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 cells ability to potentially cure, or at least ameliorate, many of our age-related diseases by regenerating tissue that makes this field so exciting.
Dr Villeponteau believes you can add many years, likely decades, to your life simply by eating right, exercising (which promotes the production of muscle stem cells, by the way) and living an otherwise clean and healthy lifestyle. Extreme life extension, on the other hand, is a different matter.
His book, Decoding Longevity, covers preventive strategies to prolong your life, mainly diet, exercise, and supplements. A portion of the book also covers future developments in the area of more radical life extension, such as stem cell technology.
If you would like to read the entire interview here is a link to the text version:
Transcript of Interview With Dr. Bryant Villeponteau by Dr. Joseph Mercola
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.
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
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.
Degeneration of the intervertebral disc is a very common problem which afflicts a large group of our population. Both neck and back pain are very often the result of progressive damage of the discs which separate our spinal vertebrae.
Healthy intervertebral discs work by absorbing stress which has occurred on the spine during movement. They then adjust our posture so we can move freely. If the discs wear out, pain develops in a variety of areas in a person’s neck and/or back.
Currently treatments for this disc degeneration have included replacing the damaged discs with new artificial ones or spinal fusion surgery. These approaches unfortunately have limited benefits because they cannot replace the full function of the discs they replace.
Now a research team at the University of Pennsylvania’s Perelman School of Medicine, School of Veterinary Medicine and the School of Engineering and Applied Science are aiming to solve this problem. They are working on developing bioengineered intervertebral discs which are harvested and made out of a person’s own stem cells. Because stem cells are undifferentiated cells which have the ability to transform into specialized cells, they are the focus of a variety of medical research studies.
For the past 15 years the team at the University of Pennsylvania has been working on these new disc models beginning with lab studies, then progressing to studies on small animals, and now recently studies on large animals.
Previously the team tested the new discs which they call disc like angle ply structures (DAPS) for 5 weeks in rat tails. In the next study, the research team further developed the engineered discs. The new model called endplate modified DAPS (eDAPS)were tested in the rats once again for up to 20 weeks. The new structure allowed the disc to retain its shape better and was more easily integrated in the surrounding tissue.
Several tests were run which included MRI scans and a variety of in depth tissue and mechanical analysis. The team discovered that in the rat model the eDAPS effectively restored the original disc function and structure.
With this success, the team was motivated to study eDAPS in goats. They proceeded to implant the device within the cervical spines of some of the goats. Goats were chosen for the study because the cervical spine discs of these animals have similar dimensions of those in humans. Goats also have semi upright stature which allowed the team to bring this study one step closer to conducting human trials.
The teams tests on goats proved to be successful. The eDAPS integrated quite well with the surrounding tissue. Additionally, the mechanic function of the discs either matched or surpassed that of the original cervical discs of the goats.
The next step will involve conducting more extensive trials on goats which will help the scientists to better understand how well eDAPS works. The team then plans to test eDAPS in human models of intervertebral disc degeneration which hopefully gets them one step closer to conducting clinical trials.
Implanting a device made of a person’s own cells is highly desirable. Using a true tissue engineered motion preserving replacement device in arthroplasty is something that has not been done yet in orthopedics. It would certainly be a large shift in treating spinal diseases and how surgeons approach motion sparing reconstruction of joints.
To view the original scientific study click here: watch-these-tissue-engineered-spinal-disks-mimic-real-thing
Researchers at the Karolinska Institute in Sweden have discovered that when we breathe through our nose rather than our mouth we are able to consolidate memories better. How breathing affects the brain has become a popular field of study in recent years and with new methodologies, more studies have been enabled.
The recent study in Sweden shows that people remember better when they breathe through their nose while the memory is being consolidated which is the process that happens between learning something and then memory retrieval. This is the first study that demonstrated this. The reason this phenomenon had not been studied earlier is that the common laboratory animals such as mice and rats do not breathe naturally through their mouths.
Memories go through 3 stages in their development. Encoding occurs first, then consolidation and finally retrieval. By breathing through the nose rather than the mouth during consolidation this enhances recognition memory. Nasal respiration is very important during the critical period where memories are activated and then strengthened. And it also suggests that the neural mechanisms which are responsible may emerge through nasal respiration.
For the study the team had the 24 Swedish participants learn twelve different smells occurring on two different occasions. Six fragrances were familiar such as strawberry and six were unfamiliar smells like pungent alcoholic scent 1 butanol.
The participants were then instructed to either breathe through their mouths or noses for one hour. When the hour was up, the participants were presented with the old set of smells along with the new set of twelve smells which also were six familiar smells and six unfamiliar smells. They were then asked if each one was from the learning session or new.
The findings indicated that when the participants breathed through their noses between the learning time and then the recognition, they remembered the smells much better. Those who breathed through their nose were twice as successful at recognizing whether the smells were old or new.
Previous research has indicated that receptors in the olfactory bulb detect not just smells but also variations in the airflow. Different parts of the brain will be activated in different phases of exhalation and inhalation. How the synchronization of brain activity and breathing happens and how that affects the brain and, subsequently our behavior, is unknown.
Growing evidence from human and animal studies indicates that respiration plays an important role in the neural and behavioral mechanisms associated with encoding and recognition. Nasal but not mouth respiration entrains neural oscillations that enhance the encoding and recognition processes and also the consolidation stage.
Smells are first processed by the olfactory bulb in mammals. This starts inside the nose and runs along the bottom of the brain. This has a direct connection to two areas of the brain that are strongly involved in memory…the hippocampus. Hippocampal rhythms are involved in the transfer of information between sensory and memory networks. With humans, bypassing nasal airflow by breathing through the mouth abolishes the rhythms and affects encoding as well as the recognition processes which reduces memory performance.
The concept that breathing affects our behavior is not new. The evidence has been around for thousands of years in areas such as meditation. However, no one has been able to scientifically prove what actually does go on in the brain. Researchers have tools now that can help reveal new clinical knowledge.
The next step for the team is to measure what really happens in the brain while breathing and how it is linked to memory. Previously it was not practical to measure this, however now the team has developed a new method of measuring activity in the brain and olfactory bulb that is non-invasive.
To view the original scientific study click here: Respiration modulates olfactory memory consolidation in humans.
Researchers at John Hopkins Bloomberg School of Public Health have conducted a study on two tribes that shed new light on the role the Western diet plays on blood pressure. The study involved a South American tribe which lives in near total isolation and has no Western dietary influences and a nearby tribe which is more exposed to Western dietary influences.
Researchers took blood pressure measurements from 72 Yanomami tribe members aged one to 60 and found no trends that pointed to lower or higher readings as the participants aged. Blood pressure measurements were also taken from 83 members of the neighboring tribe where there were Western dietary influences. They found a very clear trend pointing to higher blood pressure readings with advancing age.
The Yanomami tribe are hunter gatherers and also gardeners in a very remote rain forest region in Northern Brazil and Southern Venezuela. Their diet is low in salt and fat and high in fiber and fruits. Previous studies beginning in the 1980s have shown that obesity and atherosclerosis are virtually unknown among this tribe. They have extraordinarily low average blood pressure which does not appear to increase with age.
This study has shown that the age stability of blood pressure among this tribe begins in early childhood. It is the first study to compare this tribe to the nearby Yekwana tribe which has experienced an exposure to Western influenced lifestyles and diet.
In the United States and most other countries, blood pressure increases with age beginning early in life. The studies results support the thought that the tendency in Westernized societies for blood pressure to increase with age is not part of the natural aging process but might be the result of the cumulative effect of the Western lifestyle and diet.
The team found the blood pressures of the Yanomami tribe to be averaged at 95 systolic over 63 diastolic. In the United States the average systolic is 122 and 71 diastolic. The data shows that blood pressure within the Yanomami population remains very close to the same low levels from one to at least through the age of 60.
In contrast, the Yekwana who have been exposed to Western lifestyle and diet which includes processed foods was statistically indicating clear trends towards increasing blood pressure levels with advancing age. The Yekwana tribe members showed levels averaging 5.8 mm Hg higher by the age of 10 and 15.9 mm Hg higher by the age of 50.
With this age related increase in blood pressure which begins in early childhood, an opportunity exists for lifestyle and diet interventions to prevent later increases in blood pressure readings.
In the United States, systolic blood pressure increases by about 1.5 mm Hg. and 1.9 mm Hg per year among girls and boys respectively and 0.6 mm Hg per year among adults.
The research team involved is this study plans to follow up with a study of gut bacteria among the two tribes to determine if gut microbiome accounts for the tribe’s differences in blood pressure with aging.
To view the original scientific study click here: Association of Age With Blood Pressure Across the Lifespan in Isolated Yanomami and Yekwana Villages
A new study that analyzed more than 400 million people has revealed that genetics has a smaller impact on how long a person will live than scientists had previously thought. Researchers from Calico Life Sciences in collaboration with Ancestry (an online genealogy company), have established that inherited life span is much below what was previously estimated as earlier beliefs did not take into account people’s tendency to select partners who had similar traits to their own.
The goal of the study was to assess the heritability of lifespan…whether a person’s parents who lived long lives could predict whether that person lived a long life. Heritability measures to what extent specific genes can explain differences in a person’s traits. In the case of this study, life span. This is different than non genetic differences such as sociocultural factors, lifestyle and accidents. Previous human life span heritability estimates ranged from about 15 to 30 percent.
The researchers looked at a carefully chosen set of family trees and relevant information from over 400 million people who were surveyed by Ancestry. They began with 54 million subscribers to Ancestry which represented six billion ancestors. They then removed entries that were redundant and people who were still living thereby stitching all remaining pedigrees together.
Ancestry then stripped away any identifiable information from pedigrees leaving just the birth year, death year, birth place and familial connections that are part of the family tree structure. Most of the people were based in the U.S. and of European descent and connected to another by either spouse/spouse or parent/child relationship. The researchers then examined the similarity of life span between relatives so they could estimate heritability from each family tree.
They combined statistical and mathematical modeling to analyze data of relatives who were born during the 19th and early 20th centuries. They observed that first cousins and siblings showed same heritability estimates that were observed in previous studies. They also noted the life spans of spouses were likely to be correlated and were actually more similar than in siblings of opposite gender.
The correlation between spouses could be attributed to a variety of non genetic factors such as living in the same household or shared environment. The results then really started to surprise the researchers when they compared different types of first cousins in laws and siblings in law though there was no blood relatives and typically did not share households.
The researchers were able to focus in on correlations for other even more remote relationships which included uncles in laws and aunts, first cousins that are once removed in law and also a variety of configurations of co siblings in law. The findings which indicated that a person’s siblings, spouse siblings or their spouses siblings spouse had similar life spans, made it obvious that something besides a person’s genes was in place.
If people did not share genetic backgrounds and also did not share households, then the question became what best accounts for the life span similarity between individuals that had these types of relationships. The team went back to the data set and proceeded to perform analyses that would detect assortative mating which means the factors which are important to longevity tend to be very similar between mates. People tend to choose partners that have traits similar to their own and in this case how long they live.
Because people marry obviously before one is deceased, then assortative mating must be based on other characteristics. The mate choice could be sociocultural or genetic or both. In regards to non-genetic characteristics, wealthy people tend to marry other wealthy people for example. Or related to genetics, tall people might prefer to marry another tall person and height is somehow correlated to how long a person will live which would also inflate estimates of heritability life span.
The new analysis found that by correcting for the effects of assortative mating, life span heritability is likely no more than seven percent and perhaps even lower. The findings in this study certainly point to how low heritability of lifespan is. There are many things to learn about the biology of aging from human genes, however the recent findings temper expectations about what types of things can be learned and how easy it will be.
To view the original scientific study click here: Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating
Two separate studies have shown that consuming nuts on a daily basis may provide benefits to controlling weight gain, achieving overall metabolic health, and other cardiovascular benefits. Both studies delved into the influence eating nuts has on feeling full and improving insulin and glucose responses. These are things that can influence body weight.
The first study was conducted at the Nutrition Department at the Harvard T. H. Chan School of Public Health in Boston and involved 3 different groups of adults: 25,394 healthy men through Healthy Professionals Follow-up Study, 53,541 women through Nurses’ Health Study and another 47,255 women in Nurses Health Study II. Each of the participants in each group filled out food frequency questionnaires each year for 4 years.
The study team discovered that by replacing foods with less nutritional value with a one once serving of nuts on a daily basis resulted in a lower risk of obesity and weight gain over the 4 year length of the studies. They also found that substituting just one serving a day of nuts instead of one serving of a red meat, processed meat, desserts, potato chips or french fries, resulted in less weight gain. One serving of nuts is one ounce of whole nuts or two tablespoons of a nut butter. The study team believes their findings can be applied to the general population even though most of the participants were part of a health profession and mostly white.
Many people look at nuts as foods that are high in calories and fat and so do not consider them as a healthy snack item. However, the study shows that they actually are associated with less weight gain issues. When people reach adulthood they will begin gaining weight about one pound per year. Over 20 years that is quite a bit of weight gain. Substituting nuts for less nutritionally healthy foods can help prevent this gradual weight gain and also reduce risks of cardiovascular diseases related to weight gain and obesity.
The second study involved Brazil Nuts and was conducted at San Diego State University in 2017 with a grant provided by the American Heart Association. This study involved 22 healthy adults with two men and 20 women all age 20 or older and with a mean body mass index of 22.3. The participants ate either 20 grains of Brazil nuts which is about five nuts or 36 grams of pretzels in addition to their normal diet. The pretzels and Brazil nuts both had about the same number of calories and sodium content. They did this in two trials with 48 hours between each trial.
The team found that both the pretzels and Brazil nuts created reduced hunger feelings and a sense of fullness, however the Brazil nuts created a much fuller feeling of satiety. At forty minutes after the snacks were consumed, the team found the pretzels created a significant increase in insulin and blood glucose levels while the Brazil nuts did not. Brazil nuts actually stabilized both the insulin and blood glucose levels after they were consumed which could be beneficial for preventing weight gain.
Brazil Nuts are very rich in Selenium which is a mineral that might be associated with the insulin and blood glucose improvements noted in the study. Nuts are packed with fiber, protein, unsaturated fatty acids and a variety of beneficial chemicals. Consuming nuts can help reduce appetite and promote fullness which means people tend to eat less throughout the day. In addition to Brazil nuts, almonds, walnuts, pecans, macadamias and pistachios are other good choices!
A new study conducted by researchers at the University of Sao Paulo in Brazil in partnership with colleagues in the U.S. and Norway and published in Scientific Reports, has shown that lack of muscle stimulus results in a buildup of inadequately processed proteins in muscle cells which in turn leads to muscle wasting and weakness. This typical muscle dysfunction is a condition commonly effecting the elderly, individuals who sit for long periods of time without any exercise and bedridden patients.
Test results from rats with induced sciatic nerve injury which stopped receiving stimuli, showed the protein buildup was caused by impairment of autophagy which is the cellular machinery responsible for identifying then removing damaged toxins and proteins. The analysis of the tests on the rats subjected to a regime of aerobic exercise training which were previous to injury enabled the researchers to demonstrate that physical exercise can keep the autophagic system primed and then facilitate its activity as necessary. This is similar to muscle dysfunction due to the lack of stimulus.
Daily exercise will sensitize the autophagic system which facilitates the elimination of organelles (any of a variety of organized or specialized structures within a living cell) and proteins that are not functional in the muscles. It is important that removal of these dysfunctional components occur. When they accumulate they will become toxic and contribute to muscle cell impairment and death.
A good example of what muscle autophagy is, is by comparing muscles working in a similar manner as a refrigerator which runs on electricity. If the signal ceases due to someone pulling the plug on the frig or in the case of muscles blocks the neurons that innervate the muscles, it won’t take too long for food in a frig to spoil and proteins in muscles to spoil at different rates according to their composition. At this point an early warning mechanism in cells activates the autophagic system which will identify, isolate and then incinerate the defective material which prevents propagation of the damage. If the muscles do not receive the right electric signals for long periods of time, the early warning mechanism will stop working properly and cell collapse will occur. Without autophagy, a cascade effect will occur which leads to cell death.
In the current study, rats were submitted to sciatic nerve ligation surgery which created an effect equal to that of sciatic nerve compression in humans. The pain this injury can cause prevents people from using the leg affected by the injury which will lead to weakened muscles and eventually atrophy of those muscles.
Previous to surgery, the rats were divided into two groups. One group remained sedentary while the other group was given exercise training which consisted of running at 60% maximum aerobic capacity for one hour a day, five days per week. After four weeks of exercise training, surgery was performed. The muscular dysfunction induced by sciatic nerve injury was discovered to be less aggressive in the group which had aerobic exercise than the group of rats that were sedentary. Biochemical and functional parameters in the affected muscles were also evaluated. The aerobic training increased autophagic flux and therefore reduced dysfunctional protein levels in the muscles of the rats. Occurring at the same time was improvement in the muscle tissue’s contractility properties. Exercise is a transient stress which will leave memory in the organism and in this case via the autophagic system. When the organism is subjected to a variety of stress, it is better prepared to respond and combat the effects.
The team performed two other experiments which were designed to more thoroughly investigate the link between autophagy and exercise. One experiment involved mice in which the autophagy related gene ATG7 was silenced in the skeletal system. ATG7 encodes a particular protein responsible for synthesizing a vesicle called the autophagosome which forms around dysfunctional organelles and then transports them to the lysosome where they are broken down and then digested. This particular experiment validated the importance of autophagy in muscle biology. ATG7 will knockout mice that had not been subjected to sciatic nerve litigation although displayed muscular dysfunction.
In the second experiment, muscles from rats with sciatic nerve injury and control rats without injury were treated with chloroquine, a drug which inhibits autophagy by raising the lysosomal pH or alkalinity and therefore prevents the degradation of defective proteins. These tests showed less muscle strength in the control group of rats treated with the drug than in the untreated group. Chloroquine had no effect at all on the muscles of the rats with the sciatic nerve injury showing that the inhibition of autophagy is critical to muscular dysfunction caused by lack of stimulus.
Rather than aiming to find a treatment for people who are unable to exercise adequately, the goal of the studies was to use an experimental model for future research to help understand the cellular processes involved in muscle dysfunction. This will help facilitate the development of interventions capable of minimizing or even reversing an increasingly serious problem with muscle weakness and atrophy caused by lack of movement. By identifying a molecule that will selectively keep the autophagic system alert similar to what happens during physical exercise, treatments may be developed which can be given to people with this type of muscle disorder which includes people who are bedridden for extended periods of time, patients with degenerative muscular diseases and the elderly.
To view the original scientific study click here: Exercise prevents impaired autophagy and proteostasis in a model of neurogenic myopathy.
A collaborative study conducted by researchers at Ben Burion University of the Negev and Nanyang Technological University in Singapore, has shown the relative toxicity of six different FDA approved artificial sweeteners (sucralose, aspartame, saccharine, neotame, advantame and acesulfame potassium k) and also 10 sport supplements that contain these ingredients. Bacteria found in the digestive system became toxic when exposed to high levels of the artificial sweeteners such as just one mg/ml.
The team modified bioluminescent E coli bacteria which will illuminate when toxicants are detected and thus become a sensing model representative of the complex microbial system. This provided evidence that artificial sweeteners consumed regulartly adversely affects the activity of gut microbe which can lead to a variety of health issues.
The gut microbial system plays an important role in human metabolism. The study found that mice treated with one artificial sweetener, neotame, had different patterns than those not treated and several important genes found in the human gut decreased. Also noted were high concentrations of several fatty acids, cholesterol and lipids in the mice treated with this artificial sweetener.
Artificial sweeteners are found in many food products and diet soft drink beverages. People consume these added ingredients without even knowing it. This is especially common with athletes who devote a lot of time to their diet which often includes sport supplements taken to improve their physical performance. Additionally, artificial sweeteners have emerged as environmental pollutants and are found in surface and drinking water and in groundwater aquifers.
The study results may help in understanding the toxicity of these sweeteners and the possible negative affects on the gut microbial community and the environment. The bioluminescent bacteria panel might also be used for finding artificial sweetners that could be in the environment.
To view the original scientific study click here: Measuring Artificial Sweeteners Toxicity Using a Bioluminescent Bacterial Panel.
