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.
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.
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.
In a study of more than 17,000 Canadians published in 2009 by Dr Peter Katzmarzyk and colleagues at the Pennington Biomedical Research Center they found links between time spent sitting and mortality. “Individuals who sat the most were roughly 50% more likely to die during the follow-up period than individuals who sat the least, even after controlling for age, smoking, and physical activity levels.”
Now new research suggests that taking short but frequent walks can counteract the harm caused by sitting for long periods of time.
The researchers found that even just a five-minute stroll can help.
“American adults sit for approximately eight hours a day,” study author Saurabh Thosar, now a postdoctoral researcher at Oregon Health & Science University, said in an Indiana University news release. “The impairment in endothelial function is significant after just one hour of sitting. It is interesting to see that light physical activity can help in preventing this impairment.”
According to background information from Indiana University, sitting for a prolonged period of time can cause blood to pool in the legs. This happens because muscles are not contracting and pumping blood to the heart as effectively. As a result, the ability of blood vessels to expand from increased blood flow can become impaired. Being sedentary is also linked to high cholesterol and a larger waistline, which increase the risk for heart and metabolic disease.
“There is plenty of epidemiological evidence linking sitting time to various chronic diseases and linking breaking sitting time to beneficial cardiovascular effects, but there is very little experimental evidence,” said Thosar, who was a doctoral candidate at IU’s School of Public Health-Bloomington when the study was conducted. “We have shown that prolonged sitting impairs endothelial function, which is an early marker of cardiovascular disease, and that breaking sitting time prevents the decline in that function.”
The researchers examined the effects of three hours of sitting on 11 healthy men who were not obese. The men, who ranged in age from 20 to 35 years old, participated in two trials.
First, the men sat for three hours without moving their legs. When the study began and once every hour afterwards, the function of their femoral artery was measured with a blood pressure cuff and ultrasound technology.
During the second trial, the men sat for three hours but also walked on a treadmill for five minutes after 30 minutes, 1.5 hours and 2.5 hours. The men walked at a slow pace of 2 miles per hour. The function of their femoral artery was again measured with a blood pressure cuff and ultrasound technology.
Overall, the researchers found, the ability of the arteries in the legs to expand was reduced by as much as 50 percent after just one hour of sitting. The men who walked for five minutes for each hour they spent sitting, however, had no reduction in the function of their arteries during the three-hour period.
The researchers concluded that the increased muscle activity and blood flow from the small amount of exercise offset the negative impacts of sitting.
By Mary Elizabeth Dallas in HealthDay News. The research was published Sept. 8 in the journal Medicine & Science in Sports & Exercise.
UCLA biologists have identified a gene that can slow the aging process throughout the entire body when activated remotely in key organ systems.
Working with fruit flies, the life scientists activated a gene called AMPK that is a key energy sensor in cells; it gets activated when cellular energy levels are low.
Increasing the amount of AMPK in fruit flies’ intestines increased their lifespans by about 30 percent to roughly eight weeks from the typical six weeks and the flies stayed healthier longer as well.
Stem Cell 100TM and Stem Cell 100+TM both contain several compounds that activate AMPK. They also act on a number of additional anti-aging pathways which allowed us to double fruit fly lifespan as well as greatly increase their healthspan (the length of time they were healthy and active).
The research, published in the open-source journal Cell Reports, could have important implications for delaying aging and disease in humans, said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research.
“We have shown that when we activate the gene in the intestine or the nervous system, we see the aging process is slowed beyond the organ system in which the gene is activated,” Walker said.
Walker said that the findings are important because extending the healthy life of humans would presumably require protecting many of the body’s organ systems from the ravages of aging, but delivering anti-aging treatments to the brain or other key organs could prove technically difficult. The study suggests that activating AMPK in a more accessible organ such as the intestine, for example, could ultimately slow the aging process throughout the entire body, including the brain.
Humans have AMPK, but it is usually not activated at a high level, Walker said.
“The ultimate aim of our research is to promote healthy aging in people.”
The fruit fly, Drosophila melanogaster, is a good model for studying aging in humans because scientists have identified all of the fruit fly’s genes and know how to switch individual genes on and off. The biologists studied approximately 100,000 of them over the course of the study.
Lead author Matthew Ulgherait, who conducted the research in Walker’s laboratory as a doctoral student, focused on a cellular process called autophagy, which enables cells to degrade and discard old, damaged cellular components. By getting rid of that “cellular garbage” before it damages cells, autophagy protects against aging, and AMPK has been shown previously to activate this process.
Ulgherait studied whether activating AMPK in the flies led to autophagy occurring at a greater rate than usual.
“A really interesting finding was when Matt activated AMPK in the nervous system, he saw evidence of increased levels of autophagy in not only the brain, but also in the intestine,” said Walker, a faculty member in the UCLA College. “And vice versa: Activating AMPK in the intestine produced increased levels of autophagy in the brain and perhaps elsewhere, too.”
“Matt moved beyond correlation and established causality,” he said. “He showed that the activation of autophagy was both necessary to see the anti-aging effects and sufficient; that he could bypass AMPK and directly target autophagy.”
In research published last year, Walker and his colleagues identified another gene, called parkin, which delayed the onset of aging and extended the healthy life span of fruit flies.
By 2050, the number of people over the age of 80 will triple globally, which could come at great cost to individuals and economies. In a commentary published July 24 in Nature, three experts call for moving forward with preclinical and clinical strategies for people that have been shown to delay aging in animals. In addition to promoting a healthy diet and regular exercise, these strategies include slowing the metabolic and molecular causes of human aging, such as the incremental accumulation of cellular damage that occurs over time.
Unfortunately, medicine focuses almost entirely on fighting chronic diseases in a piecemeal fashion as symptoms develop. Instead, more efforts should be directed to promoting interventions that have the potential to prevent multiple chronic diseases and extend healthy lifespans.
The researchers, at Washington University School of Medicine in St. Louis, Brescia University in Italy, the Buck Institute for Aging and Research and the Longevity Institute at the University of Southern California, write that unfortunately, economic incentives in biomedical research and health care reward treating disease more than promoting good health.
The problems of old age come as a package. More than 70% of people over 65 have two or more chronic conditions. Studies of diet, genes and drugs indicate that delaying one age-related disease probably staves off others. At least a dozen molecular pathways seem to set the pace of physiological ageing.
Researchers have tweaked these pathways to give rodents long and healthy lives. Restricting calorie intake in mice or introducing mutations in nutrient-sensing pathways can extend lifespans by as much as 50%. And these ‘Methuselah mice’ are more likely than controls to die without any apparent diseases. In other words, extending lifespan also seems to increase ‘healthspan’, the time lived without chronic age-related conditions.
Research has highlighted potential benefits from dietary restriction in extending healthy life span. People who eat significantly fewer calories, while still getting optimal nutrition, have “younger,” more flexible hearts. They also have significantly lower blood pressure, much less inflammation in their bodies and their skeletal muscles function in ways similar to muscles in people who are significantly younger.
These insights have made hardly a dent in human medicine. Biomedicine takes on conditions one at a time. Rather, it should learn to stall incremental cellular damage and changes that eventually yield several infirmities.
The current tools for extending healthy life — better diets and regular exercise — are effective. But there is room for improvement, especially in personalizing treatments. Molecular insights from animals should be tested in humans to identify interventions to delay ageing and associated conditions. Together, preclinical and clinical researchers must develop meaningful endpoints for human trials.
Longevity pathways identified in model organisms seem to be conserved in humans and can be manipulated in similar ways. Genetic surveys of centenarians implicate hormonal and metabolic systems. Long-term calorie restriction in humans induces drastic metabolic and molecular changes that resemble those of younger people, notably in inflammatory and nutrient-sensing pathways. Mice engineered to have reduced signalling in these pathways live longer.
Several molecular pathways that increase longevity in animals are affected by approved and experimental drugs. The sirtuin proteins, involved in a similar range of cellular processes, are activated by high concentrations of naturally occurring compounds and extend lifespan in metabolically abnormal obese mice. A plethora of natural and synthetic molecules affect pathways that are shared by ageing and conditions related to ageing.
Diet has similar effects. The drugs rapamycin and metformin mimic changes observed in animals fed calorie and protein-restricted diets. And fasting triggers cellular responses that boost stress resistance, and reduce oxidative damage and inflammation. In rodents, fasting protects against diabetes, cancer, heart disease and neurodegeneration9. There are many anti-ageing interventions that could be considered for clinical trials.
Scientists are not set up to capitalize on these leads to combat the looming ageing crisis. Clinicians do not realize how much is understood about the molecular mechanisms of ageing and its broad effects on diseases. Researchers of all stripes focus too much on easing or reversing the progression of diseases.
The problem is calcified by the funding gap. Budgets for ageing research are small compared to disease-centred research. The Division of Aging Biology in the US National Institute on Aging receives less than 1% of the National Institutes of Health’s budget even though it supports research into the mechanisms underlying most disabilities and chronic diseases. Most grants focus on diseases of specific systems. Most study sections are not set up to evaluate multidisciplinary research on healthspan. The situation is similar in Europe and Japan.
How should we test interventions that extend healthspan? Human data from dietary restriction and genetic-association studies of healthy ageing could help to channel the most promising pathways identified in preclinical studies. Animal studies should be designed to better mimic human ageing. For example, frailty indices are often used in human studies. Comparable indices should be developed for mice.
Suitable endpoints for human trials are needed. Animal work suggests many candidates as potential biomarkers, such as accumulation of molecular damage to DNA, proteins and lipids from oxidative stress. Publicly funded clinical trials could also collect crucial samples of blood, muscle and fat for molecular analysis.
Funding agencies should establish committees of translational scientists to review which markers of biological ageing are most consistent between animals and humans, and prioritize the most practical for further assessment. Chosen biomarkers could be evaluated in clinical studies over a broad age range of patients already being treated with drugs that increase lifespan in animal models. Assessments must also be developed for dietary or other interventions that do not involve drugs.
The most important change must be in mindset. Economic incentives in both biomedical research and health care reward treating diseases more than promoting health. The launch of a few anti-ageing biotech companies such as Calico, created last year by Google, is promising. But public money must be invested in extending healthy lifespan by slowing ageing. Otherwise we will founder in a demographic crisis of increased disability and escalating health-care costs.
A number of studies show that people who sleep approximately 6 1/2 – 7 hours each night live longer and have better cognitive function than those sleeping 8 hours or more.
Daniel F. Kripke, an Emeritus Professor of Psychiatry at the University of California San Diego, analyzed the data on 1.1 million people over a six year period who participated in a cancer study. Published in JAMA Psychiatry the study showed that people who reported they slept 6.5 – 7.4 hours had a lower mortality rate than those who slept for a shorter or longer length of time.
In another study, published in the journal Sleep Medicine in 2011, Dr. Kripke found further evidence that the optimal amount of sleep might be less than the traditional eight hours. The researchers recorded the sleep activity of about 450 elderly women using devices on their wrist for a week. Some 10 years later the researchers found that those who slept fewer than five hours or more than 6.5 hours had a higher mortality.
A study in the journal Frontiers in Human Neuroscience last year used data from users of the cognitive-training website Lumosity. Researchers looked at the self-reported sleeping habits of about 160,000 users who took spatial-memory and matching tests and about 127,000 users who took an arithmetic test. They found that cognitive performance increased as people got more sleep, reaching a peak at seven hours before starting to decline.
A study in the current issue of Journal of Clinical Sleep Medicine tracked five healthy adults who were placed in what the researchers called Stone-Age-like conditions in Germany for more than two months without electricity, clocks, or running water. Participants fell asleep about two hours earlier and got on average 1.5 hours more sleep than was estimated in their normal lives, the study said. Their average amount of sleep per night was 7.2 hours.
We do not have to lose our independence and ability to live life in our 70′s or 80′s. Even at the age of 100 years old Fauja Singh completed a marathon.
The race ended just after Fauja Singh crossed the line in 3,851st place. By finishing then he would do what no man before him had ever done. Amid the bundled and cheering crowd in Toronto, underneath a distended but gracious sky, he would complete a marathon. And he would do so at 100 years old.
Was it pain he felt as he approached the end, just footsteps away from redefining the limits of human endurance? No, this wasn’t pain. Fauja knew pain. This wasn’t pain but exhaustion. And Fauja could handle exhaustion, because exhaustion foreshadowed euphoria. When Fauja got tired, it often meant a record would soon fall.
He’d already broken a few. Fastest to run a marathon (male, over age 90), fastest to run 5,000 meters (male, over age 100), fastest to run 3,000 meters (male, over age 100), and on and on they went. But those records didn’t roll off the tongue the way this one would. Oldest person to complete a marathon (male): Fauja Singh.
So Fauja ran in Toronto, arms swinging, yellow turban bobbing, chest-length Zeusian beard swaying in the wind. He was joined by other runners with roots in the Indian region of Punjab, their appearance in keeping with the traditions of their Sikh faith. Fauja trotted for the first three miles, until his coach encouraged him to slow to a jog. Speed was fleeting, the enemy of endurance. By mile 6, he’d downshifted to a toddle. After a break for a rubdown and some tea at mile 18, he settled into a walk.
The exhaustion took hold sometime around mile 20, but Fauja stayed upbeat about the remaining distance. Finally Fauja saw the only mile-marker that mattered: the finish line. What had been silence between footsteps was now music and cheers. The slog to the finish reminded Fauja of his wedding day, of the joy that awaited at the end of the long aisle. He waved to the crowd as he walked across the line, then lifted his arms and accepted a medal. He’d finished in 8 hours, 25 minutes. There were smiles and handshakes and photos with friends and strangers, then a rambling news conference for Fauja to reflect on his record.
Researchers at the University of California, Berkeley, have discovered that the hormone oxytocin plays a critical role in healthy muscle maintenance and repair. After a nine-day treatment of old mice, scientists found that the muscles of the group that had received oxytocin injections healed far better than those of a control group without oxytocin.
“The action of oxytocin was fast,” said Elabd a University of California Researcher. “The repair of muscle in the old mice was at about 80 percent of what we saw in the young mice.”
A few other biochemical factors in blood have been connected to aging and disease in recent years, but oxytocin is the first anti-aging molecule identified that is approved by the Food and Drug Administration for clinical use in humans.
Oxytocin is a hormone associated with maternal nurturing, social attachments, childbirth and sex and is indispensable for healthy muscle maintenance and repair, and that in mice, it declines with age.
The new study published in the journal Nature Communications, presents oxytocin as the latest treatment target for age-related muscle wasting, or sarcopenia.
A few other biochemical factors in blood have been connected to aging and disease in recent years, but oxytocin is the first anti-aging molecule identified that is approved by the Food and Drug Administration for clinical use in humans, the researchers said. Pitocin, a synthetic form of oxytocin, is already used to help with labor and to control bleeding after childbirth. Clinical trials of an oxytocin nasal spray are also underway to alleviate symptoms associated with mental disorders such as autism, schizophrenia and dementia.
Oxytocin is sometimes referred to as the “trust hormone” because of its association with romance and friendship. It is released with a warm hug, a grasped hand or a loving gaze, and it increases libido. The hormone kicks into high gear during and after childbirth, helping new mothers bond with and breastfeed their new babies.
“This is the hormone that makes your heart melt when you see kittens, puppies and human babies,” said Conboy, who is also a member of the Berkeley Stem Cell Center and of the California Institute for Quantitative Biosciences (QB3). “There is an ongoing joke among my research team that we’re all happy, friendly and trusting because oxytocin permeates the lab.”
The researchers pointed out that while oxytocin is found in both young boys and girls, it is not yet known when levels of the hormone start to decline in humans, and what levels are necessary for maintaining healthy tissues.
Christian Elabd and Wendy Cousin, both senior scientists in Conboy’s lab, were co-lead authors on this study.
Previous research by Elabd found that administering oxytocin helped prevent the development of osteoporosis in mice that had their ovaries removed to mimic menopause.
The new study determined that in mice, blood levels of oxytocin declined with age. They also showed that there are fewer receptors for oxytocin in muscle stem cells in old versus young mice.
To tease out oxytocin’s role in muscle repair, the researchers injected the hormone under the skin of old mice for four days, and then for five days more after the muscles were injured. After the nine-day treatment, they found that the muscles of the mice that had received oxytocin injections healed far better than those of a control group of mice without oxytocin.
“The action of oxytocin was fast,” said Elabd. “The repair of muscle in the old mice was at about 80 percent of what we saw in the young mice.”
Interestingly, giving young mice an extra boost of oxytocin did not seem to cause a significant change in muscle regeneration.
“This is good because it demonstrates that extra oxytocin boosts aged tissue stem cells without making muscle stem cells divide uncontrollably,” Cousin added.
The researchers also found that blocking the effects of oxytocin in young mice rapidly compromised their ability to repair muscle, which resembled old tissue after an injury.
The researchers also studied mice whose gene for oxytocin was disabled, and compared them with a group of control mice. At a young age, there was no significant difference between the two groups in muscle mass or repair efficiency after an injury. It wasn’t until the mice with the disabled oxytocin gene reached adulthood that signs of premature aging began to appear.
“When disabling other types of genes associated with tissue repair, defects appear right away either during embryonic development, or early in life,” said Conboy. “To our knowledge, the oxytocin gene is the only one whose impact is seen later in life, suggesting that its role is closely linked to the aging process.”
Cousin noted that oxytocin could become a viable alternative to hormone replacement therapy as a way to combat the symptoms of both female and male aging, and for long-term health. Hormone therapy did not show improvements in agility or muscle regeneration ability, and it is no longer recommended for disease prevention because research has found that the therapy’s benefits did not outweigh its health risks.
In addition to healthy muscle, oxytocin is predicted to improve bone health, and it might be important in combating obesity.
Conboy said her lab plans to examine oxytocin’s role in extending a healthy life in animals, and in conserving its beneficial anti-aging effects in humans.
She noted that there is a growing circle of scientists who believe that aging is the underlying cause of a number of chronic diseases.
“If you target processes associated with aging, you may be tackling those diseases at the same time,” said Conboy. “Aging is a natural process, but I believe that we can meaningfully intervene with age-imposed organ degeneration, thereby slowing down the rate at which we become progressively unhealthy.”
The reduced ability to respond to stress is a major characteristic of aging. Indeed, aging itself is a stressful condition. Therefore, reducing chronic causes of stress can promote longevity. Some of the best protein protectors against stress and aging are the Heat Shock Proteins (HSPs). The protective HSPs are induced whenever your body is exposed to stressing agents such as:
1. Alcohol, which is one of the likely reasons that one drink per day helps prolong life
2. Elevated body temperature
3. Environmental toxins such as heavy metals or toxic chemicals
4. Oxidative stress, which may explain part of the reason that limited exercise is beneficial
Besides their effects on stress response, HSPs also have a protective role in disease and aging. For example, much research has shown that HSPs help with cardiovascular, metabolic, and neurological disorders.
At the recent AGE research conference (May 31 to June 2, 2014), new data on HSPs was presented by Kalie Kavanagh at Wake Forest University in North Carolina. Long lived Centenarians have better heat shock response and some may have gene variants of HSPs that are protective. HSP levels typically decline with age. Experiments in monkeys to raise their HSPs preserved insulin sensitivity, lowered blood pressure, and increased endurance.
The most interesting information to come out of the HSP talk was the potential to increase your own HSP levels. The HSPs can be stimulated by raising your body temperature slightly for 10 to 30 minutes using available methods: soaking in a hot tub at 104 degrees or sitting in a steam sauna bath, or participating in any exercise in which you build up a sweat for 5 minutes or more. These activities all lead to higher HSP levels, which can remain elevated and protective for 24 hours or more.