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

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

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

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

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

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

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

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

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

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

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

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

lroot on October 10th, 2018

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

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

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

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

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

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

lroot on October 8th, 2018

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

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

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

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

Blood from world’s oldest woman suggests life limit

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

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

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

lroot on October 5th, 2018

neural cells

Researchers at the University of California, Irvine, have made a discovery that may improve the ability to control the formation of mature cells after stem cell transplants. Intrinsic cell properties have been identified that affect the fate of neural stem cells. The discovery could help scientists in predicting or controlling the fate of stem cells thereby improving their use in transplant therapies.

Neural stem cells can become one of 3 types of brain cells: neurons, astrocytes or oligendrocytes. The study revealed that neural stem cells which differed in fate potential expressed distinct patterns of sugars on the cell’s surface. The sugars contribute to electrical properties of the neural cell membrane and ultimately result in cell fate. Stem cells which hold great promise for disease treatments, can also pose difficulties in knowing what a stem cell will become after transplantation. The same number of stem cells can be transplanted in different patients, but the outcomes can be significantly different if cells transplanted in one patient become astrocytes and the cells in another patient become neurons. With the new discovery, scientists were able to predict what a neural stem cell will become and potentially direct cell fate. This would greatly enhance the success of stem cell transplantation therapies for a variety of diseases.

By using electrical properties, the research team discovered a new way to identify and then sort neural stem cells. They built on these findings by showing that differences in cell surface sugars are the reason these cells have different electrical properties. This study examined a variety of pathways that add sugars to cells and were able to find one that differed between cells that make astrocytes and cells that made neurons. The team stimulated the pathway in neural cells, changed the cell electrical properties, and caused the cells to make more astrocytes and fewer neurons. This showed that cell surface sugars can control cell fate. This pathway is active in cells which are grown for transplants and also in cells of developing brains. This pathway could also control how neural stem cells form astrocytes and neurons when the brain is being formed during development.

The researchers are now studying whether this pathway changes how cells will behave in transplants or how a developing brain is formed. To see how the process is regulated, they are focusing on the machinery inside the cell which adds the sugars in the first place. They have also found that particular proteins on cell surfaces are altered by this pathway which will help them uncover how the sugars go about telling stem cells which type of cell to form. The long term goal of the studies is to find methods to improve the effectiveness stem cell transplants for treating disease and injury.

To view the original scientific study click here: The Long Noncoding RNA Lncenc1 Maintains Naive States of Mouse ESCs by Promoting the Glycolysis Pathway.

mouse

Researchers at Boston Children’s Hospital have conducted a study that shows new insight as to why people with spinal cord injuries become paralyzed from the injury site down, even when the spinal cord has not become completely severed. Using paralyzed mice, they have shown that a small molecule compound when given systemically can revive these circuits and restore their ability to walk. They saw 80% of mice treated with the compound recover their stepping ability.

The researchers took a new approach from earlier studies which was inspired by the success of epidural electrical stimulation based strategies, the only treatment that was effective in treating patients with spinal cord injury. The treatment applied a current to the lower portion of the spinal cord and combined with rehabilitation training enabled some parties to regain movement. The epidural stimulation seemed to affect the excitability of neurons. When the stimulation was turned off, the effect was gone. The researchers tried to find a pharmacologic approach to mimic the stimulation and understand how it works.

The researchers selected a handful of compounds already known to alter the excitability of neurons and able to cross the blood brain barrier. The compound was given to mice in groups of 10 by intraperitoneal injection. All the mice used in the study had spinal cord injuries but with some nerves still intact. Each group including a control group that was given a placebo were treated for 8 to 10 weeks.

One of the compounds used, called COP290, had the most potent effect. It enabled paralyzed mice to regain stepping ability after 4 to 5 weeks of the treatment. Electromyography recordings showed that the 2 relevant groups of hind limb muscles were active. And the walking scores remained higher than the control groups up to 2 weeks after stopping treatment and side effects were minimal.

CLP290 is known to activate a protein called KCC2 which is found in cell membranes and transports chloride out of neurons. The current research shows that inhibitory neurons in an injured spinal cord are crucial to the recovery of motor function. These neurons produce drastically less KCC2 after a spinal cord injury and they are unable to properly respond to signals from the brain. They only respond to excitatory signals which tell them to keep firing. This results in too much inhibitory signaling in the overall spinal circuit. In other words, the brain’s commands telling the limbs to move aren’t relayed.

Restoring KCC2 with either genetic techniques or CLP290, the inhibitory neurons can receive inhibitory signals from the brain which tells them to fire less. The researchers found that this shifts the overall circuit back toward excitation making it more responsive to brain input. This had the same effect of reanimating spinal circuits which were disabled due to injury. By restoring inhibition, the whole system will be excited more easily. However, there does need to be a balance as too much excitation is not good and too much inhibition is not good either.

The team is now investigating other compounds that will act as agonists to KCC2. They believe such gene therapy to restore KCC2 might be combined with epidural stimulation to maximize function after spinal cord injuries.

To view the original scientific study click here: Reactivation of Dormant Relay Pathways in Injured Spinal Cord by KCC2 Manipulations

lroot on September 23rd, 2018

high fiber foods

As all mammals age, microglia which are immune cells in the brain become chronically inflamed. When this occurs, they produce chemicals which are known to impair cognitive and motor functions. This is one explanation in regards to why memory fades and other brain functions also decline during the aging process. According to a new study at the University of Illinois College of Agricultural, Consumer and Environmental Sciences however, there might be a remedy to delay this inevitability and that is with dietary fiber.

Consuming dietary fiber promotes the growth of good bacteria in the gut. As these bacteria digest ingested fiber, they produce SCFAs (short chain fatty acids) which includes butyrate, as byproducts. Butyrate is of particular interest as it has been shown to produce antiinflammatory properties on microglia. It has also been shown to improve memory in mice when it has been administered pharmacologically.

In previous studies, butyrate in drug form (sodium butyrate) showed positive outcomes although the mechanism wasn’t clear. The new study however reveals in old mice that butyrate inhibits the production of damaging chemicals produced by inflamed microglia. One of these damaging chemicals has been associated with Alzheimers disease in humans.

Researchers have been interested in how sodium butyrate works, however they are more interested in knowing whether similar effects can be obtained by feeding mice more fiber. People are highly unlikely to consume sodium butyrate due to its noxious odor, however a more practical way to get elevated butyrate is by consuming a diet high in soluble fiber. The idea goes directly to the fact that gut bacteria naturally convert fiber to butyrate.

Diet has a major influence on the function and composition of microbes found in the gut. Diets high in fiber benefit these good microbes. Diets high in fat and protein on the other hand, can have a negative influence on microbial function and composition. It was believed that butyrate which is derived from dietary fiber would have the same benefits in the brain as the drug form, sodium butyrate. However, it had not been previously tested. The research team fed low and high fiber diets to groups of both young and old mice. They then measured the levels of butyrate and other SCFAs contained in the blood and additionally, inflammatory chemicals in the intestine.

The diet high in fiber elevated butyrate and SCFAs in the blood in both the young and old mice. However, only the old mice showed intestinal inflammation on the low fiber diet. The young adult mice did not have the inflammatory response on the same low fiber diet as the old mice. This indicates the vulnerability of the aging process and diet. When the old mice were fed the high fiber diet, the intestinal inflammation was drastically reduced revealing that dietary fiber can manipulate the inflammatory environment in the gut.

The next step the researchers took was to look at signs of brain inflammation. They examined about 50 unique genes in microglia and discovered that high fiber diet reduced the inflammatory profile in older mice.

The next step for the researchers is to examine the effects of diet on behavior and cognition and the precise mechanisms in the gut brain axis. Although the current study was conducted on mice, the team is comfortable in extending the finding to humans if only in a general way. What we eat matters and it is known that older adults consume 40% less dietary fiber than is recommended. By not consuming enough fiber, negative consequences can occur. Most people do not make the connection to brain health and inflammation in general.

To view the original scientific study click here: Butyrate and Dietary Soluble Fiber Improve Neuroinflammation Associated With Aging in Mice. Frontiers in Immunology, 2018; 9 DOI: 10.3389/fimmu.2018.01832

lroot on September 21st, 2018

senior injured

Researchers at the Georgia Institute of Technology have engineered a molecular matrix which will deliver stem cells referred to as muscle satellite cells (MuSCs), directly to muscle tissue in patients such as the elderly whose muscles don’t regenerate very well. This molecular matrix, a hydrogel, has successfully delivered MuSCs to injured, aged muscles in mice. The hydrogel boosted the healing process while also protecting the stem cells from any harsh immune reactions.

The development has provided a new method by which an aging patient after a car accident for instance, can receive treatment to severe muscle injuries that won’t typically heal. Previously, muscle stem cells from a donor have not been able to be successfully delivered to restore damaged tissue. Simply injecting additional MuSCs into the inflamed, damaged tissue was inefficient. This was mostly due to the stem cells encountering an immune system on the warpath.

Muscle injuries attract immune cells and typically this would help with muscle stem cell repair. However, in the aged or dystropic muscles, immune cells will lead to the release of toxic chemicals such as cytokines and free radicals which kill the new stem cells. Young Jang, one of the researchers says that only about 1 and 20 percent of injected MuSCs actually make it to damaged tissue and those that do will arrive in a weakened state. Additionally, some tissue damage makes any injection unfeasible.

The new hydrogel will protect the cells which will multiply and thrive inside the matrix. The hydrogel is applied to the injured muscles with the cells engrafting onto the tissues which will help them heal. Hydrogels very often start out as a water-based solution of molecular components which resemble crosses and other components that make the ends of the crosses attach to each other. When these components come together, they will fuse into molecular nets suspended in water. This results in a material that resembles the consistency of a gel.

If stem cells are mixed into the solution, when the matrix forms it ensnares the treatment for delivery and also protects the payload from dissipation or death in the body. Researchers can custom engineer hydrogels and can reliably and easily synthesize them by tweaking their components. This physically traps the MuSCs in a net and the cells also grab onto chemical latches that have been engineered into the net or matrix.

The hydrogel’s added latches bond with proteins protruding from stem cells membranes and not only increase the cell’s adhesion to the net, but also hinder them from suicide. Stem cells will tend to kill themselves when they are detached and free floating.

The cells and chemical components are mixed in solution then applied to the muscle that has been injured. The mixture sets to a matrix gel patch which glues the stem cells in place. The gel is biodegradable and biocompatible. The stem cells thrive and multiply in the gel once it has been applied. The hydrogel then degrades and leaves behind the cells engrafted onto muscle tissue in much the same way natural stem cells would be.

In healthier, younger individuals MuSCs are part of the natural healing mechanism in the body. MuSCs are resident stem cells found in the skeletal muscles. They are key players in producing new muscle tissue and live on muscle strands like specks.

As people age they lose muscle mass and the number of satellite cells will also decrease. The ones that do remain get weaker. At very advanced age, a person stops regenerating muscle altogether.

With the new system the researchers engineered, donor cells can be introduced to enhance the repair mechanism in older, injured people. If the new method goes to clinical trials, researchers will most likely have to work around the possibility for donor cell rejection in human patients.

To view the original scientific study click here: Synthetic matrix enhances transplanted satellite cell engraftment in dystrophic and aged skeletal muscle with comorbid trauma

lroot on September 17th, 2018

brain

Scientists at the University of Virginia School of Medicine have discovered that improving the function of the lymphatic vessels in mice has led to dramatic enhancement of their ability to learn and improve their memory. The work which was led by neuroscientist Jonathan Kipnis, Ph.D., may provide doctors a new path to treat and prevent a variety of age related memory loss and other conditions.

In 2015 the team discovered that the brain is surrounded by lymphatic vessels. These were vessels science textbooks said did not exist. The discovery made headlines around the globe and was named one of the year’s biggest discoveries by Science. Dr. Kipnis sees the newest discovery as the most important yet. He notes that if they can make old mice learn better, then there is something that can be done. The pathology in the mice subjects looked very similar to what is seen in human samples in terms of all the amyloid protein. When the team obstructed vessels in mice models, there was a significant accumulation of harmful plaques in the brain.

The team were able to use a compound to improve the flow of brain waste to the lymph nodes in the necks of aged mice. When done, the vessels became larger and drained better which had a direct effect on the mice’s ability to remember and learn. By targeting the lymphatic vasculature around the brain, they observed enhanced cognitive ability in old mice.

The team determined that obstructing vessels in mice worsened the accumulation of harmful amyloid plaques in the brain which are associated with memory related disease. This could help explain the buildup of such plaques in people. Since 98 percent of cases are not familial, it is really a matter of what effects aging has on these types of diseases. By figuring out what specific changes are happening in aged lymphatics in humans, specific approaches can be developed to treat age related memory diseases.

The team believes that the best way to treat memory related diseases in the aged might be to combine vasculature repair with other approaches. By improving the flow through meningeal lymphatic vessels, it might be possible to overcome some of the obstacles that have hindered previously promising treatments. Additionally the new discovery may offer ways to stave off the onset of these types of diseases to the point that treatments won’t be necessary. It may even be possible to delay them indefinitely.

To view the original scientific study click here: Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease.

lroot on August 31st, 2018

probiotic

In a study conducted by the Medical College of Georgia at Augusta University researchers have discovered a significant accumulation of bacteria in the small intestine from probiotic use which can result in disorientating brain fogginess and rapid, severe belly bloating. The study was conducted on 30 patients with 22 of them reporting problems with difficulty concentrating and confusion. They also reported bloating and gas.

The researchers found large colonies of breeding bacteria in the patient’s small intestines and also high levels of D-lactic acid which was being produced by the bacteria lactobacilus fermentation of sugars in the food they consumed. D-lactic acid can be temporarily toxic to brain cells which can interfere with thinking, sense of time and cognition. Some of the patients in the study showed two to three times the normal amount of D-lactic acid in their blood. Most of the patients said the brain fogginess they were experiencing lasted from half an hour to several hours after eating and some reported that the fogginess was so severe they had to quit their job.

This is the first time the connection has been made between bacterial overgrowth in the small intestine, high levels of D-lactic acid in the gut, and brain fogginess associated with probiotic use. Probiotic bacteria has the capacity to break down sugar and produce D-lactic acid. If the small bowel is inadvertently colonized with probiotic bacteria then the stage has been set for potentially developing lactic acidosis and brain fogginess. Probiotics can be very beneficial in some scenarios such as restoring gut bacteria after taking antibiotics, but with excessive or indiscriminate use complications such as noted in the study can arise. The researchers warn that probiotics should be treated as a drug rather than as a food supplement.

The patients in the study who experienced brain fogginess took protiotics and small intestinal bowel overgrowth (SIBO) was more common in this group (68% compared to 28%),. The patients with brain fogginess also showed a higher prevalence of D-lactic acidosis (77% compared to 25%). When the patients experiencing the brain fogginess stopped taking the probiotics and took a course of antibiotics, their brain fogginess resolved. The actual movement of food in the gastrointestinal tract was slow in one third of the patients with brain fogginess and one fourth in the other group. Slower passage of food can increase the chance of SIBO.

Normally the small intestines do not make much D-lactic acid. SIBO appears to change that by causing bacteria to go into a feeding frenzy which ferments sugars resulting in methane and hydrogen gas that causes bloating. When probiotics are added to that the acid gets absorbed in the blood and can reach the brain.

By identifying the problem, it can be treated. Diagnosis includes urine, blood and breath tests to detect lactic acid and an endoscopy which examines fluid from the small intestine can identify the specific bacteria and antibiotic treatment can be administered.

In the study, the patients with brain fogginess, SIBO and/or D-lactic acidosis were asked to discontinue probiotic products and were given antibiotics which were targeted to their bacterial population. Those patients who did not exhibit SIBO were asked to stop probiotics and stop eating yogurt. Those patients with SIBO and D-lactic acidosis but no brain fogginess were also administered antibiotics. After treatments, 70 percent of patients reported significant improvements in their symptoms. 85 percent of patients reported their brain fogginess had disappeared. Those patients with SIBO and high levels of D-lactic acid and no brain fogginess reported significant improvement in regards to cramping and bloating with three months.

All patients who participated in the study had extensive examination of the gastrointestinal tract which included a motility test to rule out any other potential causes of their symptoms. Questionnaires were filled out which included questions about symptoms such as belching, gas and abdominal pain along with other related issues about antibiotic and probiotic use and food fads and consumption of yogurt.
Patients were given carbohydrates which were followed by metabolic testing to see the impact of things like insulin and blood glucose levels. Levels of D-lactic acid and L-lactate acid were also measured as these acids which result from muscle use of glucose as energy can also cause muscle cramps.

Probiotics are meant to work in the colon and not in the stomach or small intestines. However, people with motility issues, those taking opioids and proton pump inhibitors, can result in issues with probiotic bacteria reaching the proper place. Other problems from use of antidepressants and minerals like iron and people with diabetes, can also slow movement and increase the change that probiotics will remain too long in the upper intestine where they can cause harm.

For many people probiotics can help especially in those suffering from gastroenteritis or stomach flu where diarrhea and other problems from antibiotic use can wipe out natural gut bacteria. This is when probiotic use is beneficial in building up the bacterial flora. Good sources of probiotics are sauerkraut, yogurt, kefir, kimchi and dark chocolate. These are all generally safe due to their small amounts of bacteria. Helpful gut bacteria or microbiome are essential to a well functioning immune system and general health overall.

Future studies will include following patients for longer periods of time to ensure problems remain resolved. Some of the patients in the current study required two rounds of antibiotics.

To view the original scientific study click here: Brain fogginess, gas and bloating: a link between SIBO, probiotics and metabolic acidosis.

lroot on August 24th, 2018

peoplle eating

Through a variety of studies involving timing of breakfast and dinner and eating during an 8-10 hour window each day, health benefits have been discovered. From weight loss and reduction of body fat to protection against obesity and metabolic diseases, the research has revealed a host of health benefits to controlled eating.

One study conducted by scientists at the Salk Institute, discovered that mice who lacked the biological clocks thought necessary for a healthy metabolism, could still be protected against metabolic diseases and obesity when their daily access to food was restricted to a 10 hour window. The research suggests that health problems which are associated with disruptions to an animals 24 hour rhythms of rest and activity, which in humans is linked to doing shift work or eating throughout most of the day, can be corrected by consuming all calories in a 10 hour window.

For many people their day begins with a cup of coffee first thing in the morning and doesn’t end until a bedtime snack 14 to 15 hours later. Restricting food intake to 10 hours per day and then fasting the rest of the time can lead to better health says Satchidananda Panda, a Professor in Salk’s Regulatory Biology Lab.

All cells in a mammal’s body operate on a 24 hour cycle which is known as the circadian rhythm which are cellular cycles that control when various genes are active. In humans, digestive genes are more active earlier in the day while genes which control cellular repair are more active at night. In previous studies researchers found that mice which were allowed 24 hour access to a high fat diet became obese and developed a variety of metabolic diseases including fatty liver, diabetes and high cholesterol. When these same mice were restricted to the high fat diet for an 8 to 10 hour window, they became lean, fit and healthy. The results were attributed to the mice being in better sync with their cellular clocks by eating most of the calories when the genes for digestion were most active.

In the current study, the researchers aimed to better understand the role circadian rhythm plays in metabolic diseases through disabling the genes responsible for maintaining the biological clock in mice, including the liver which regulates many metabolic functions. The genetic defects in these clock less mice, makes them more susceptible to diabetes, fatty liver disease and high blood cholesterol. These diseases were further escalated when the mice were allowed to eat sugary and fatty foods.

To test time restricted eating, the clock less mice were put on one of two high fat diet regimes. One group had access to food around the clock while the other group had access to the same number of calories but only during a 10 hour window. As was expected, the group of mice that ate at any time became obese and developed metabolic diseases. The other group which only ate during a 10 hour window remained healthy and lean despite not having an internal clock and genetically programmed to be morbidly sick. This revealed to the researchers that health benefits derived from the 10 hour window were not only due to restricting eating times when digestive genes were most active.

From previous studies, researchers were under the impression that the biological clock was internally timing the process of turning metabolic genes on and off at predetermined times. And while this may still be true, the research shows that by controlling the mice’s feeding and fasting cycles the internal timing system can be overridden with an external timing system.

The work suggests that the main role of circadian clocks might be to tell an animal when to eat and when not to eat. This strikes a balance between sufficient nutrition during the “eat” state and the necessary rejuvenation and repair during the fasting state. When the clock is disrupted as can be seen in humans who do shift work or when it might be compromised due to genetic defects, the balance between rejuvenation and nutrition breaks down and disease can occur. As a person ages, the circadian clock weakens. This parallels the increased risk for heart disease, cancer, dementia and metabolic diseases.

The good news is that simply making a lifestyle change by eating all food within a 10 hour window can restore balance, help maintain health and stave off metabolic diseases. This finding that a good lifestyle can beat bad effects of defective genes opens up new hope for staying healthy.

The researchers plan to study whether eating within an 8 to 10 hour window can prevent or reverse many age related diseases as well as looking at how the current study on mice can apply to humans.

Another study in regards to controlled eating involved making modest changes to breakfast and dinner times to help reduce body fat. This study led by Dr. Jonathan Johnston at the University of Surrey investigated what impact changing meal times has on dietary intake, blood risk markers for heart disease and diabetes, and dietary intake.

Participants in the study were divided into two groups. One group was required to delay their breakfast time by 90 minutes and have their dinner time 90 minutes earlier than normal. The other group was allowed to eat their meals as they normally would. Blood samples and complete diet diaries were given by all participants before and during the 10 week intervention and were asked to complete a feedback questionnaire immediately following the study. Participants were not asked to follow a strict diet and could eat freely provided it was within a certain eating window.

The researchers found that those who changed their eating times lost on average more than twice as much body fat as those who ate their meals as they normally would. And while there were no restrictions on what the participants could eat, the researchers found that the group who changed mealtimes ate less food overall than the other group. The questionnaire confirmed this with 57% of participants noting a reduction in food intake either due to decreased eating opportunities, reduction in food intake or a cutback in snacking particularly in the evening. The researchers did note that they were uncertain whether the longer fasting time with this group may have contributed to the reduction in body fat.

The researchers also examined if fasting diets are compatible with long term commitment and everyday life. When questioned, 57% of participants thought they could not have maintained the new mealtimes past the prescribed 10 weeks due to incompatibility with social and family life. However, 43% felt they would consider continuing if eating times were a bit more flexible.

Although the study was small, it did provide researchers with invaluable insights into how alterations to meal times can have benefits to the body. Reduced body fat lessens chances of obesity and related diseases and is vital to improving overall health. However, fasting diets can be difficult to follow and can be challenging given most people’s lifestyle. These preliminary findings will help researchers design larger and more comprehensive studies of time restricted fasting.

Both studies summarized above do reveal that changing eating habits can influence a person’s health and help protect against disease and obesity. As more studies involving fasting and eating times are conducted, more insights will be revealed as to further health benefits and how people can incorporate new diet and fasting lifestyles into their everyday life in a compatible manner.

To view the original scientific study click here: A pilot feasibility study exploring the effects of a moderate time-restricted feeding intervention on energy intake, adiposity and metabolic physiology in free-living human subjects.