Western Diet and Blood Pressure

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

Why it Takes So Long to Wake Up in the Morning

A study conducted by Raphael Vallat, Ph.D. at The University of California, Berkeley, has shown why people have a hard time waking up in the morning. Sleep Inertia or brain fog is real and makes it difficult for some people to drag themselves out of bed in the morning.

Early risers might deny it but as evidenced by the study, brain fog can take quite a while to dissipate and prior to the current study, researchers weren’t sure why it existed. Dr. Vallat asserts that even though the body is awake and moving in the morning, the brain can be asleep in some capacity following the wake up time.

When a person wakes up from sleeping, the brain doesn’t immediately switch from that sleeping state to a fully awakened state. Instead it goes through a transition period called sleep inertia which can last even up to 30 minutes after awakening. During this particular period, the brain will progressively switch from sleep to a normal wakefulness and our mental & cognitive performance does also.
To test this transitional period and prove how real it is, the team had 34 participants take 45 minute naps during which time they entered two periods of a deep sleep which are known as N2 and N3. The participants did not however enter REM (Rapid Eye Movement) sleep which is the deepest type of sleep. Upon awakening, Dr. Vallat tested the participants alertness using two subtraction tests which was one five minutes after awakening and one 25 minutes after awakening.

Similar to anyone who has experienced brain fog, the participants tended to make more mistakes after awakening, and their brain scans revealed why this happened. When a person is awake, the brain switches between two different modes which occur in two separate circuits. One is the task active mode such as when we are being productive or reading, and the second one is non focused task negative mode which is mind wandering. When we are awake we oscillate between the two modes and when the task active mode is functioning, there will usually be a decrease in activity with the task negative circuit.

What causes the sleep inertia to be different is the brain struggling to switch fluidly between the two circuits. It seems the brain is not really able to switch between these two different modes during sleep inertia resulting in lower performance with a mental calculation task.

The research team’s results indicate that during the period of sleep inertia the brain will slowly regain its ability to switch between the two modes divided by functional segregation. They believe it will take about 30 minutes to ultimately achieve this.

Unfortunately, they know there isn’t much a person can do to speed up their wake up process. Even a caffeine boost is not a true solution. There were some results that indicated caffeine increased the functional segregation between the two modes (task active and task negative networks) resulting in an enhancement of the brain’s ability to switch between the two modes. But it seems it does not actually work rapidly enough to cut through sleep inertia.

Caffeine takes about 30 to 60 minutes to reach peak level. Sleep inertia dissipates in about 30 minutes which is before the caffeine would even begin to work on the body. Instead of trying to caffeinate through slow brain functioning, Dr. Vallat suggests the only real fix for sleep inertia is time. Waiting a few minutes before making important decisions or hitting the road running is the best tonic especially if waking up from a very deep slumber.

How Important is Genetics for Longevity?

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

Nuts Help Control Weight Gain

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!

Exercise Improves Elimination of Toxic Proteins from Muscles

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.

Artificial Sweeteners and Toxic Effects on Gut Microbes

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.

Does Nutrition have More Impact on Bone Strength than Exercise?

Researchers at the University of Michigan have answered the question that fitness experts and scientists have wondered about. Does nutrition or exercise have the biggest impact on bone strength?

The tests were conducted on male, 16 week old mice which were assigned to 9 groups that were weight matched. This included a baseline group, an exercise with detraining group and a group that was non-exercised. 0.5% Calcium and 0.5% Phosphorus was fed to the control group and 5% Calcium and 1% Phosphorus was fed to the supplemented diet.

The exercise employed was treadmill running for 30 minutes at 12 metres per minute and this lasted for eight weeks. At the end of the eight week period, the mice that consumed the supplemented diet had more BMC (tibial cortical bone mineral content) and vBMD (bone mineral density) than the mice that were in the controlled diet group.

It was additionally noted that exercise was only able to increase BMC when the supplemented diet was also included. At the end of 16 weeks, both exercise and non-exercise groups of mice that were fed a supplemented diet were able to maintain greater tibial cortical BMC as well as vBMD as compared to the mice in the control group.

After looking at exercise and mineral supplementation in mice, they found some very interesting results. Nutrition played a much bigger role in bone strength and mass than exercise. Additionally, after exercise was stopped the mice continued to retain gains in bone strength if they continued to consume a diet supplemented with minerals.

David Kohn, a professor in the schools of engineering and dentistry, noted that long term mineral supplements will lead not only to increases in strength and bone mass, but also the ability to retain the increases even when training stops. And as people age, it is much easier to maintain diet over exercise.

Another finding was that diet alone will have positive effects on bone even when exercise isn’t happening. This was a big surprise to the team who anticipated exercise with a pretty ordinary diet to prove to have bigger gains in a persons bone strength.

Their data indicates that long term use of a mineral supplemented diet can be beneficial in the prevention of bone loss and strength even if you aren’t exercising. Combining both mineral supplementation and exercise serves to amplify the gains.

Previous studies looked at the effects of dietary calcium. The current study looked at increased calcium along with increased phosphorus and discovered benefits by increasing both. This doesn’t mean people should start running out and buying phosphorus and calcium supplements since their findings don’t directly correlate from mice to humans, but it does give the team a concept to study.

It is well known that peak bone mass occurs in people in the early twenties and then begins to decline. The goal then is to figure out how to maximize bone mass at an early age so when bone mass begins to decline, people are able to start in a better position.

The researchers also performed a variety of mechanical assessments that relate to the bone. The mechanical quality of bone tissue doesn’t always correlate with bone mass. The mice were tested following eight weeks of exercise training and a normal diet or a supplemented diet and then following another eight weeks of no training.

To view the original scientific study click here: Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice.

Too Much Sleep can be Bad for the Brain

Neuroscientists from Western University’s Brain and Mind Institute have released early results from the world’s most intense sleep study which reveals that sleeping an average of 7-8 hours per night have better cognitive performance than people that sleep less than that or more.

The article published in SLEEP, shows results from the study which was started in June 2017 with more than 40,000 people from all over the world included in the scientific investigation that was online. The study involved a very detailed questionnaire including a list of cognitive performance activities. The goal was to find out the sleeping habits of people all around the world. Sleep studies of a smaller degree have been conducted in laboratories, however this study’s goal was to find out what sleep is really like.

The study involved a very diverse group of participants which allowed the researchers to compare sleep deprivation on people of different professions, lifestyles and ages. The extensive questionnaire asked questions about where they lived, education level, medications they took and other information that helped the team consider factors that would contribute to results of the study. The participants also underwent 12 established cognitive tests so that mental ability and amount of sleep could be correlated.

About one half of the participants reported that they slept less than 6.3 hours each night. This is about sixty minutes less than what the study recommends for healthy sleep habits. One very surprising revelant factor was that participants who had slept less than four hours performed like they were nine years older than they were.

An additional interesting discovery was the fact that adults were affected equally. People who got seven to eight hours of sleep per night showed the highest functional cognitive behavior and this was regardless of age. The impairment related to too much or too little sleep was not dependent on age. However, older adults were much more likely to have shorter sleep duration which meant they were much more impacted by sleep deprivation than the other age groups of people.

Less sleep and more sleep both negatively impacted several cognitive functions such as information manipulation for problem solving and recognizing complex patterns. Verbal ability and reasoning were the most impacted by sleep with short term memory ability being barely impacted.

The study confirmed that getting 7 to 8 hours of sleep per night is optimal. Data from a previous study conducted on about one million people showed that both sleep deprivation and too many hours sleeping should be avoided for optimal health of the heart. 7 to 8 hours of sleep is recommended to keep the brain performing at its very best.

The studies findings show how significant real world implications are. Many people including those in positions that require a lot of responsibility may operate on too little sleep which may impair problem solving, reasoning and communication skills on a regular basis. Getting too much sleep on the other hand can be just as damaging.

To view the original scientific study click here: Dissociable effects of self-reported daily sleep duration on high-level cognitive abilities.

Skeletal Stem Cells Identified

Researchers have isolated human skeletal stem cells from adult and fetal bones that become cartilage, bone or stroma cells. This is the first time that skeletal stem cells have been identified in humans. The team was also able to derive the skeletal stem cells from human induced pluripotent stem cells which opens up the possibility of therapeutic applications.

By identifying this human skeletal stem cell and elucidating its lineage map, the researchers believe molecular diagnosis and treatment of skeletal diseases will occur. There is a tremendous burden imposed by neoplastic, post traumatic, post surgical and degenerative skeletal disorders. Skeletal dysfunction can develop into a broad spectrum of health conditions and despite its significant impact on disease and health, treatments aimed at improving skeletal function are currently limited. A major hurdle is that stem cell regulation in the human skeletal system is largely unexplored.

Bones posses skeletal tissues which have exceptionally regenerative potential. Defects of the bone heal readily and some vertebrates can actually regenerate portions of their limbs. However, regenerative capacities of skeletal tissues in other vertebrates are much more restricted. Bones in humans and mice can recover from small to moderate sized defects. However, adult cartilage tissue possess little to no regenerative ability. Both humans and mice exhibit severe age related degeneration of skeletal tissues with aging.

In the recent study, the team addressed the knowledge gap by identifying and characterizing human skeletal stem cells and downstream cartilage and bone progeny in a variety of tissues. These self renewing and multipotent cells were present in both adult and fetal human bone marrow tissues. They could be derived from iPSCs (induced pluripotent stem cells). By identifying the relationships between downstream skeletal progenitors and human skeletal stem cells, the team was able to create a lineage map of stem cell mediated formation of human skeletal tissues.

Additionally, transcriptomic (the study of the complete set of RNA transcripts that are produced by the genome under specific circumstances or in a specific cell) and epigenetic (the study of changes in organisms caused by modification of gene expression) comparisons with mouse skeletal stem cells revealed evolutionary conserved pathways regulating stem cell mediated formation of skeletal tissues. Divergent molecular pathways which may regulate species specific differences in skeletal structure and bone development were also revealed.

Comparing functional and molecular differences in specific types of stem cells between different species of vertebrates may lead to the uncovering of divergent and convergent mechanisms which underlie tissue growth and regeneration. This understanding could be applied towards enhancing health and rejuvenation in humans.

To view the original scientific study click here: Identification of the Human Skeletal Stem Cell

Are BPA Free Plastics Any Better Than BPA?

Twenty years ago a research team discovered by accident that BPA had leached out of plastic cages that were used to house female lab mice which caused an increase in chromosomally abnormal eggs. They have now discovered that a variety of alternative bisphenols now being used to replace earlier BPA in BPA free cups, cages, bottles and other items appear to have similar problems with their mice. Patricia Hunt of Washington State University reports a strange deja vu experience in their laboratory.

The recent findings were uncovered very similarly as the team once again noticed changes in the data coming from studies on control animals. The problem was once again traced to contamination from damaged cages, however the effects were more subtle than what presented in the original discovery. That was due to not all of the cages being damaged and the contamination source remained less certain.

The team was able to determine that the mice were being exposed to bisphenol replacements. They also observed that the disturbance in the lab was causing problems in the production of both sperm and eggs. After getting the contamination under control, they conducted additional controlled studies to test the effects of a variety of replacement bisphenols including one of the more common replacements known as BPS. The studies confirmed that the dispenol replacements produce remarkably similar chromosomal abnormalities as those seen in the earlier BPA study.

Patricia Hunt noted that the initial accidental exposure of the mice was remarkably similar to what could happen in people who use plastics in that the exposure was highly variable and accidental. Not all of the mice’s cages were damaged therefore the findings differed among mice in different cages. She adds that although determining levels of human exposure is difficult, the controlled experiments were conducted using low doses of BPS and other disphenol replacements thought to be relevant in people who use BPA free plastics.

The problems if they remain true in people as has been shown with BPA, will carry to future generations through their effects on the germ line. The team has shown that if it were possible to completely eliminate bisphenol contaminants, the effects would still persist for about three generations.

The team says more work is needed to determine whether some bisphenol replacements might be safer than others as there are dozens of these types of chemicals now in use. They also suspect that other widely used and endocrine disrupting chemicals such as parabens, flame retardants and phthalates may have similar adverse affects on fertility and they warrant study also.

The team agrees that the ability to rapidly enhance properties of chemicals has tremendous potential for treating a variety of diseases, controlling dangerous infectious agents, and enhancing medical and structural materials. The technology has paved the way for green chemistry which is a healthier future achieved by engineering chemicals to protect against hazardous effects. Currently however, regulatory agencies which are charged with assessing chemical safety cannot keep up with the introduction of new chemicals. Furthermore, as disphenol replacements illustrate, it is more cost effective and easier under current regulations to replace a chemical of concern with structural analogs instead of determining the attributes that make it hazardous.

The teams advice to consumers is simple: BPA free or not, plastic products which show physical signs of aging or damage cannot be deemed safe.

To view the original scientific study click here: Replacement Bisphenols Adversely Affect Mouse Gametogenesis with Consequences for Subsequent Generations.

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