all conditions linked to older age “inflammaging”. Some inflammation is part of the normal repair process for healing and is essential in keeping us safe from viral and bacterial infection along with noxious environmental agents. However, not all inflammation is good. When it becomes prolonged and persists, it can become destructive and damaging.

When a younger person is affected by an infection or injury, their immune system switches to an anti-inflammatory response. This does not happen as effectively in older people which is due to the accumulation of “senescent” or aged immune cells.

Senescent cells contain shorter telomeres which are the protective caps at the tips of chromosomes. They prevent vital genetic material from becoming lost when the chromosome is duplicated during the replication of cells.

Telomeres become shorter every time a cell divides and division eventually ceases completely. If the cell survives, it slowly becomes more dysfunctional. Senescent immune cells will produce more immune signaling molecules which are known as cytokines which promote inflammation. They turn out more interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).

High levels of IL-6 and TNF-alpha have been linked to mortality and disability in older people. They have a noticeably strong association with cardiovascular disease, type 2 diabetes, cancer and
neurodegenerative disease.

When the number of pro-inflammatory cells increase, there is also an increase in the number of immune cells known as M1 macrophages which are more pro-inflammatory and a decrease in the number of M2 macrophages which increase immunoregulatory.

These particular changes in the frequency of both M1 and M2 cells seems to be linked to an increased risk of developing plaques which are comprised of debris and fat which will block the arteries in atherosclerosis.

The immune system will learn to recognize and neutralize particular pathogens through adaptive immunity. An immune cell known as a T cell plays a critical role in adaptive immunity. When an infection occurs, naive T cells will learn to recognize the specific pathogen that is involved. They then will differentiate into cells which are specialized to mount additional responses against the identical pathogen.

The number of T cells remains constant throughout a person’s life. However, the pool of naive undifferentiated cells will steadily shrink over the years as more cells commit to taking on specific infections. As a result, the bodies of older people become less able to mount immune responses that are effective to new infections. And for the same reason, vaccines provoke weaker response from the immune system that is aging and therefore provide less protection. Research has suggested that repeated flu immunizations may lead to reduced antibody responses.

Many older people harbor a latent infection that is known as human cytomegalovirus which is very common and persistent but doesn’t typically produce symptoms. In some older people, this particular infection may slowly deplete their immune resources which makes them more susceptible to other viral infections and reduces the effect of flu vaccines.

Additionally with this slow decline in immunity with age, senescent T cells will produce more pro-inflammatory cytokines including IL-6. These will in turn stoke the chronic and systemic inflammation of inflammaging.

Although there isn’t anything that will prevent aging, there are a variety of lifestyle changes a person can make to help in staying healthy into old age.

Exercise has a significant effect on the immune system. Unfortunately, people become less active as they age. However, there is evidence that suggests getting as much exercise as is possible can slow or even reverse some of the effects caused by immunosenescence.

Skeletal muscle will produce a range of proteins that are known as myokines which reduce inflammation and can preserve immune function. It would make sense therefore, that maintaining muscle mass through exercise will help protect the body against infection and a variety of diseases.

One study discovered that aerobic fitness engaged in by 102 healthy males aged 18 to 61, was inversely proportional to the number of senescent T cells found in their blood after adjusting for age. This means that increased physical fitness was linked to less immunosenescence. The males who were most fit not only had fewer senescent T cells, but also a greater number of naive T cells.

Another study compared immune responses from 61 healthy males aged 65 to 85 to a flu vaccine. About 1/3 of the males were intensively active through sports or running, 1/3 were moderately active, and 1/3 were mostly inactive. After adjusting for age, the study found that the intensively and moderately active males produced more antibodies in response to the vaccine than the less active participants.

Amazingly, the males who were more active had higher serum concentrations of antibodies to some of the flu strains even prior to undergoing vaccination.

In regards to diet, there is plenty of indirect evidence to suggest that diet helps determine older adult’s risk of developing sarcopenia. This condition will cause a loss of muscle mass, functionality and strength. There seems to be a two way relationship between the immune system and skeletal muscle. Muscles will produce anti-inflammatory myokines. However, recent evidence has suggested that chronic inflammation also speeds up the muscle loss caused by sarcponenia.

Dietary supplements such as Vitamin D and polyunsaturated fatty acids may help reduce the risk of sarcopenia due to their anti-inflammatory properties. In addition, growing evidence suggests that people who consume a Mediterranean diet are less likely to become frail as they age. Frailty meaning losing muscle strength, tiring easily and walking slowly.

The Mediterranean diet consists of large amounts of leafy vegetables, fruits and olive oil; moderate amounts of poultry, dairy and fish; and low amounts of added sugar and red meat. Earlier studies have shown that this diet is linked to the lower risk of obesity, type 2 diabetes, cancer, and cardiovascular disease.

A 2018 review of observational studies, shows people who adhere the most closely to this type diet were less than half as likely to develop frailty over a 4 year period compared to those who followed it the least likely.

People who are frail have higher levels of inflammatory markers and inflammation is thought to be closely linked to frailty. The Mediterranean diet is associated with low levels of inflammatory markers and may help reduce the risk of frailty through this mechanism.

And while muscle plays a role in decreasing inflammation in older people, fat or adipose tissue may have the exact opposite effect. Normal aging will often lead to weight gain due to an accumulation of adipose tissue around the organs and beneath the skin. And adipose tissue may make a profound contribution to inflammaging.

Close to 30% of the pro-inflammatory cytokine IL-6 in the bloodstream may originate from adipose tissue. Having overweight and obesity in older age may therefore contribute to chronic inflammation. Animal and human studies have suggested that the immune system of people with obesity may produce fewer antibodies in response to the flu vaccine. Eating a healthful diet such as the Mediterranean diet and exercising appear to counter the effects of immune aging. This may be in part due to the way these two lifestyle habits prevent excessive weight gain. Studies suggest that older people who have a moderate weight gain and who exercise regularly have fewer senescent T cells and lower levels of inflammatory cytokines in their blood.

Whether or not exercise, diet and weight loss can reverse immunosenescence remains open for future research.

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