Discovery of a New Source of Neurons

It has been the belief that mammals are born with an entire supply of neurons which have to last for a lifetime. New research has discovered a particular type of stem cell that makes neurons, which are the source of new cells in the brain’s hippocampus.

Neuroscientists have found at least two different regions of the brain that grow new neurons. They are the center for our sense of smell and the seat of learning and memory, the hippocampus.

The study conducted by researchers at the Perelman School of Medicine, University of Pennsylvania, have discovered in mice a type of stem cell that is the source of this recently discovered supply of new cells in the hippocampus. The findings could help neuroscientists discover how to better maintain youthful conditions for memory and learning, and also regenerate and repair of parts of the brain following injury and with aging.

They have shown for the first time in mammals that neurons in the part of the hippocampus called the dentate gyrus, grow and then develop from a single population of stem cells over a lifetime. These new immature neurons are much more flexible in making the connections in the hippocampus compared to more mature neurons. This is vitally important for healthy memory, learning and adjusting mood.

The team has shown that the neural stem cells they have found have a common molecular signature across the lifetime of the mice. They were able to do this by labeling neural stem cells in embryos while the brain was developing and then following these cells from birth to adulthood.

This approach revealed that these new neural stem cells with their precursor’s label were constantly creating new neurons throughout the animal’s lifespan. The process is unique to the brain. Within the hippocampus these cells never cease replicating and contributing to the brain’s flexibility in mammals.

This capacity is known as plasticity which is the ability of the brain to form new connections throughout a lifetime to compensate for disease and injury and to adjust in response to new input from the environment. The team compares this process of new neuron growth within the hippocampus to adding new units to the circuitry of the brain’s motherboard.

The research team’s next steps will be to look at the same neural stem cells in other types of mammals and most importantly in humans. They plan to start the search in post mortem brain tissue to investigate how the neural stem cells population are regulated.

To view the original scientific study click below.

A Common Origin of Stem Cells Drives Developmental and Adult Neurogenesis

Longer Life from Lifting Weights

A new study has a great new message…you can help prolong your life by increasing the power of your muscles. The study has shown for the first time that people tend to live longer lives when they have more muscle power.

Power is reliant on the ability to generate velocity and force and coordinate our movement. It is the measure of work performed per unit of time (force times distance). Greater power is produced when the identical amount of work is finished in a shorter period of time or when more work is done during the same time.

Stair climbing requires power and the faster a person climbs the more power is required. Pushing or holding a heavy object needs strength.

Power training is done by finding the ideal combination of weight being moved or lifted and speed. When at the gym most people think about strength training such as weight being lifted and repetitions of the weight lifting without paying any attention to the speed. However, for optimal power training, we need to go beyond the typical strength training by adding speed to the weight lifting.

Our muscle power begins decreasing after about 40. It is known that power is strongly associated to all cause mortality. The good news is that we only need to be above the median for our sex for the best survival with no additional benefit from becoming even more powerful.

The study conducted by the European Society of Cardiology enrolled 3,878 non athletic people aged 41 to 85. The participants underwent a maximal muscle power test using upright rowing exercises between 2001 and 2016. The average age was 59 with 5% of participants over 80 and 68% of these were men.

The highest value that was achieved after two to three attempts with increasing loads was considered as the maximal muscle power and expressed relative to body weight. The values were then divided into quartiles for survival analysis and were analyzed separately by sex.

During the median 6.5 year follow up, 247 men and 75 women had died. Median power value was 2.5 watts kg for the men and 1.4 watts kg for the women. The participants with the maximal muscle power above the median for their sex had the greatest survival (quartiles three and four). Those participants in two and one quartiles respectively had 4 to 5 and 10 to 13 times higher risk of dying compared to those above the median.

This is the first time prognostic value of muscle power had been assessed. Prior research focused on muscle strength by using the hand grip exercise. The upright row exercise was used for the current study because it is a common action as part of daily life such as picking up groceries and grandchildren.

The best way to train to increase muscle power is through multiple exercises for the lower and upper body. A weight should be chosen with the load to achieve maximal power which is not too easy to lift and not too heavy that it can barely be lifted. One to three sets of six to eight repetitions is ideal. The weight should be moved as fast as possible while contracting muscles. A 20 second rest should occur between the sets which will sufficiently replenish energy stores in muscles. The above should be repeated for all exercises for the lower and upper body.

The best way to progress is to begin with six repetitions then increase to eight when they become easy. Once that becomes easy, the weight should be increased and go back to six repetitions and increase to eight once again.

Repairing Muscles with Stem Cells

A new study has given insights into muscle boosting therapies for age related muscle decline and muscular dystrophies. The study conducted by scientists from Sanford Burnham Prebys, have discovered a molecular signaling pathway involving proteins that regulate how muscle stem cells decide whether to differentiate or renew.

Stem cells in the muscles can burn out while trying to regenerate tissue while natural aging processes occur or due to a variety of chronic diseases of the muscles. The team believes they have found possible drug targets that will direct stem cells in the muscles to make the right decision that will lead to muscle repair. This can potentially help regeneration of muscle tissue and help in the maintenance of muscle function due to distrophy of muscles and the aging process.

As part of the natural aging process muscle wasting occurs. This is called Sarcopenia. Sarcopenia affects almost 10% of adults over 50 and nearly ½ of these individuals are in their 80s. This condition can lead to loss of independence and contributes to accidents involving falls which is a leading cause of accidental death in those 65 and older.

Muscle wasting also can occur due to genetic diseases of the muscles. There are more than 30 genetic diseases characterized by progressive muscle degeneration and weakness.

Stem cells of the muscle choose between two different fates over a person’s life. They either self renew to replenish the population of stem cells, or they become adult muscle cells. Mounting evidence has shown that mitochondrial respiration or cellular breathing, is a key switch that will drive stem cells of the muscle to differentiate which is an energy intensive process instead of self renewing.

For the current study, the team used mouse models to demonstrate that protein Stat3 promotes mitochondrial respiration. Stat3 regulates many of the cellular processes. This led the team to comb through genes which are expressed during muscle growth to locate additional proteins which are regulated by Stat3 which might serve as more specific targets.

Their efforts led to the protein Fam3a. They conducted further work which included generating a mouse model and cell lines that lacked the Fam3a protein and demonstrated that this protein is required for differentiation and muscle growth. They also showed that Fam3a is secreted by muscle cells while muscle repair occurs. Treatment with the protein restored mitochondrial respiration and stem cell differentiation in stem cells of the muscle which lacked Stat3. This demonstrated the integral role Fam3a plays in determining the fate of muscle stem cells.

Due to the aging of the baby boomer generation with people over the age of 60, it is important to help extend health span as well as life span. The ability to maintain and boost muscle tissue function can assist more people in living an independent and active life. The results of the study can help scientists find applications for muscle wasting diseases and challenges associated with the aging process.

The hope is their findings could also apply to stem cells that differentiate in efforts to create other tissues to treat other degenerative diseases of tissues. They are currently conducting preclinical studies to validate the protein Fam3a as a therapeutic target.

To view the original scientific study click below.

The Stat3-Fam3a axis promotes muscle stem cell myogenic lineage progression by inducing mitochondrial respiration. Nature Communications

Young At Any Age

There is much we can do to slow down and even reserve the body’s trend to decline. A new long term study examined how changes in physical activity in post middle age affects mortality rates.

The study included 2,205 men who were surveyed from 1970 to 1973 at the age of 50. Each participant was categorized into groups that were based on their level of physical activity. The four groups were physical activity that was high, medium, low or sedentary. A follow up was conducted when the participants turned 60, 70, 72 and 82.

The results from the study were positive. As was expected, exercising more translated into lower mortality rates in each of the four groups. The participants who increased their activity levels between ages 50 to 60 were found to have the same mortality rate as those who had always maintained high levels of exercise.

The results were so pronounced, the mortality reductions were compared to people who stopped smoking. However, it is noted that low level exercisers needed to maintain regular physical activity for a minimum of 5 years to catch up. These findings confirm that we have the ability to reverse some damage that has been created in earlier years so as to become healthy as those who have maintained healthy lifestyle choices for a great portion of their lives.

The University of Pittsburgh team that conducted the study have quite possibly answered questions to the possibility of frailty not be inevitable as we age. Their have been recent studies showing that after reaching 40 we will typically lose 8% and more of our muscle mass with each decade. This accelerates after 70. These losses translate into less mobility, independence, strength and have been linked to early mortality.

Exercise on a regular basis may rewrite the future of our muscles. Little evidence for deterioration in older athletes musculature was found. The 70 to 80 year old athletes had just about as much thigh muscle as did the athletes in their 40s. They also showed minor if any fat infiltration.

These older athletes remained strong, although there did occur a drop off in leg muscle strength at around the age of 60. They might not have been quite as strong as those in their 50s, however the difference was small and very little additional decline followed.

The athletes aged 70 to 80 were found to be just about as strong as those in their 60s. This means that we do not have to lose muscle function and mass as we age. Changes that have been assumed to be due to the aging process and unstoppable, are actually related to sedentary and inactive lifestyles. This can be changed and intervened upon.

Those participants who had been sedentary but chose to become fit were able to cut their risk of heart attack by 75% to 80% over a 5 year period. According to the Harvard Alumni Health Study, vigorous activity can significantly lower the risk of coronary heart disease.

There is currently an increasing trend of people 60+ being on their way to being in better shape than the average 35 year old. If a person is exercising now, it doesn’t really matter if they are 25 or 85, they can double their strength in about 3 months and possibly double it again in an additional 3 months. Muscle growth in these older participants was found to be statistically equal to those of younger years doing the same degree of training. Strength and flexibility is not limited to the young. Percentage of body fat and aerobic capacity was found to be more related to training than age.

Additionally, exercise is known to be great for attitude, sex drive and appearance. It helps maintain hormone levels which decline with age. Exercise also increases lymph flow and metabolism as well as helping to increase DHEA while also reducing cortisol, the stress hormone.

Exercise can be aerobic cardio training or anaerobic weight/strength training. Resistance training and weight training can help wake up neural connections. Not only will this lead to improved strength and agility, but will also lead to better coordination.

It is important to note than anyone new to an exercise routine should consider consulting a personal trainer. These trained professionals can help design a program, keep their students motivated and on track, and also insure they are moving correctly to avoid injury.

The body was designed to move. Our bodies signal our cells to grow when we exercise. This creates a ripple effect and spreads growth processes to every cell in our body to help us function in a younger manner. On the other hand, sedentary muscles trickle chemicals which will signal cells to wither away. We can choose to be lazy and decay or choose to be active to help maintain a powerful body as we age. Based on the study, it is never too late to improve!

To view the original scientific study click below.

Total mortality after changes in leisure time physical activity in 50 year old men 35 Year follow-up of population based cohort

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Lower your Stress Hormone Levels with Nature

Taking a stroll or sitting in a place near nature can have some very positive benefits. The findings from a recent study have established for the first time that communing with nature will significantly lower stress hormone levels.

“Nature pills” which is what the discovery is calling the natural stress relieving remedy of being in nature, has real measurable effect. An experiment was designed that would give the researchers a realistic estimate of an effective dose for relieving stress hormone levels.

Participants were asked to engage in a 10 minute or more nature pill three times a week for a period of 8 weeks. Levels of cortisol which is a stress hormone, were measured using saliva samples which were take before and after a nature pill once every two weeks.

The participants were able to choose the time of day, the duration and the place of their nature experience. The chosen place was defined as any place outside that in the participant’s opinion made them feel like they have interacted with nature.

There were just a few constraints put in place to minimize factors which are known to influence stress. They included taking the nature pill during daylight, no aerobic exercise, and to avoid internet, phone calls, social media, reading and conversations.

By building personal flexibility in their experiment, the research team was able to identify the optimal duration of a participant’s nature pill – no matter where or when the nature pill was taken and under normal circumstances of modern life which can be hectic and unpredictable.

Furthermore, to make allowances for participant’s busy lifestyles and also provide meaningful results, the design was also novel in other aspects. Day to day differences in participant’s stress status were accommodated day to day.

The team did this by collecting four snapshots of cortisol change due to a nature pill. That also allowed them to identify and account for any impact of the ongoing, natural drop in cortisol levels as a day goes on. This resulted in a more reliable estimate of the effective duration.

The results of the data revealed that just a mere twenty minutes of a nature experience was sufficient to significantly reduce levels of cortisol. The results also showed that spending even a little more time immersed in the nature experience, 20 to 30 minutes walking or sitting, caused levels of cortisol dropped at their greatest rate.

The experiment gives healthcare practitioners great results as an evidence based rule of thumb on what to include in a nature pill prescription. The studies results provide the first estimates of how experiences in nature impact our stress levels in the context of a normal day.

The experiment’s approach might be used as a tool for further study in this area. Further studies could assess how gender, age, physical ability, seasonality and culture influence the effectiveness of nature experiences in regards to well being. These additional studies could help healthcare practitioners develop customized nature pill prescriptions as well as deeper insights into city designs and well being programs for the public.

To view the original scientific study click below.

Urban Nature Experiences Reduce Stress in the Context of Daily Life Based on Salivary Biomarkers

Prevent Cartilage Damage with Exercise

A new study has given us yet another good reason to exercise! The study found that exercise helps to prevent degradation of cartilage that is due to osteoarthritis.

The study conducted at Queen Mary University of London has shown for the first time how the mechanical forces which are experienced by joint cells during exercise, prevents cartilage degradation. Exercise does this by suppressing the action of inflammatory molecules which lead to osteoarthritis.

The research team demonstrated exercise benefits on tissues which form our joints and how this is down to tiny hair like structures which are called primary cilia found on living cells.

When we exercise joint cartilage such as the knee and hip is squashed. Living cells in the cartilage detect this mechanical distortion which then block inflammatory molecules which are associated with conditions such as arthritis.

The anti inflammatory effect of physical activity is due to the activation of a protein called HDAC6. This protein triggers changes in the proteins that form the primary cilia.

Blocking the HDAC6 with pharmaceutical drugs prevented the anti inflammatory effects due to physical activity. Other drug treatments were able to mimic exercise benefits.

Changes which occurred in the length of the primary cilia which are only a few 1000th of a millimeter, provided a biomarker for the level of inflammation. During inflammation the cilia got longer. However, treatments that prevented the elongation successfully prevented this inflammation.

Additionally, the team’s findings might explain the anti inflammatory effects of normal blood flow in the arteries. This is important for the prevention of arterial disease such aneurysm and atherosclerosis.

The team hopes the findings will help in the development of treatments for diseases such as arthritis. These diseases affect more than 3 million people just in the United Kingdom. The results might lead to whole new therapeutic approaches which are known as mechano medicine in which drugs simulate the effect of mechanical forces to prevent the damaging effects of inflammation and treat arthritic conditions accordingly.

To view the original scientific study click below.

Mechanical loading inhibits cartilage inflammatory signalling via an HDAC6 and IFT-dependent mechanism regulating primary cilia elongation

High Fructose Corn Syrup Linked to Tumor Growth

A new study shows that consuming even a modest amount of high fructose corn syrup on a daily basis accelerates the growth of tumors in the intestines of mouse models. And the findings are independent of obesity. Just 12 ounces of a sugar sweetened beverage daily feeds cancer cells, boosting their growth.

The study team also found the mechanism by which the consumption of sugar laden beverages can directly feed the growth of cancer which suggests the potential of novel therapeutic strategies. There have been more observational studies lately which have raised awareness of the link between consuming sugary beverages, colorectal cancer and obesity.

The thought has been that sugar is harmful mostly because consuming too much can lead to obesity. And obesity increases risks of many types of cancer. However, there has been uncertainty whether a casual and direct link exists between cancer and the consumption of sugar. This was the important question that led to the study conducted by researchers at Baylor College of Medicine and Weill Cornell Medicine.

The team generated a mouse model of early stage cancer of the colon where APC gene is deleted. The APC gene is a gatekeeper in colorectal cancer. Deleting APC is compared to removing the breaks on a car. Without this gene, normal intestinal cells will neither stop nor die which leads to the forming of early stage tumors known as polyps. It is estimated that more than 90% of patients with colorectal cancer have this type of APC mutation.

The team tested the effect consuming sugar sweetened water had on tumor development in the mouse model with the disease. The water contained 25% high fructose corn syrup which is the main sweetener in a variety of sugary drinks people consume. This sweetener consists of glucose and fructose with a 45:55 ratio.

When the team provided the sweetened beverage in a water bottle for the APC model mice to consume at their will, they rapidly gained weight in a months time. To keep the mice from being obese and mimicking a humans daily consumption of a single can of soda, they instead gave the mice a modest amount of the sweetened water orally with a special syringe once a day. When they controlled their consumption, after two months the mice did not become obese, however they did develop tumors that were of higher grade and larger than mice who were treated with regular water.

The study results indicate that when animals have early state of tumors in their intestines, consuming even modest amounts of high fructose corn syrup in the form of liquid can boost tumor progression and growth even independently of obesity.

Further research is needed to translate the discoveries to people, however the findings in the mouse model suggest that constant consumption of sugary beverages can shorten the time for cancer to develop. With humans, it typically takes 20 to 30 years for cancer of the colon to grow from early stage benign tumors to aggressive cancers.

The research team continued their study by investigating the mechanism through which this type of sweetener promoted tumor growth. They found that the APC model mice receiving the modest quantities of high fructose corn syrup had high amounts of fructose in their colons. Sugary beverages increased the levels of glucose and fructose in the colon and blood respectively. The tumors could then efficiently take up both fructose and glucose by different routes.

By using cutting edge technologies to trace the fate of fructose and glucose in tumor tissues, the research team showed that fructose was first chemically changed and the process enabled it to efficiently promote the production of fatty acids which then contribute to tumor growth.

The findings suggested the role of fructose in tumors is to enhance glucose’s role of directing synthesis of fatty acids. This abundance of fatty acids can potentially be used by the cancer cells to form cellular membranes and signaling molecules to influence or grow inflammation.

To see whether fructose metabolism or the increased fatty acid production was responsible for the sugar induced tumor growth, the team modified the APC model mice to lack genes coding for enzymes that are involved in either fatty acid synthesis or fructose metabolism. One group of the mice lacked an enzyme KHK which is involved in the metabolism of fructose. The other group lacked enzyme FASN which is involved in fatty acid synthesis.

The team discovered that mice lacking either of these two genes did not develop large tumors unlike the APC model mice when fed the same small amounts of high fructose corn syrup.

The study showed results that colorectal cancers use high fructose corn syrup as fuel to increase rates of tumor growth. This is the major ingredient in most sugary sodas along with a variety of processed foods.

Fructose is not essential for the growth and survival of normal cells. This suggests that potential therapies targeting fructose metabolism may be worth exploring. And of course avoiding beverages and foods containing high fructose corn syrup as much as possible could significantly reduce the availability of sugar in the colon.

To view the original scientific study click below.

High-fructose corn syrup enhances intestinal tumor growth in mice.

Do Eggs and Cholesterol Cause Heart Disease?

Sobering news has just come out for those who love their omelets! A new study of nearly 30,000 people has reported that adults who consumed more dietary cholesterol and eggs showed a significantly higher risk of cardiovascular disease and death from any cause.

The study conducted by Northwestern Medicine indicates that the current U.S. dietary guideline recommendations for dietary eggs and cholesterol needs to be reevaluated. The recent study looked at data of 29,615 ethnically and racially diverse adults from six prospective cohort studies.

The diet data was collected using a questionnaire for food frequency and by getting diet history. Each participant was asked what they had eaten for the previous month or year. All data was collected with a single visit. The study had up to 31 years of follow up with a median of 17.5 years. During this time 5,400 cardiovascular events and 6,132 all causes of deaths were diagnosed.

The study results found that eating 300 mg of dietary cholesterol a day (the amount found in 2 eggs) was found to be associated with a 17% higher risk of incident cardiovascular disease and 18% higher risk of all causes of death. They found that cholesterol was the main factor independent of saturated fat and other dietary fats.

They also found that eating 3 to 4 eggs in a week was associated with a 6% higher risk of cardiovascular disease and an 8% higher risk of any cause of death. Overall diet quality, exercise and the type and amount of dietary fat did not change the association between dietary cholesterol and cardiovascular disease and death.

The study showed that if two people consumed the same diet and the only thing different in the diet was eggs, then they could directly measure the effect eggs have on heart disease. Earlier studies found eating eggs did not raise the risk of cardiovascular disease. However, those studies had a less diverse sample, a shorter follow up timeline and limited ability to adjust for other parts of someones diet.

The study did have a major limitation of long term eating patterns which were not assessed. The study team had just one snapshot of what each individuals eating pattern looked like. However, they do think they represented a good estimate of a person’s dietary intake although any changes in a person’s diet couldn’t be accounted for.

Based on the new study, people should watch their dietary intake of cholesterol by keeping it low. Reducing foods that are cholesterol rich such as red meat and eggs is the recommendation. However, eggs and red meat are good sources of great nutrients such as iron, choline and amino acids so they don’t need to be banished for good. It would be wise to eat egg whites instead of whole eggs and red meat consumption kept to a minimum.

To view the original scientific study click below.

Associations of Dietary Cholesterol or Egg Consumption With Incident Cardiovascular Disease and Mortality.

Lack of Sleep and Aging Go Hand in Hand

New research from Oxford University has brought scientists closer to understanding the mysterious function of sleep. What the scientists have discovered is how oxidative stress leads to sleep. Oxidative stress is believed to be one of the reasons we age and is also a cause of degenerative diseases.

The study confirms just what scientists have suspected…chronic lack of sleep will shorten life. Professor Gero Miesenbock who led the team, compares oxygen tanks which carry explosion hazard labels to humans who face a similar risk when oxygen we breathe to convert food into energy leads to oxidative stress in cells. He calls this imperfectly contained combustion.

This oxidative stress is believed to be one of the causes of aging and associated degenerative diseases which hinder of later years in life. The new research shows that oxidative stress also activates neurons which control whether we go to sleep.

The research team studied sleep regulation in fruit flies which are the animals that provided the first insight into the circadian clock almost 50 years ago. Each individual fly has a special set of neurons which control sleep. In a previous study the team discovered that the sleep control neurons function like an on off switch. When the neurons are electrically active the fly will be sleeping. When the neurons are silent the fly is awake.

The team decided to look for the signals which will switch the sleep control neurons on. They knew from previous research that a major difference between waking and sleep is how much electrical current will flow through two ion channels which are called Sandman and Shaker. Most of the current will be through Shaker during sleep.

The function of ion channels is to generate and control these electrical impulses through which brain cells will communicate. This made the team of scientists think about turning the question of, why we sleep, into a solvable and concrete problem. The team then sought to discovered what causes the electrical current to go through Shaker.

The answer was found in a component of the Shaker channel. They found that suspended below the electrically conducting portion of Shaker is another component. A small molecule, NADPH, flips back and forth between the chemical states which regulates the Shaker current. In turn, the state of NADPH reflects the degree of oxidative stress the cell has experienced. Sleeplessness leads to oxidative stress and this in turn drives the chemical conversion.

In a demonstration of this mechanism, a flash of light which flipped the chemical state of NADPH put flies to sleep.

Sleep disturbances are very common and sleeping pills are one of the most commonly prescribed drugs. These medications carry a variety of side effects and risks including addiction, forgetfulness and confusion. By targeting the mechanism the team has discovered, some of the side effects could be avoided.

To view the original scientific study click below.

Sleep and Aging: Two Side of One Coin?

A Good Reason to Follow the Mediterranean Diet

New research has shown that following the Mediterranean Diet for just a period of 4 days will boost exercise performance! Which is another great reason to follow one of the healthiest diets! The research team at St. Louis University in Missouri conducted the study to see if this diet would improve exercise performance and endurance. What they found was evidence that the Mediterranean diet which is already known for good health, did boost exercise performance in the study group.

The team recruited four men and seven women who were already recreationally active. The participants were asked to follow a diet that included eating lots of fresh vegetables and fruits, olive oil, nuts, whole grains, and a moderate consumption of red wine while also avoiding processed and red meats, trans and saturated fats, refined sugars and also limiting dairy products.

Following the first four days with the participants on this predominantly plant based diet, they were asked to run 5 kilometers on a treadmill. Nine to sixteen days later the participants were asked to follow a Western diet for an additional four days and then run 5 kilometers once again. The Western diet they followed was the traditional Western diet which consists of over consumption of refined sugars, salt, and saturated fats and little intake of fresh fruits and vegetables.

The team additionally wanted to test the effects the two diets would have on muscle strengthening and anaerobic exercise. They asked the participants to take a vertical jump test, a cycle test and a hand grip test at the same time points throughout the study.

The study found that overall the participants were 6 percent faster in the 5 kilometer treadmill run after following the Mediterranean diet than they were following the Western diet. The improvement occurred even though the heart rates of the participants were about the same and ratings of perceived exertion were the same on both occasions. However, the different diets did not show any effect on performance with the anaerobic exercise.

A variety of individual nutrients that are found in foods in the Mediterranean diet improve performance immediately or within just a few days. However, the benefits were quickly lost when a switch was made back to the Western diet. The study provides an incentive not only for athletes but also the general population to eat a healthier diet such as the Mediterranean diet.

To view the original scientific study click below.

Short-Term Mediterranean Diet Improves Endurance Exercise Performance: A Randomized-Sequence Crossover Trial.

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