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.
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.
A recent study showed that “cells age faster with a sedentary lifestyle. Chronological age doesn’t always match biological age,” according to Aladdin Shadyab, PhD, lead author of the study with the Department of Family Medicine and Public Health at UC San Diego School of Medicine.
Telomeres are tiny caps found on the ends of DNA strands, like the plastic tips of shoelaces, that protect chromosomes from deterioration. As a cell ages, its telomeres naturally shorten and fray, but health and lifestyle factors, such as obesity and smoking, may accelerate that process.
The study, publishing online January 18 in the American Journal of Epidemiology, found elderly women with less than 40 minutes of moderate-to-vigorous physical activity per day and who remain sedentary for more than 10 hours per day have shorter telomeres.
The researchers also found that elderly women who sit for more than 10 hours a day with low physical activity have cells that are biologically older by eight years compared to women who are less sedentary.
Shadyab and his research team believe they are the first to objectively measure how the combination of sedentary time and exercise can impact the aging biomarker.
Nearly 1,500 women, ages 64 to 95, participated in the study. The women are part of the larger Women’s Health Initiative (WHI), a national, longitudinal study investigating the determinants of chronic diseases in postmenopausal women. The participants completed questionnaires and wore an accelerometer on their right hip for seven consecutive days during waking and sleeping hours to track their movements.
“We found that women who sat longer did not have shorter telomere length if they exercised for at least 30 minutes a day, the national recommended guideline,” said Shadyab. “Discussions about the benefits of exercise should start when we are young, and physical activity should continue to be part of our daily lives as we get older, even at 80 years old.”
Shadyab said future studies will examine how exercise relates to telomere length in younger populations and in men.
Reference: Aladdin H. Shadyab et al. Associations of Accelerometer-Measured and Self-Reported Sedentary Time With Leukocyte Telomere Length in Older Women. American Journal of Epidemiology, January 2017 DOI: 10.1093/aje/kww196
Abstract: Few studies have assessed the association of sedentary time with leukocyte telomere length (LTL). In a cross-sectional study conducted in 2012–2013, we examined associations of accelerometer-measured and self-reported sedentary time with LTL in a sample of 1,481 older white and African-American women from the Women’s Health Initiative and determined whether associations varied by level of moderate- to vigorous-intensity physical activity (MVPA). The association between sedentary time and LTL was evaluated using multiple linear regression models. Women were aged 79.2 (standard deviation, 6.7) years, on average. Self-reported sedentary time was not associated with LTL. In a model adjusting for demographic characteristics, lifestyle behaviors, and health-related factors, among women at or below the median level of accelerometer-measured MVPA, those in the highest quartile of accelerometer-measured sedentary time had significantly shorter LTL than those in the lowest quartile, with an average difference of 170 base pairs (95% confidence interval: 4, 340). Accelerometer-measured sedentary time was not associated with LTL in women above the median level of MVPA. Findings suggest that, on the basis of accelerometer measurements, higher sedentary time may be associated with shorter LTL among less physically active women.
Like spicy food? If so, you might live longer, say researchers at the Larner College of Medicine at the University of Vermont, who found that consumption of hot red chili peppers is associated with a 13 percent reduction in total mortality in a large prospective study.
For centuries, peppers and spices have been thought to improve health and longevity, but only one other scientific study conducted in China and published in 2015 has previously examined chili pepper consumption and its association with mortality. This new study corroborates the earlier study’s findings.
Using National Health and Nutritional Examination Survey (NHANES) III data collected from more than 16,000 Americans who were followed for up to 23 years, medical student Mustafa Chopan ’17 and Professor of Medicine Benjamin Littenberg, M.D., examined the baseline characteristics of the participants according to hot red chili pepper consumption. They found that consumers of hot red chili peppers tended to be “younger, male, white, Mexican-American, married, and to smoke cigarettes, drink alcohol, and consume more vegetables and meats,” in comparison to participants who did not consume red chili peppers. They examined data from a median follow-up of 18.9 years and observed the number of deaths and then analyzed specific causes of death.
“Although the mechanism by which peppers could delay mortality is far from certain, Transient Receptor Potential (TRP) channels, which are primary receptors for pungent agents such as capsaicin (the principal component in chili peppers), may in part be responsible for the observed relationship,” say the study authors.
There are some possible explanations for red chili peppers’ health benefits, state Chopan and Littenberg in the study. Among them are the fact that capsaicin is believed to play a role in cellular and molecular mechanisms that prevent obesity and modulate coronary blood flow, and also possesses antimicrobial properties that “may indirectly affect the host by altering the gut microbiota.”
“Because our study adds to the generalizability of previous findings, chili pepper or even spicy food consumption may become a dietary recommendation and/or fuel further research in the form of clinical trials,” says Chopan.
Reference: Mustafa Chopan, Benjamin Littenberg. The Association of Hot Red Chili Pepper Consumption and Mortality: A Large Population-Based Cohort Study. PLOS ONE, 2017; 12 (1): e0169876 DOI: 10.1371/journal.pone.0169876
Abstract: “The evidence base for the health effects of spice consumption is insufficient, with only one large population-based study and no reports from Europe or North America. Our objective was to analyze the association between consumption of hot red chili peppers and mortality, using a population-based prospective cohort from the National Health and Nutritional Examination Survey (NHANES) III, a representative sample of US noninstitutionalized adults, in which participants were surveyed from 1988 to 1994. The frequency of hot red chili pepper consumption was measured in 16,179 participants at least 18 years of age. Total and cause-specific mortality were the main outcome measures. During 273,877 person-years of follow-up (median 18.9 years), a total of 4,946 deaths were observed. Total mortality for participants who consumed hot red chili peppers was 21.6% compared to 33.6% for those who did not (absolute risk reduction of 12%; relative risk of 0.64). Adjusted for demographic, lifestyle, and clinical characteristics, the hazard ratio was 0.87 (P = 0.01; 95% Confidence Interval 0.77, 0.97). Consumption of hot red chili peppers was associated with a 13% reduction in the instantaneous hazard of death. Similar, but statistically nonsignificant trends were seen for deaths from vascular disease, but not from other causes. In this large population-based prospective study, the consumption of hot red chili pepper was associated with reduced mortality. Hot red chili peppers may be a beneficial component of the diet.”
Like everything else in the body, the white-matter fibers that allow communication between brain regions also decline with age. In a new study, researchers found a strong association between the structural integrity of these white-matter tracts and an older person’s level of daily activity not just the degree to which the person engaged in moderate or vigorous exercise, but also whether he or she was sedentary the rest of the time.
The study, reported in the journal PLOS ONE, tracked physical activity in 88 healthy but “low-fit” participants aged 60 to 78. The participants agreed to wear accelerometers during most of their waking hours over the course of a week, and also submitted to brain imaging.
“To our knowledge, this is the first study of its kind that uses an objective measure of physical activity along with multiple measures of brain structure,” said University of Illinois postdoctoral researcher Agnieszka Burzynska, who conducted the research with U. of I. Beckman Institute director Arthur Kramer and kinesiology and community health professor Edward McAuley.
Most studies ask subjects to describe how much physical activity they get, which is subjective and imprecise, Burzynska said. The accelerometer continuously tracks a person’s movement, “so it’s not what they say they do or what they think they do, but we have measured what they are actually doing,” she said.
The researchers assumed that participants’ activity levels over a week accurately reflected their overall engagement, or lack of engagement, in physical activity.
The study also relied on two types of brain imaging. The first, diffusion tensor imaging, offers insight into the structural integrity of a tissue by revealing how water is diffused in the tissue. The second method looks for age-related changes in white matter, called lesions. Roughly 95 percent of adults aged 65 and older have such lesions, Burzynska said. While they are a normal part of aging, their early onset or rapid accumulation may spell trouble, she said.
The team found that the brains of older adults who regularly engaged in moderate-to-vigorous exercise generally “showed less of the white-matter lesions,” Burzynska said.
The association between physical activity and white-matter structural integrity was region-specific, the researchers reported. Older adults who engaged more often in light physical activity had greater structural integrity in the white-matter tracts of the temporal lobes, which lie behind the ears and play a key role in memory, language, and the processing of visual and auditory information.
In contrast, those who spent more time sitting had lower structural integrity in the white-matter tracts connecting the hippocampus, “a structure crucial for learning and memory,” Burzynska said.
“This relationship between the integrity of tracts connecting the hippocampus and sedentariness is significant even when we control for age, gender and aerobic fitness,” she said. “It suggests that the physiological effect of sitting too much, even if you still exercise at the end of the day for half an hour, will have a detrimental effect on your brain.”
The findings suggest that engaging in physical activity and avoiding a sedentary lifestyle are both important for brain health in older age, Burzynska said.
“We hope that this will encourage people to take better care of their brains by being more active,” she said.
Reference: Agnieszka Zofia Burzynska ,Laura Chaddock-Heyman,Michelle W. Voss,Chelsea N. Wong,Neha P. Gothe,Erin A. Olson,Anya Knecht,Andrew Lewis,Jim M. Monti,Gillian E. Cooke,Thomas R. Wojcicki,Jason Fanning,Hyondo David Chung,Elisabeth Awick,Edward McAuley,Arthur F. Kramer. Physical Activity and Cardiorespiratory Fitness Are Beneficial for White Matter in Low-Fit Older Adults. PLoS ONE 9(9): e107413. doi:10.1371/journal.pone.0107413
The stem cells in our teeth can be energized to fill in chips, cracks, and cavities, researchers say, and the findings could one day possibly make dental cement obsolete.
The work has been conducted just in mice so far, but the research, published Monday in the journal Scientific Reports, highlights a way to motivate stem cells to repair tooth defects at a scale they normally can’t, with a drug that already has some safety testing behind it. It also demonstrates the potential of a type of stem cell therapy in which the cells are stimulated in place, rather than taken out, manipulated, and put back in.
“We’re mobilizing stem cells in the body and it works,” said Paul Sharpe, a researcher at King’s College London and an author of the new paper. “If it works for teeth, chances are it could work for other organs.”
Experts not involved with the work noted that while it is in early stages, the simplicity of the approach should ease its path into the next phases of research that show whether it might produce the same results in people.
“These important steps close down the translational gap and bring this discovery a step closer to future clinical applications,” Dr. Vanessa Chrepa, a researcher at the University of Washington, wrote in an email. “This work will hopefully set the stage for clinical studies in the near future.”
When teeth lose some of their dentin — the bony tissue beneath the enamel that makes up the bulk of the tooth — the stem cells tucked deep inside mount a recovery effort and manufacture new dentin (which is also spelled dentine). The problem, Sharpe said, is that the natural repair mechanism can only regrow small amounts of dentin and can’t make up all that is lost when a tooth suffers a serious injury, contracts a major infection, or takes on the sharp end of a dentist’s drill.
Because of the limits of the teeth’s ability to repair themselves, dentists have to fill or seal teeth to prevent further infection and degradation. But dental cement also prevents the tooth from ever returning to its natural, pearly white self.
Sharpe and his team have been trying to understand how the natural repair mechanism works in hopes of converting that understanding into a way to super-power it. As part of their research, they discovered that a group of molecules called glycogen synthase kinase inhibitors (or GSK-3 inhibitors) boosts the stem cells’ ability to stimulate production of dentin beyond what normally occurs.
For the new study, the researchers drilled tiny holes into mice’s molars to expose the tooth’s pulp, where the stem cells live. They then inserted collagen sponges that had been soaked in one of three types of GSK-3 inhibitors and covered the tooth.
After six weeks, the researchers removed the teeth and found that the sponges had dissolved and the lost dentin had mostly been regenerated.
“They’ve harnessed the signaling pathway that promotes natural repair,” said Megan Pugach, a researcher at the Forsyth Institute in Cambridge, Mass., and at the Harvard School of Dental Medicine, who was not involved with the research.
Sharpe and his team are now conducting similar studies in rats to make sure the approach can generate enough dentin to fill in larger holes in larger teeth before trying to study the method in people. But two aspects of the approach could help ease its path into clinical trials.
A new study shows that older people who followed a Mediterranean diet retained more brain volume over a three-year period than those who did not follow the diet as closely. The study is published in the January 4, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. But contrary to earlier studies, eating more fish and less meat was not related to changes in the brain.
The Mediterranean diet includes large amounts of fruits, vegetables, olive oil, beans, whole grains, moderate amounts of fish, dairy and wine, and limited red meat and poultry.
“As we age, the brain shrinks and we lose brain cells which can affect learning and memory,” said study author Michelle Luciano, PhD, of the University of Edinburgh in Scotland. “This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health.”
Researchers gathered information on the eating habits of 967 Scottish people around age 70 who did not have dementia. Of those people, 562 had an MRI brain scan around age 73 to measure overall brain volume, gray matter volume and thickness of the cortex, which is the outer layer of the brain. From that group, 401 people then returned for a second MRI at age 76. These measurements were compared to how closely participants followed the Mediterranean diet.
The participants varied in how closely their dietary habits followed the Mediterranean diet principles. People who didn’t follow as closely to the Mediterranean diet were more likely to have a higher loss of total brain volume over the three years than people who followed the diet more closely. The difference in diet explained 0.5 percent of the variation in total brain volume, an effect that was half the size of that due to normal aging.
The results were the same when researchers adjusted for other factors that could affect brain volume, such as age, education and having diabetes or high blood pressure.
There was no relationship between grey matter volume or cortical thickness and the Mediterranean diet.
The researchers also found that fish and meat consumption were not related to brain changes, which is contrary to earlier studies.
“It’s possible that other components of the Mediterranean diet are responsible for this relationship, or that it’s due to all of the components in combination,” Luciano said.
Luciano noted that earlier studies looked at brain measurements at one point in time, whereas the current study followed people over time.
“In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain,” said Luciano. “Still, larger studies are needed to confirm these results.”
Reference: 1.Michelle Luciano, Janie Corley, Simon R. Cox, Maria C. Valdés Hernández, Leone C.A. Craig, David Alexander Dickie, Sherif Karama, Geraldine M. McNeill, Mark E. Bastin, Joanna M. Wardlaw, Ian J. Deary. Mediterranean-type diet and brain structural change from 73 to 76 years in a Scottish cohort. Neurology, 2017; 10.1212/WNL.0000000000003559 DOI: 10.1212/WNL.0000000000003559