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:
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.
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.
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.
UC San Francisco scientists identified a previously unknown pool of blood making stem cells in the lungs capable of restoring blood production when the stem cells of the bone marrow, previously thought to be the principal site of blood production, are depleted. Using video microscopy in the living mouse lung, the scientists have revealed that the lungs play this previously unrecognized role in blood production. As reported online March 22, 2017 in Nature, the researchers found that the lungs produced more than half of the platelets blood components required for the clotting that stanches bleeding in the mouse circulation.
“This finding definitely suggests a more sophisticated view of the lungs that they’re not just for respiration but also a key partner in formation of crucial aspects of the blood,” said pulmonologist Mark R. Looney, MD, a professor of medicine and of laboratory medicine at UCSF and the new paper’s senior author. “What we’ve observed here in mice strongly suggests the lung may play a key role in blood formation in humans as well.”
The findings could have major implications for understanding human diseases in which patients suffer from low platelet counts, or thrombocytopenia, which afflicts millions of people and increases the risk of dangerous uncontrolled bleeding. The findings also raise questions about how blood stem cells residing in the lungs may affect the recipients of lung transplants.
Mouse lungs produce more than 10 million platelets per hour, live imaging studies show
The new study was made possible by a refinement of a technique known as two-photon intravital imaging recently developed by Looney and co-author Matthew F. Krummel, PhD, a UCSF professor of pathology. This imaging approach allowed the researchers to perform the extremely delicate task of visualizing the behavior of individual cells within the tiny blood vessels of a living mouse lung.
Looney and his team were using this technique to examine interactions between the immune system and circulating platelets in the lungs, using a mouse strain engineered so that platelets emit bright green fluorescence, when they noticed a surprisingly large population of platelet-producing cells called megakaryocytes in the lung vasculature. Though megakaryocytes had been observed in the lung before, they were generally thought to live and produce platelets primarily in the bone marrow.
“When we discovered this massive population of megakaryocytes that appeared to be living in the lung, we realized we had to follow this up,” said Emma Lefrançais, PhD, a postdoctoral researcher in Looney’s lab and co-first author on the new paper.
More detailed imaging sessions soon revealed megakaryocytes in the act of producing more than 10 million platelets per hour within the lung vasculature, suggesting that more than half of a mouse’s total platelet production occurs in the lung, not the bone marrow, as researchers had long presumed. Video microscopy experiments also revealed a wide variety of previously overlooked megakaryocyte progenitor cells and blood stem cells sitting quietly outside the lung vasculature estimated at 1 million per mouse lung.
Newly discovered blood stem cells in the lung can restore damaged bone marrow
The discovery of megakaryocytes and blood stem cells in the lung raised questions about how these cells move back and forth between the lung and bone marrow. To address these questions, the researchers conducted a clever set of lung transplant studies:
First, the team transplanted lungs from normal donor mice into recipient mice with fluorescent megakaryocytes, and found that fluorescent megakaryocytes from the recipient mice soon began turning up in the lung vasculature. This suggested that the platelet-producing megakaryocytes in the lung originate in the bone marrow.
“It’s fascinating that megakaryocytes travel all the way from the bone marrow to the lungs to produce platelets,” said Guadalupe Ortiz-Muñoz, PhD, also a postdoctoral researcher in the Looney lab and the paper’s other co-first author. “It’s possible that the lung is an ideal bioreactor for platelet production because of the mechanical force of the blood, or perhaps because of some molecular signaling we don’t yet know about.”
In another experiment, the researchers transplanted lungs with fluorescent megakaryocyte progenitor cells into mutant mice with low platelet counts. The transplants produced a large burst of fluorescent platelets that quickly restored normal levels, an effect that persisted over several months of observation — much longer than the lifespan of individual megakaryocytes or platelets. To the researchers, this indicated that resident megakaryocyte progenitor cells in the transplanted lungs had become activated by the recipient mouse’s low platelet counts and had produced healthy new megakaryocyte cells to restore proper platelet production.
Finally, the researchers transplanted healthy lungs in which all cells were fluorescently tagged into mutant mice whose bone marrow lacked normal blood stem cells. Analysis of the bone marrow of recipient mice showed that fluorescent cells originating from the transplanted lungs soon traveled to the damaged bone marrow and contributed to the production not just of platelets, but of a wide variety of blood cells, including immune cells such as neutrophils, B cells and T cells. These experiments suggest that the lungs play host to a wide variety of blood progenitor cells and stem cells capable of restocking damaged bone marrow and restoring production of many components of the blood.
“To our knowledge this is the first description of blood progenitors resident in the lung, and it raises a lot of questions with clinical relevance for the millions of people who suffer from thrombocytopenia,” said Looney, who is also an attending physician on UCSF’s pulmonary consult service and intensive care units.
In particular, the study suggests that researchers who have proposed treating platelet diseases with platelets produced from engineered megakaryocytes should look to the lungs as a resource for platelet production, Looney said. The study also presents new avenues of research for stem cell biologists to explore how the bone marrow and lung collaborate to produce a healthy blood system through the mutual exchange of stem cells.
“These observations alter existing paradigms regarding blood cell formation and lung biology. The observation that blood stem cells and progenitors seem to travel back and forth freely between the lung and bone marrow lends support to a growing sense among researchers that stem cells may be much more active than previously appreciated, Looney said. “We’re seeing more and more that the stem cells that produce the blood don’t just live in one place but travel around through the blood stream. Perhaps ‘studying abroad’ in different organs is a normal part of stem cell education.”
Reference: 1.Emma Lefrançais, Guadalupe Ortiz-Muñoz, Axelle Caudrillier, Beñat Mallavia, Fengchun Liu, David M. Sayah, Emily E. Thornton, Mark B. Headley, Tovo David, Shaun R. Coughlin, Matthew F. Krummel, Andrew D. Leavitt, Emmanuelle Passegué, Mark R. Looney. The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors. Nature, 2017; DOI: 10.1038/nature21706
A simple tablespoon daily of coconut oil could promote weight loss and improve cardiovascular health, reveals a new clinical study.
Coconut oil was once considered a “bad fat” since it contains saturated fatty acids, however it has a different chemical structure than saturated fats from animals or those that are synthetically produced such as margarine and other hydrogenated oils. Natural sources of saturated fats are gaining appreciation as beneficial, particularly for the brain. Even saturated fats from animals are not necessarily bad. It is excessive arachidonic acid which is found in the fat of grain fed animals such as most beef that is best avoided. That is caused by their diet which is too high in omega-6 polyunsaturated fatty acids and lacking omega-3 fatty acids. Meat from 100% grass fed beef or buffalo contains less arachidonic acid and a healthy balance of the two types of polyunsaturated fats.
The new study evaluated the health effects of consuming extra virgin coconut oil, focusing on how it affects heart health and a range of measurements including body weight, size, and circumference.
The average age of the participants was 62.4 years, 70% were elderly individuals, and 63.2% were males. During the first phase which lasted three months, 136 enrollees were put on a standardized diet. From the third month onward, the 116 who completed the first phase were placed in two groups with 22 remaining on the diet while 92 were put on the diet with .43 ounces daily of extra virgin coconut oil, which is equivalent to about 1 Tablespoon.
The results of the 3 month study showed that relative to the standard diet, the coconut oil group saw a decrease in all six of the bodily parameters measured, including weight loss of 1.3 pounds and waist size reduction of almost an inch. Additional testing also showed improvements in cardiovascular health. Previous studies of coconut oil have shown many benefits including improved cognition and enhanced nutrient absorption.
One of the advantages of coconut oil is that it does not oxidize during cooking as is the case with most other oils. That is one of the reasons why hydrogenated oils were created. Unfortunately they contain dangerous trans fatty acids so are best avoided. Back in the 1980’s many doctors and dieticians thought that coconut oil was bad because of it’s saturated oil content. Since then dozens of studies have found the opposite to be true. Also demographic studies have typically shown better heart health in countries where coconuts are eaten regularly.
A molecular key to aging of the blood and immune system has been discovered in new research conducted at UC San Francisco, raising hope that it may be possible to find a way to slow or reverse many of the effects of aging.
The key is a link between the health of a rare population of adult stem cells that arise early in development and are responsible for replenishing all blood cell types throughout a lifetime, and a newly identified role for autophagy, an important cellular cleanup and recycling process that was the focus of the 2016 Nobel Prize in Physiology or Medicine.
In their new study, published online March 1 in Nature, the UCSF team discovered that in addition to its normal role in cellular waste-processing, autophagy also is needed for the orderly maintenance of blood-forming hematopoietic stem cells (HSCs), the adult stem cells that give rise to red blood cells, which carry oxygen, and to platelets, as well as the entire immune system.
The researchers found that autophagy keeps HSCs in check by allowing metabolically active HSCs to return to a resting, quiescent state akin to hibernation. This is the default state of adult HSCs, allowing their maintenance for a lifetime.
According to Emmanuelle Passegué, PhD, the senior scientist for the study, “This is a previously unknown role for autophagy in stem cell biology.”
Failure to activate autophagy has profound impacts on the blood system, Passegué’s team found, leading to the unbalanced production of certain types of blood cells. Defective autophagy also diminished the ability of HSCs to regenerate the entire blood system when they were transplanted into irradiated mice, a procedure similar to bone marrow transplantation.
The researchers determined that 70 percent of HSCs from old mice were not undergoing autophagy, and these cells exhibited the dysfunctional features common among old HSCs. However, the 30 percent of old HSCs that did undergo autophagy looked and acted like HSCs from younger mice.
Passegué led the study while she was a professor of medicine with the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at UCSF. In January she became an Alumni Professor in the Department of Genetics & Development and the director of the Columbia Stem Cell Initiative at Columbia University Medical Center.
Scientists have identified many different tissue-specific stem cells, all of whose performance declines with age, Passegué said. Finding out how this occurs has been an active area of research, and a focus of her laboratory group in recent years.
In a large series of experiments and analyses, many conducted by the study’s first author, Theodore Ho, a UCSF graduate student, the scientists compared characteristics of HSCs from old mice with those of HSCs from younger mice that had been genetically programmed so that they could not undergo autophagy. They found that loss of autophagy in young mice was sufficient to drive many of the defects that arise naturally in the blood of old mice, including changes in the cellular appearance of HSCs and a disruption in the normal proportions of the various types of blood cells, characteristics of old age.
Previous research had shown that autophagy causes the formation of “sacs” within cells that can engulf and enzymatically digest molecules and even major cellular structures, including mitochondria, the cell’s biochemical power plants. But in the new study, the researchers found that genetically programmed loss of autophagy resulted in the accumulation of activated mitochondria with increased oxidative metabolism that triggered chemical modifications of DNA in HSCs.
These “epigenetic” DNA modifications altered the activities of genes in a way that changed the developmental fate of HSCs. They triggered disproportionate production of certain blood cells and reduced the ability of HSCs to regenerate the entire blood system when transplanted. This result was similar to what the researchers observed in the majority of old HSCs that failed to activate autophagy.
In contrast, the minority of old HSCs that still exhibited significant levels of autophagy were able to keep their mitochondria and metabolism in check, and could re-establish a healthy blood system following transplantation, similar to HSCs from young mice.
However, in a hopeful sign for potential future therapies to rejuvenate blood stem cells, the researchers succeeded in restoring autophagy to old HSCs by treating them with pharmacological agents in a lab dish.
“This discovery might provide an interesting therapeutic angle to use in re-activating autophagy in all of the old HSCs, to slow the aging of the blood system and to improve engraftment during bone marrow or HSC transplantation,” Passegué said. “It is our hope that the end point will be a way to really improve the fitness of stem cells and to use that capability to help the immune systems.”
Reference: Theodore T. Ho, Matthew R. Warr, Emmalee R. Adelman, Olivia M. Lansinger, Johanna Flach, Evgenia V. Verovskaya, Maria E. Figueroa & Emmanuelle Passegué; Autophagy maintains the metabolism and function of young and old stem cells, Nature (2017). DOI: 10.1038/nature21388
Our blood stem cells generate around a thousand billion new blood cells every day. But the blood stem cells’ capacity to produce blood declines as we age. This leads to lowered immunity and other age related problems. Now for the first time, a research team at Lund University in Sweden has succeeded in rejuvenating blood stem cells that had become less functional in aging mice. The study is published in Nature Communications.
When we are young, our blood stem cells produce an even and well-balanced number of red and white blood cells according to need. As we age, however, the capacity of the blood stem cells to produce the number of blood cells we need declines.
“This type of age-related change can have major consequences as it can lead to an imbalance in stem cell production. For example, a reduced production of immune cells or excessive production of other types of cells” explains David Bryder, who headed the study at Lund University.
A fundamental question was whether blood stem cells age differently within a single individual or whether all blood stem cells are equally affected by advancing age. In an initial stage, it was therefore important to genetically mark old blood stem cells, to enable the identification and tracking of those most affected by age. In the next step, these traceable cells were reprogrammed to another type of stem cell known as iPS cells, which can generate all cells in an individual and not only blood cells. When the cells are reprogrammed, their identity is ?re-set”; when these reprogrammed iPS cells formed new blood stem cells, the researchers observed that the re-set had entailed a rejuvenation of the cells.
“We found that there was no difference in blood-generating capacity when we compared the reprogrammed blood stem cells with healthy blood stem cells from a young mouse. This is, as far as we know, the first time someone has directly succeeded in proving that it is possible to recreate the function of young stem cells from a functionally old cell?, says Martin Wahlestedt, the first author of the study.
The research team’s studies have also thereby shown that many age-related changes in the blood system cannot be explained by mutations in the cells’ DNA. If the changes depended on permanent damage at the DNA level, the damage would still be present after the re-set. Instead, epigenetic changes appear to underlie the decline in function associated with advancing age.
“Our findings justify further research to improve the function of human blood stem cells” concludes David Bryder.
Reference: Martin Wahlestedt, Eva Erlandsson, Trine Kristiansen, Rong Lu, Cord Brakebusch, Irving L. Weissman, Joan Yuan, Javier Martin-Gonzalez, David Bryder. Clonal reversal of ageing-associated stem cell lineage bias via a pluripotent intermediate. Nature Communications, 2017; 8: 14533 DOI: 10.1038/ncomms14533
Adult stem cells collected directly from human fat have been used in stem cell treatments in many countries during the past 10 years. They are more stable than other cells such as fibroblasts from the skin and have the potential for use in anti-aging treatments, according to researchers from the Perelman School of Medicine at the University of Pennsylvania. They made the discovery after developing a new model to study chronological aging of these cells. They published their findings this month in the journal Stem Cells.
Chronological aging shows the natural life cycle of the cells as opposed to cells that have been unnaturally replicated multiple times or otherwise manipulated in a lab. In order to preserve the cells in their natural state, Penn researchers developed a system to collect and store them without manipulating them, making them available for this study. They found stem cells collected directly from human fat called adipose-derived stem cells (ASCs) can make more proteins than originally thought. This gives them the ability to replicate and maintain their stability, a finding that held true in cells collected from patients of all ages.
“Our study shows these cells are very robust, even when they are collected from older patients,” said Ivona Percec, MD, director of Basic Science Research in the Center for Human Appearance and the study’s lead author. “It also shows these cells can be potentially used safely in the future, because they require minimal manipulation and maintenance.”
Stem cells are currently used in a variety of anti-aging treatments and are commonly collected from a variety of tissues. But Percec’s team specifically found ASCs to be more stable than other cells, a finding that can potentially open the door to new therapies for the prevention and treatment of aging-related diseases.
“Unlike other adult human stem cells, the rate at which these ASCs multiply stays consistent with age,” Percec said. “That means these cells could be far more stable and helpful as we continue to study natural aging.”
ASCs are not currently approved for direct use by the Food and Drug Administration in the United States. Percec said the next step for her team is to study how chromatin is regulated in ASCs. Essentially, they want to know how tightly the DNA is wound around proteins inside these cells and how this affects aging. The more open the chromatin is, the more the traits affected by the genes inside will be expressed. Percec said she hopes to find out how ASCs can maintain an open profile with aging.
You can rebuild them, even if you are middle-aged or older.
“Our lab and others have shown repeatedly” that older muscles will grow and strengthen, says Marcas Bamman, a professor of integrative biology at the University of Alabama at Birmingham. In his studies, men and women in their 60s and 70s who began supervised weight training developed muscles that were as large and strong as those of your average 40-year-old. Jack LaLanne continued to work out and maintain large and strong muscles until he passed away at the age of 96 years old.
The process of bulking up works differently in older people than in the young. Skeletal muscles are composed of various types of fibers and “two things happen” to those fibers after we reach middle age, Dr. Bamman says. Some muscle fibers die, especially if we have not been exercising our muscles much. Sedentary adults can lose 30 to 40 percent of the total number of fibers in their muscles by the time they are 55, Dr. Bamman says.
Others of the fibers remain alive but shrink and atrophy as we age.
Young people who work out add new muscle fibers and also plump up their existing ones. Older people do not. We increase the size of our atrophied muscle fibers with exercise but, for a variety of physiological reasons, do not add to the number of fibers, Dr. Bamman says.
But in practical terms, who cares? Older muscles will become larger and stronger if you work them, Dr. Bamman says.
The key, he continues, is regular and progressive weight training. If you don’t belong to a gym, consider joining one, and then plan on tiring yourself. In order to initiate the biochemical processes that lead to larger, stronger fibers, Dr. Bamman says, you should push your muscles until they are exhausted.
In his studies, volunteers used weights calibrated so that the lifters could barely complete a set of eight to 12 repetitions before their arms or legs grew leaden and they had to rest. They repeated each set two or three times and visited the gym three times per week. If you are new to weight workouts, ask for an orientation at your gym or consult an athletic trainer who often works with older clients.
Reference: Bickel CS1, Cross JM, Bamman MM. Exercise dosing to retain resistance training adaptations in young and older adults. Med Sci Sports Exerc. 2011 Jul;43(7):1177-87.
Companies advertise “BPA-free” as a safer version of plastic products ranging from water bottles to sippy cups to toys. Many manufacturers stopped using Bisphenol A to strengthen plastic after animal studies linked it to early puberty and a rise in breast and prostate cancers.
Yet new UCLA research demonstrates that BPS (Bisphenol S), a common replacement for BPA, speeds up embryonic development and disrupts the reproductive system.
Reported in the Feb. 1 edition of the journal Endocrinology, the animal study is the first to examine the effects of BPA and BPS on key brain cells and genes that control the growth and function of organs involved in reproduction.
“Our study shows that making plastic products with BPA alternatives does not necessarily leave them safer,” explained senior author Nancy Wayne, a reproductive endocrinologist and a professor of physiology at the David Geffen School of Medicine at UCLA.
Using a zebrafish model, Wayne and her colleagues found that exposure to low levels of BPA and BPS—equivalent to the traces found in polluted river waters—altered the animals’ physiology at the embryonic stage in as quickly as 25 hours.
“Egg hatching time accelerated, leading to the fish equivalent of premature birth,” said Wayne, who is also UCLA’s associate vice chancellor for research. “The embryos developed much faster than normal in the presence of BPA or BPS.”
The UCLA team, which included first author Wenhui Qiu, a visiting graduate student from Shanghai University, chose to conduct the study in zebrafish because their transparent embryos make it possible to “watch” cell growth as it occurs.
Using fluorescent-green protein tags, the researchers tracked the fishes’ development of reproductive endocrine brain cells, which control puberty and fertility. In a second finding, the team discovered that the number of endocrine neurons increased up to 40 percent, suggesting that BPA overstimulates the reproductive system.
“Exposure to low levels of BPA had a significant impact on the embryos’ development of brain cells that control reproduction, and the genes that control reproduction later in life,” said Wayne. “We saw many of these same effects with BPS found in BPA-free products. BPS is not harmless.”
Wayne suspects that overstimulation of the neurons that regulate reproduction could lead to premature puberty and disruption of the reproductive system. Her lab plans to investigate this question in a future study.
After uncovering her first finding about BPA in 2008, Wayne immediately discarded all of the plastic food containers in her home and replaced them with glass. She and her family purchase food and drinks packaged in glass whenever possible.
“Our findings are frightening and important,” emphasized Wayne. “Consider it the aquatic version of the canary in the coal mine.”
Finally, the researchers were surprised to find that both BPA and BPS acted partly through an estrogen system and partly through a thyroid hormone system to exert their effects.
“Most people think of BPA as mimicking the effects of estrogen. But our work shows that it also mimics the actions of thyroid hormone,” said Wayne. “Because of thyroid hormone’s important influence on brain development during gestation, our work holds important implications for general embryonic and fetal development, including in humans.”
Researchers have proposed that endocrine-disrupting chemicals may be contributing to the U.S.’ rise in premature human births and early onset of puberty over the past couple of decades.
“Our data support that hypothesis,” said Wayne. “If BPA is impacting a wide variety of animal species, then it’s likely to be affecting human health. Our study is the latest to help show this with BPA and now with BPS.”
BPA can leach into food, particularly under heat, from the lining of cans and from consumer products such as water bottles, baby bottles, food-storage containers and plastic tableware. BPA can also be found in contact lenses, eyeglass lenses, compact discs, water-supply pipes, some cash register and ATM receipts, as well as in some dental sealants and composites. The U.S. and Europe were expected to manufacture more than 5 million tons of products containing the additives in 2015.