Have you ever wondered why aging occurs and how one might slow its progression? Aging expert Dr. Villeponteau describes dietary, exercise, and supplement routines that can add decades to your healthspan. Decoding Longevity condenses a wealth of practical information for those interesting in extending their health and longevity. Decoding Longevity also discusses the exponential increases in technology that will likely lead to greatly expanded longevity while maintaining health and indpendence in the next 20 to 40 years.

Decoding Longevity offers a full spectrum biological and genetic analysis of the aging process in layman’s language. Starting with an analysis of why life expectancy increased 57% in the 20th Century, it then focuses on recommended lifestyle choices that can significantly extend your healthspan and youthful fitness. The third part looks in some detail at the last 20 years of aging research, while the final section explores future developments that will provide powerful tools for extending healthspan and longevity in the next 20 to 40 years.

The Author: Dr. Bryant Villeponteau has 25 years of scientific leadership in aging research and some 60 scientific journal and patent publications. He has a Ph.D. in Biology from UCLA and was Assistant Professor of Biological Chemistry at the University of Michigan Medical School in the Institute of Gerontology. Dr. Villeponteau later led the research group at Geron Corporation, where he was the lead inventor in cloning human telomerase, thereby winning the Distinguished Inventor Award for the 2nd best US patent of 1997. Since 2008, Dr. Villeponteau has used genetics and machine learning technologies to develop antiaging supplements and drugs. He also cofounded Centagen, a Colorado stem cell company.

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That chicken wing you’re eating could be as deadly as a cigarette. In a new study that tracked a large sample of adults for nearly two decades, researchers have found that eating a diet rich in animal proteins during middle age makes you four times more likely to die of cancer than someone with a low-protein diet — a mortality risk factor comparable to smoking.

“There’s a misconception that because we all eat, understanding nutrition is simple. But the question is not whether a certain diet allows you to do well for three days, but can it help you survive to be 100?” said corresponding author Valter Longo, the Edna M. Jones Professor of Biogerontology at the USC Davis School of Gerontology and director of the USC Longevity Institute.

Not only is excessive protein consumption linked to a dramatic rise in cancer mortality, but middle-aged people who eat lots of proteins from animal sources — including meat, milk and cheese — are also more susceptible to early death in general, reveals the study to be published March 4 in Cell Metabolism. Protein-lovers were 74 percent more likely to die of any cause within the study period than their more low-protein counterparts. They were also several times more likely to die of diabetes.

But how much protein we should eat has long been a controversial topic — muddled by the popularity of protein-heavy diets such as Paleo and Atkins. Before this study, researchers had never shown a definitive correlation between high protein consumption and mortality risk.

Rather than look at adulthood as one monolithic phase of life, as other researchers have done, the latest study considers how biology changes as we age, and how decisions in middle life may play out across the human lifespan.

In other words, what’s good for you at one age may be damaging at another. Protein controls the growth hormone IGF-I, which helps our bodies grow but has been linked to cancer susceptibility. Levels of IGF-I drop off dramatically after age 65, leading to potential frailty and muscle loss. The study shows that while high protein intake during middle age is very harmful, it is protective for older adults: those over 65 who ate a moderate- or high-protein diet were less susceptible to disease.

? High protein intake especially if from animal sources is linked to increased cancer, diabetes, and overall mortality

? Higher protein consumption may be protective for older adults

? Plant-derived proteins are associated with lower mortality than animal-derived proteins

? High IGF-1 levels increased the relationship between mortality and high protein

The latest paper draws from Longo’s past research on IGF-I, including on an Ecuadorian cohort that seemed to have little cancer or diabetes susceptibility because of a genetic mutation that lowered levels of IGF-I; the members of the cohort were all less than five-feet tall.

“The research shows that a low-protein diet in middle age is useful for preventing cancer and overall mortality, through a process that involves regulating IGF-I and possibly insulin levels,” said co-author Eileen Crimmins, the AARP Chair in Gerontology at USC. “However, we also propose that at older ages, it may be important to avoid a low-protein diet to allow the maintenance of healthy weight and protection from frailty.”

Crucially, the researchers found that plant-based proteins, such as those from beans, did not seem to have the same mortality effects as animal proteins. Rates of cancer and death also did not seem to be affected by controlling for carbohydrate or fat consumption, suggesting that animal protein is the main culprit.

“The majority of Americans are eating about twice as much proteins as they should, and it seems that the best change would be to lower the daily intake of all proteins but especially animal-derived proteins,” Longo said. “But don’t get extreme in cutting out protein; you can go from protected to malnourished very quickly.”

Longo’s findings support recommendations from several leading health agencies to consume about 0.8 grams of protein per kilogram of body weight every day in middle age. For example, a 130-pound person should eat about 45-50 grams of protein a day, with preference for those derived from plants such as legumes, Longo explains.

The researchers define a “high-protein” diet as deriving at least 20 percent of calories from protein, including both plant-based and animal-based protein. A “moderate” protein diet includes 10-19 percent of calories from protein, and a “low-protein” diet includes less than 10 percent protein.

Even moderate amounts of protein had detrimental effects during middle age, the researchers found. Across all 6,318 adults over the age of 50 in the study, average protein intake was about 16 percent of total daily calories with about two-thirds from animal protein — corresponding to data about national protein consumption. The study sample was representative across ethnicity, education and health background.

People who ate a moderate amount of protein were still three times more likely to die of cancer than those who ate a low-protein diet in middle age, the study shows. Overall, even the small change of decreasing protein intake from moderate levels to low levels reduced likelihood of early death by 21 percent.

For a randomly selected smaller portion of the sample – 2,253 people – levels of the growth hormone IGF-I were recorded directly. The results show that for every 10 ng/ml increase in IGF-I, those on a high-protein diet were 9 percent more likely to die from cancer than those on a low-protein diet, in line with past research associating IGF-I levels to cancer risk.

The researchers also extended their findings about high-protein diets and mortality risk, looking at causality in mice and cellular models. In a study of tumor rates and progression among mice, the researchers show lower cancer incidence and 45 percent smaller average tumor size among mice on a low-protein diet than those on a high-protein diet by the end of the two-month experiment.

“Almost everyone is going to have a cancer cell or pre-cancer cell in them at some point. The question is: Does it progress?” Longo said. “Turns out one of the major factors in determining if it does is is protein intake.” The study suggests that low protein intake during middle age followed by moderate to high protein consumption in old adults may optimize healthspan and longevity.

Reference: https://www.cell.com/cell-metabolism/retrieve/pii/S155041311400062X

The power of regenerative medicine appears to have turned science fiction into scientific reality — by allowing scientists to transform skin cells into cells that closely resemble beating heart cells. However, the methods required are complex, and the transformation is often incomplete. But now, scientists at the Gladstone Institutes have devised a new method that allows for the more efficient — and, importantly, more complete — reprogramming of skin cells into cells that are virtually indistinguishable from heart muscle cells. These findings, based on animal models and described in the latest issue of Cell Reports, offer new-found optimism in the hunt for a way to regenerate muscle lost in a heart attack.

Heart disease is the world’s leading cause of death, but recent advances in science and medicine have improved the chances of surviving a heart attack. In the United States alone, nearly 1 million people have survived an attack, but are living with heart failure — a chronic condition in which the heart, having lost muscle during the attack, does not beat at full capacity. So, scientists have begun to look toward cellular reprogramming as a way to regenerate this damaged heart muscle.

The reprogramming of skin cells into heart cells, an approach pioneered by Gladstone Investigator, Deepak Srivastava, MD, has required the insertion of several genetic factors to spur the reprogramming process. However, scientists have recognized potential problems with scaling this gene-based method into successful therapies. So some experts, including Gladstone Senior Investigator Sheng Ding, PhD, have taken a somewhat different approach.

“Scientists have previously shown that the insertion of between four and seven genetic factors can result in a skin cell being directly reprogrammed into a beating heart cell,” explained Dr. Ding, the paper’s senior author and a professor of pharmaceutical chemistry at UCSF, with which Gladstone is affiliated. “But in my lab, we set out to see if we could perform a similar transformation by eliminating — or at least reducing — the reliance on this type of genetic manipulation.”

To that effect, the research team used skin cells extracted from adult mice to screen for chemical compounds, so-called ‘small molecules,’ that could replace the genetic factors. Dr. Ding and his research team have previously harnessed the power of small molecules to reprogram skin cells into neurons and, more recently, insulin-producing pancreas cells. They reasoned that a similar technique could be used to do the same with heart cells.

“After testing various combinations of small molecules, we narrowed down the list to a four-molecule ‘cocktail,’ which we called SPCF, that could guide the skin cells into becoming more like heart cells,” said Gladstone Postdoctoral Scholar Haixia Wang, PhD, the paper’s lead author. “These newly reprogramed cells exhibited some of the twitching and contracting normally seen in mature heart cells, but the transformation wasn’t entirely complete.”

So, Drs. Ding and Wang decided to add one genetic factor, called Oct4, to the small molecule cocktail. And by doing so, the research team was able to generate a completely reprogrammed beating heart cell.

“Once we added Oct4 to the mix, we observed clusters of contracting cells after a period of just 20 days,” explained Dr. Ding. “Remarkably, additional analysis revealed that these cells showed the same patterns of gene activation and electric signaling patterns normally seen in the ventricles of the heart.”

Dr. Ding and his team believe that these results may point to a more desirable method for reprogramming, as ventricular heart cells are the type of cells typically lost during a heart attack. These findings give the team newfound optimism that the research is well on its way towards an entirely pharmaceutical-based method to regrow heart muscle.

“The fact that the combination of Oct4 and small molecules appears to generate beating heart cells in an accelerated fashion is encouraging,” said Joseph Wu, MD, PhD, Director of the Stanford Cardiovascular Institute, who was not involved in this study. “Future advances by Dr. Ding and others will likely focus on improving the efficiency of conversion as well as duplicating the data in adult human cells.”

Reference:

Haixia Wang, Nan Cao, C. Ian Spencer, Baoming Nie, Tianhua Ma, Tao Xu, Yu Zhang, Xiaojing Wang, Deepak Srivastava, Sheng Ding. Small Molecules Enable Cardiac Reprogramming of Mouse Fibroblasts with a Single Factor, Oct4. Cell Reports, February 2014 DOI: 10.1016/j.celrep.2014.01.038

One of the major causes of hearing loss is damage to the sound-sensing hair cells in the inner ear. For years, scientists have thought that these cells are not replaced once they’re lost, but new research appearing online February 20 in the journal Stem Cell Reports reveals that supporting cells in the ear can turn into hair cells in newborn mice. If the findings can be applied to older animals, they may lead to ways to help stimulate cell replacement in adults and to the design of new treatment strategies for people suffering from deafness due to hair cell loss.

Whereas previous research indicated that hair cells are not replaced, this latest study found that replacement does indeed occur, but at very low levels. “The finding that newborn hair cells regenerate spontaneously is novel,” says senior author Dr. Albert Edge of Harvard Medical School and Massachusetts Eye and Ear Infirmary.

The team’s previous research revealed that inhibition of the Notch signaling pathway increases hair cell differentiation and can help restore hearing to mice with noise-induced deafness. In their latest work, the investigators found that blocking the Notch pathway increases the formation of new hair cells not from remaining hair cells but from certain nearby supporting cells that express a protein called Lgr5.

“By using an inhibitor of Notch signaling, we could push even more cells to differentiate into hair cells,” says Dr. Edge. “It was surprising that the Lgr5-expressing cells were the only supporting cells that differentiated under these conditions.”

Combining this new knowledge about Lgr5-expressing cells with the previous finding that Notch inhibition can regenerate hair cells will allow the scientists to design new hair cell regeneration strategies to treat hearing loss and deafness.

Reference:

Naomi F. Bramhall, Fuxin Shi, Katrin Arnold, Konrad Hochedlinger, Albert S.B. Edge. Lgr5-Positive Supporting Cells Generate New Hair Cells in the Postnatal Cochlea. Stem Cell Reports, February 2014 DOI: 10.1016/j.stemcr.2014.01.008

A cure for type 1 diabetes has alluded researchers. Not because scientists do not know what must be done — but because the tools have not been available to do it. Now scientists at the Gladstone Institutes, harnessing the power of regenerative medicine, have developed a technique in animal models that could replenish the very cells destroyed by the disease. The team’s findings, published online in the journal Cell Stem Cell, are an important step towards freeing an entire generation of patients from the life-long injections that characterize this devastating disease.

Type 1 diabetes, which usually manifests during childhood, is caused by the destruction of ?-cells, a type of cell that normally resides in the pancreas and produces a hormone called insulin. Without insulin, the body’s organs have difficulty absorbing sugars, such as glucose, from the blood. Once a death sentence, the disease can now be managed with regular glucose monitoring and insulin injections. A more permanent solution, however, would be to replace the missing ?-cells. But these cells are hard to come by, so researchers have looked towards stem cell technology as a way to make them.

“The power of regenerative medicine is that it can potentially provide an unlimited source of functional, insulin-producing ?-cells that can then be transplanted into the patient,” said Dr. Ding, who is also a professor at the University of California, San Francisco (UCSF), with which Gladstone is affiliated. “But previous attempts to produce large quantities of healthy ?-cells — and to develop a workable delivery system — have not been entirely successful. So we took a somewhat different approach.”

One of the major challenges to generating large quantities of ?-cells is that these cells have limited regenerative ability; once they mature it’s difficult to make more. So the team decided to go one step backwards in the life cycle of the cell.

The team first collected skin cells, called fibroblasts, from laboratory mice. Then, by treating the fibroblasts with a unique ‘cocktail’ of molecules and reprogramming factors, they transformed the cells into endoderm-like cells. Endoderm cells are a type of cell found in the early embryo, and which eventually mature into the body’s major organs — including the pancreas.

“Using another chemical cocktail, we then transformed these endoderm-like cells into cells that mimicked early pancreas-like cells, which we called PPLC’s,” said Gladstone Postdoctoral Scholar Ke Li, PhD, the paper’s lead author. “Our initial goal was to see whether we could coax these PPLC’s to mature into cells that, like ?-cells, respond to the correct chemical signals and — most importantly — secrete insulin. And our initial experiments, performed in a petri dish, revealed that they did.”

The research team then wanted to see whether the same would occur in live animal models. So they transplanted PPLC’s into mice modified to have hyperglycemia (high glucose levels), a key indicator of diabetes.

“Importantly, just one week post-transplant, the animals’ glucose levels started to decrease gradually approaching normal levels,” continued Dr. Li. “And when we removed the transplanted cells, we saw an immediate glucose spike, revealing a direct link between the transplantation of the PPLC’s and reduced hyperglycemia.”

But it was when the team tested the mice eight weeks post-transplant that they saw more dramatic changes: the PPLC’s had given rise to fully functional, insulin-secreting ?-cells.

“These results not only highlight the power of small molecules in cellular reprogramming, they are proof-of-principle that could one day be used as a personalized therapeutic approach in patients,” explained Dr. Ding.

“I am particularly excited about the prospect of translating these findings to the human system,” said Matthias Hebrok, PhD, one of the study’s authors and director of the UCSF Diabetes Center. “Most immediately, this technology in human cells could significantly advance our understanding of how inherent defects in ?-cells result in diabetes, bringing us notably closer to a much-needed cure.”

If you’re eating better and exercising regularly, but still aren’t seeing improvements in your health, there might be a reason: pollution. According to a new research report published in the September issue of The FASEB Journal, what you are eating and doing may not be the problem, but what’s in what you are eating could be the culprit. The study described below gives one more very good reason for eating organically raised foods.

“This study adds evidences for rethinking the way of addressing risk assessment especially when considering that the human population is widely exposed to low levels of thousands of chemicals, and that the health impact of realistic mixtures of pollutants will have to be tested as well,” said Brigitte Le Magueresse-Battistoni, a researcher involved in the work from the French National Institute of Health and Medical Research (INSERM). “Indeed, one pollutant could have a different effect when in mixture with other pollutants. Thus, our study may have strong implications in terms of recommendations for food security. Our data also bring new light to the understanding of the impact of environmental food contaminants in the development of metabolic diseases.”

To make this discovery, scientists used two groups of obese mice. Both were fed a high-fat, high-sucrose enriched diet, with one group receiving a cocktail of pollutants added to its diet at a very low dosage. These pollutants were given to the mice throughout — from pre-conception to adulthood. Although the researchers did not observe toxicity or excess of weight gain in the group having received the cocktail of pollutants, they did see a deterioration of glucose tolerance in females, suggesting a defect in insulin signaling. Study results suggest that the mixture of pollutants reduced estrogen activity in the liver through enhancing an enzyme in charge of estrogen elimination. In contrast to females, glucose tolerance was not impacted in males exposed to the cocktail of pollutants. However, males did show some changes in liver related to cholesterol synthesis and transport. This study fuels the concept that pollutants may contribute to the current prevalence of chronic diseases including metabolic diseases and diabetes.

“This report that confirms something we’ve known for a long time: pollution is bad for us,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “But, what’s equally important, it shows that evaluating food contaminants and pollutants on an individual basis may be too simplistic. We can see that when “safe” levels of contaminants and pollutants act together, they have significant impact on public health.”

Data from a new study of British adults suggest that adherence to the Western diet (fried and sweet food, processed and red meat, refined grains, and high-fat dairy products) reduces a person’s likelihood of achieving older ages in good health and with higher functionality. Study results appear in the May issue of The American Journal of Medicine.

“The impact of diet on specific age related diseases has been studied extensively, but few investigations have adopted a more holistic approach to determine the association of diet with overall health at older ages,” says lead investigator Tasnime Akbaraly, PhD, Inserm, Montpellier, France. “We examined whether diet, assessed in midlife, using dietary patterns and adherence to the Alternative Healthy Eating Index (AHEI), is associated with aging phenotypes, identified after a mean 16-year follow-up.”

The AHEI is a validated index of diet quality, originally designed to provide dietary guidelines with the specific intention to combat major chronic conditions such as cardiovascular diseases and diabetes.

Investigators analyzed findings from the British Whitehall II cohort study, which suggest that following the AHEI can double the odds of reversing metabolic syndrome, a condition known to be a strong predictor of heart disease and mortality. The research team sought to identify dietary factors that can not only prevent premature death, but also promote ideal aging.

Researchers followed 3,775 men and 1,575 women from 1985-2009 with a mean age of 51 years from the Whitehall II study. Using a combination of hospital data, results of screenings conducted every five years, and registry data, investigators identified mortality and chronic diseases among participants. The outcomes at follow up stage, classified into 5 categories were:

1. Ideal aging, defined as free of chronic conditions and high performance in physical, mental, and cognitive functioning tests — 4.0%

2. Nonfatal cardiovascular event — 12.7%

3. Cardiovascular death — 2.8%

4. Noncardiovascular death — 7.3%

5. Normal aging — 73.2%

The study determined that participants with low adherence to the AHEI increased their risk of cardiovascular and noncardiovascular death. Those who followed the Western diet consisting of fried and sweet food, processed food and red meat, refined grains, and high-fat dairy products lowered their chances for ideal aging.

“We showed that following specific dietary recommendations such as the one provided by the AHEI may be useful in reducing the risk of unhealthy aging, while avoidance of the ‘Western-type foods’ might actually improve the possibility of achieving older ages free of chronic diseases and remaining highly functional,” notes Dr. Akbaraly. “A better understanding of the distinction between specific health behaviors that offer protection against diseases and those that move individuals towards ideal aging may facilitate improvements in public health prevention packages.”

Exercise, even in small doses, changes the expression of our innate DNA. New research from Lund University in Sweden has described for the first time what happens on an epigenetic level in fat cells when we undertake physical activity.

“Our study shows the positive effects of exercise, because the epigenetic pattern of genes that affect fat storage in the body changes,” says Charlotte Ling, Associate Professor at Lund University Diabetes Centre.

The cells of the body contain DNA, which contains genes. We inherit our genes and they cannot be changed. The genes, however, have ‘methyl groups’ attached which affect what is known as ‘gene expression’ — whether the genes are activated or deactivated. The methyl groups can be influenced in various ways, through exercise, diet and lifestyle, in a process known as ‘DNA methylation’. This is epigenetics, a relatively new research field that in recent years has attracted more and more attention.

In the study, the researchers investigated what happened to the methyl groups in the fat cells of 23 slightly overweight, healthy men aged around 35 who had not previously engaged in any physical activity, when they regularly attended spinning and aerobics classes over a six-month period.

“They were supposed to attend three sessions a week, but they went on average 1.8 times,” says Tina R?nn, Associate Researcher at Lund University.

Using technology that analyses 480 000 positions throughout the genome, they could see that epigenetic changes had taken place in 7,000 genes (an individual has 20-25 000 genes). They then went on to look specifically at the methylation in genes linked to type 2 diabetes and obesity.

“We found changes in those genes too, which suggests that altered DNA methylation as a result of physical activity could be one of the mechanisms of how these genes affect the risk of disease,” says Tina R?nn, adding that this has never before been studied in fat cells and that they now have a map of the DNA methylome in fat.

In the laboratory, the researchers were able to confirm the findings in vitro (studying cell cultures in test tubes) by deactivating certain genes and thus reducing their expression. This resulted in changes in fat storage in fat cells.

The world?s oldest living person reached another milestone Sunday when she celebrated her Sweet 116. When asked for her secret to living such a long life she said ?I mind my own business and I don?t eat junk food.?

Besse Cooper has become only the 8th person in the world and the 4th American verified to have turned that age, according to Guinness World Records.

Cooper, whose maiden name was Brown, was born on Aug. 26, 1896, in northern Tennessee the same year as comedian George Burns and writer F. Scott Fitzgerald.

In 1917 during World War I, she moved to Georgia to work as a schoolteacher. She later married Luther Cooper, and they raised four children together. He died in 1963 at age 68, according to The Walton Tribune.

The newspaper reported last year that the supercentenarian is also a grandmother of 12, great-grandmother of 15 and great-great-grandmother of one.

Walton County officials held a ribbon cutting Friday to name a bridge in honor of Cooper, who resides in a nursing home and was unable to attend the ceremony.

?The older she has gotten the more wittier she has gotten,? Cooper?s third child, Sidney, reportedly said, adding that she had a message for the bridge-naming ceremony: ?I?m glad I gave them a reason to name it.?

Although Guinness World Records first called her the world?s oldest living person in January 2011, she lost the title when it was discovered Maria Gomes Valentin, of Brazil, was born 48 days earlier.

Valentin died on June 21, 2011, just shy of her 115th birthday, and Cooper was again crowned the world?s super senior.

Cooper could still surpass another Tennessean, Elizabeth Bolden, who was 116 years and 118 days when she died in 2006.

The person with the longest human lifespan ever recorded was Jeanne Calment, of France, who was born in 1875 and died in 1997 at the age of 122.