When we first tested Stem Cell 100 on drosophila we were very pleased that it doubled both their average (mean) and maximum lifespans. As far as we know no one had ever accomplished that before. The study was conducted with a control group that received a normal diet and the SC100 group which received the same diet with Stem Cell 100 added starting the second day after hatching.

People who take Stem Cell 100 are typically middle age or older. They did not start taking the nutraceutical supplement during childhood. So we wondered what would happen if the fruit flies started it much later in life. The study was repeated with a third group added which started Stem Cell 100 at the age of 36 days. For perspective the oldest 5% of the fruit flies in the control group typically live 45 – 50 days. In the first study the average (mean) lifespan was about 20 days for the control group and 40 days for the SC100 group. So 36 days is fairly old for a fruit fly.

The results of the study with the third group starting Stem Cell 100 much later in life were better than expected. As you can see in the graphs below the maximum lifespan of the oldest 5% averaged 120 days which was almost as old as the SC100 group that started with the supplement added to their food from the second day after hatching. This result implies that one can take Stem Cell 100 later in life and still get excellent longevity benefits! Also as we described in an earlier blog post the SC100 drosophila regardless of when they started Stem Cell 100 were still flying around, fertile and laying eggs long after the oldest of the control group had died of old age showing that they stayed youthful and healthy.

Stem Cell 100+ contains the same botanical extracts as Stem Cell 100 with additional ingredients and an improved formula that make it even more effective.

It has been known for some time that reducing caloric intake tends to lengthen lifespan and improve overall health. The history of caloric restriction goes all the way back to Luigi Cornaro a nobleman who lived during the 1400’s. At the age of 40 he was suffering from failing health so he began eating less to see if that would help. As a result he recovered his health, stayed on the limited diet, and lived to be 102 years old. Of course that was an amazing achievement back when the average lifespan was only 40 to 50 years. He even wrote several books on the subject which have been translated into English.

In modern animal studies that have been conducted on caloric restriction those that were given a lower calorie diet still received the same nutrient intake of vitamins, minerals, EFA’s, amino acids, etc., but ate food with less calories. The increase in lifespan was significant in many of the studies with the restricted animals living as much as 30% – 40% longer. The results were an increase in both average and maximum lifespan as well as better health.

While it is not possible to do a scientific test of lifespan on humans it is expected that it would have a similar effect. Of course few people would not want to go through life hungry all the time even if they knew they would live a much longer lifespan.

Is there a way to achieve the benefits of caloric restriction without eating less food? Scientists have discovered that reducing calories up regulates the SIRT1 gene. What is interesting is that resveratrol has a similar effect on SIRT1. The problem is that resveratrol has a very short half life of about 14 – 17 minutes. Because it degrades so rapidly it has limited effect on humans and animals.

Is there a better way to up regulate SIRT1? The solution is to take resveratrol analogs. They have half lives that are hours long and so can reach cells deep in the human body and continue to be active for a much longer time. So by taking resveratrol analogs it is possible that many of the benefits of caloric restriction can be achieved without limiting calories.

Stem Cell 100 and Stem Cell 100+ both contain resveratrol anaologs. That is just one example of the multi-pathway approach that was taken by Dr. Villeponteau to formulate supplements that act on many different anti-aging and regenerative mechanisms at the same time.

A 20 year long study of nearly 30,000 women in Sweden showed that those who spent more time in the sun lived longer than those who reported less sun exposure. Those with the greatest sun exposure received an extra 7 months to 2 years of life.

Because the sun?s UV light triggers chemical reactions in the skin that lead to the production of vitamin D, it?s possible that vitamin D is responsible for the health benefits of sun exposure described in this study. And that could mean vitamin D supplements would promote longer life, even without sun exposure. However, that?s only speculation and prior studies have not been able to prove this.

The authors of this study speculate that recommendations to limit sun exposure might actually do more harm than good. As long as you avoid getting burned, they suggest that avoiding the sun could have a negative health impact similar in magnitude to smoking. That?s quite a statement!

While it is very important to avoid sunburn there are problems with some sunscreens that contain chemicals that are toxic or that become oxidized by the sun so they may do more harm than good. Wearing sunscreen hasn?t reduced skin cancer cases. In fact, melanoma rates have tripled since the 1970s.

The sun is our primary source of vitamin D, an important vitamin that strengthens our bone health, helps balance our hormones, boosts our immune system and nourishes brain function. But when we apply sunscreen, we block the sun?s rays and subsequently, the production of vitamin D in our bodies.

With these simple tips, you can protect yourself from toxic sunscreen chemicals and reap the sun?s benefits at the same time!

1. Get your sunshine during off-peak hours.

The sun can cause the most damage when it?s high in the sky: anywhere from 10am to 4pm., but that may differ slightly depending on where you live.

Stick to the sunshine early in the morning or later in the day, with one little caveat: spend 10-15 minutes in the sun during peak hours to get your daily dose of vitamin D. This is all the time you need to grab your essential amount of vitamin D.

2. Don’t wash off the vitamin D.

Vitamin D is formed on the surface of your skin when it’s exposed to UVB rays from the sun, but that vitamin D doesn’t sink in right away ? it can take up to 48 hours to absorb the majority of it. But at the end of a sunny day, most of us are in the shower scrubbing off the sunscreen, sweat and sand … and sending all that lovely vitamin D down the drain.

Try to rinse your body in the shower with just water if you can. Limit your soap usage to just your pits and your bits.

3. Eat your sunscreen.

UV radiation increases free radicals in our bodies. Boost your consumption of antioxidant-rich foods like berries, leafy greens, black beans, bell peppers, carrots, green tea, raw cacao, garlic and salmon.

There?s a reason nature offers us such a beautiful bounty of foods like berries in the summertime. Sure, they’re delicious, but they’ll also help us boost our consumption of important free radical-fighters.

4. Avoid sunburns and cover up.

Wearing sunscreen lulls us into a false sense of protection. Some people believe they can frolic through the surf for hours and be 100% shielded from the sun. This is how sunburns happen!

No one wants to end up looking like a leather handbag. Don?t spend too much time in the sun all at once, and wear lightweight clothing that’ll allow you to cover your skin and still beat the heat.

5. Buy sun block that is made from natural ingredients, oil free and based on titanium oxide and/or zinc oxide.

By using these sun protection strategies, you can get the essential sun nutrients that will ultimately benefit your health and well-being.

Reference:

Avoidance of sun exposure as a risk factor for major causes of death J Intern Med. 2016 Mar 16. doi: 10.1111/joim.12496; Lindqvist PG1, Epstein E2, Nielsen K3, Landin-Olsson M4, Ingvar C5, Olsson H6.

I was sitting in the front row of the auditorium when Jack LaLanne walked by in one of his famous jumpsuits. On his way up to the stage he had a spring in his step and excellent posture like a young person. The difference was that he was 87 years old. He gave an autobiographical talk about his life and how to retain youthful health and vitality. He was an excellent speaker. At one point he looked fondly at his wife and said “Each morning I get up at 4:30 AM and leave this beautiful women to work out for 2 hours. I want to see how long I can keep it going.”

When Jack was young he had a long list of health issues from headaches to behavioral problems that resulted in dropping out of high school for a year. He described himself as addicted to sugar and junk food. Then he attended a lecture by the famous nutrition expert Paul Bragg who talked about eating more natural and unprocessed foods. Jack changed his diet, started working out, and the rest is history. Besides his long running television show Jack invented exercise equipment that is still used in gyms today, started a chain of health clubs that grew to 200 locations, and performed amazing feats of endurance and strength even at the age of 70 years old that most people would not be capable of in their 20’s.

After the lecture was over a line formed of people who wanted Jack’s autograph or to have their picture taken with him. I waited until the line had disappeared and then was able to talk with Jack and his wife for about 15 minutes. He was so healthy and clear minded it was difficult to imagine that he was approaching the age of 90. He looked just like the picture above so it must have been taken close to when I met him.

The message is that at an age when most people (if they are still alive) are disabled and shuffling around a nursing home with a walker Jack Lalanne was still doing heavy duty workouts each morning and able to engage in the same activities as a young person. He aged, but he never became “old”. How long did he keep it going? He did his last 2 hour workout the day before he past away from pneumonia at the age of 96. Was all that luck or was it because he controlled his own destiny with nutrition and exercise?

Of course we are not recommending a 2 hour extensive workout each day, but the fact that a man could continue that lifestyle for so many years speaks volumes. We can’t stop our chronological age from increasing, however each year we are learning more about how to slow down and reverse many of the effects of biological aging. Don’t accept old age and disability as inevitable. The knowledge and tools to maintain youth and vitality for as long as you live are improving each year. Given the exponential increase in scientific knowledge the day is approaching when staying healthy and active even after the age of 100 becomes common.

?Anything in Life is Possible, if YOU Make it Happen!? ~ Jack LaLanne

Recently one of our customers told me about a comic he saw. It showed a drawing of an old and sickly looking man who was seeing his doctor. The doctor said “you know those extra 15 years you were told you would get by eating a healthy diet and exercising? Well this is it”. This is a common myth in America. That the people who follow a healthy lifestyle will live longer, but it will be additional years of disability and major health problems added to the end of their life. The reality is quite different. The same healthy approach to nutrition, exercise and a healthy lifestyle will not only lengthen life it will also greatly improve quality of life.

The Blue Zones is a book by Dan Buettner about 4 places where there are an unusually large number of centenarians. Those people are over one hundred years old and still typically active and healthy even at that advanced age. Unlike so many Americans that end up shuffling around a nursing home with a walker at the age of 75 or 80 and sitting in bed most of the day watching television they are enjoying life and able to live independently. Of course there are people everywhere that are genetically gifted with long lived parents and grand parents. If they follow the Western diet of unhealthy foods they may still live to an old age, but they will likely be in very poor health with a low quality of life. Most people would prefer a high quality of life over a longer life, although we now have the scientific knowledge about how to achieve both.

The 4 locations are in Sardinia, Italy; Okinawa, Japan; Loma Linda, California and the Nicoya Penninsula, Costa Rica. In each place there are groups of people with excellent nutrition who get lots of exercise and follow a healthy more relaxed lifestyle. They also tend to have many friends and family member that they spend a lot of time socializing with. The book is available on Amazon.com in paperback for less than $10 so you might want to buy a copy.

The lesson is that we do not have to accept old age. If we are willing to do some work to eat healthy and exercise we can choose to stay young and enjoy life even as we add more chronological years to our age. This is also an exciting time because we are uncovering the fundamental causes of aging and developing therapies and nutraceuticals to help increase our quality of life and lifespan even beyond what is possible with a healthy diet and exercise alone. But, it all goes together. Although supplements can help you stay young and live longer you will get better results by combining them with a healthy lifestyle.

A long term study middle-aged men has shown that the impact of low physical capacity on risk of death is second only to smoking. Low aerobic capacity has been associated with increased mortality in short-term studies. The aim of this study was to evaluate the predictive power of aerobic capacity for mortality during 45-years of follow-up. The research was published in the European Journal of Preventive Cardiology.

“The benefits of being physically active over a lifetime are clear,” said lead author Dr Per Ladenvall, a researcher in the Department of Molecular and Clinical Medicine, Sahlgrenska Academy at University of Gothenburg, Sweden. “Low physical capacity is a greater risk for death than high blood pressure or high cholesterol.”

The study included 792 men from the “Study of Men Born in 1913,” a representative sample of 50 year old men in Gothenburg recruited in 1963. The study was designed to investigate risk factors for cardiovascular disease and mortality.

In 1967, at 54 years of age, the 792 men did an exercise test. Of those, 656 men also did a maximum exercise test in which they pushed themselves to the limit. The remaining men were excluded from the maximum exercise test because they had a health condition that could make it unsafe. Maximal oxygen uptake, called VO2 max, was measured in a subpopulation of the 656 men using ergospirometry.

Dr Ladenvall said: “VO2 max is a measure of aerobic capacity and the higher the figure, the more physically fit a person is. In 1967 it was difficult to do ergospirometry in large populations, so the researchers derived a formula using the measurements in the subpopulation, and then calculated predicted VO2 max for the remaining 656 men who had done the maximum exercise test.”

After the initial examination in 1967, the men were followed up until 2012, at the age of 100 years. Several physical examinations were performed, about one every 10 years. Data on all-cause death was obtained from the National Cause of Death Registry.

To analyse the association between predicted VO2 max and mortality the men were divided into three groups (tertiles) ranging from low to high: 2.00 l/min, 2.26 l/min, and 2.56 l/min.

The researchers found that each tertile increase in predicted VO2 max was associated with a 21% lower risk of death over 45 years of follow up, and after adjusting for other risk factors (smoking, blood pressure and serum cholesterol).

Dr Ladenvall said: “We found that low aerobic capacity was associated with increased rates of death. The association between exercise capacity and all-cause death was graded, with the strongest risk in the tertile with the lowest maximum aerobic capacity. The effect of aerobic capacity on risk of death was second only to smoking.”

“The length of follow up in our study is unique,” continued Dr Ladenvall. “When this study began, most data was derived from hospital cohorts and there was very limited data on exercise testing in a large general population. Our sample is representative of the male population in Gothenburg at that time. The risk associated with low aerobic capacity was evident throughout more than four decades and suggests that being physically active can have a big impact over a lifetime.”

He concluded: “We have come a long way in reducing smoking. The next major challenge is to keep us physically active and also to reduce physical inactivity, such as prolonged sitting.”

Reference: 1.P. Ladenvall, C. U. Persson, Z. Mandalenakis, L. Wilhelmsen, G. Grimby, K. Sva rdsudd, P.-O. Hansson. Low aerobic capacity in middle-aged men associated with increased mortality rates during 45 years of follow-up. European Journal of Preventive Cardiology, 2016; DOI: 10.1177/2047487316655466

One would expect that each time a women carries a baby that the stress and depletion would speed up the aging process and shorten her life. At Simon Fraser University, health sciences professor Pablo Nepomnaschy and postdoctoral researcher Cindy Barha followed a group of 75 Kaqchikel Mayan women over a 13 year period. They discovered just the opposite of what they expected to find. The women who had more children had longer telomeres which is associated with a longer life span and a slower aging process. While it is true that pregnant women receive higher social support and experience an increase in the actions of the gonadal steroid estradiol, which increases during pregnancy those do not seem to offer a sufficient explanation. By combining this study with information that has been discovered from several others we have an interesting answer to the mystery.

An article published in Scientific American during December 2012 holds the key. When a mother is carrying a baby they are connected by the placenta. It acts as a conduit to carry nutrients, oxygen, wastes and other substances between the mother and the fetus. This has been known for a long time. What is new is the discovery that stem cells from the fetus also travel through the placenta passing from the unborn baby back into the mother. They implant in the mother and can live for decades in the brain, lung, thyroid, muscle, liver, heart, kidney, skin and other organs. There is even evidence that if the mother has an internal injury that some of the stem cells from her child may repair the damage. Young stem cells are very powerful for healing and especially appropriate for a mother because half of their genetic material came from her. Not only does a mother carry in her body cells of all her children, but the younger children may carry cells that traveled from the fetus to the mother and then into a different child later on. So oddly enough many women and even some men carry cells in their body that is partly from their children or siblings.

Very young stem cells are powerful and that is basically what a mother is receiving each time she carries a baby. No wonder women who have more children age at a slower rate.

References

Cindy K. Barha, Courtney W. Hanna, Katrina G. Salvante, Samantha L. Wilson, Wendy P. Robinson, Rachel M. Altman, Pablo A. Nepomnaschy. Number of Children and Telomere Length in Women: A Prospective, Longitudinal Evaluation. PLOS ONE, 2016; 11 (1): e0146424 DOI: 10.1371/journal.pone.0146424

Robert Martone Scientists Discover Children?s Cells Living in Mothers. Scientific American, 2012

Autophagy keeps the molecules in your cells in good working order. Cells make a lot of defective molecules. They misread genes, for example, and misfold proteins. Even a perfectly crafted molecule does not stay perfect for long. ?Proteins go bad with time,? said Daniel Klionsky of the University of Michigan. ?They age, and they wear out.?

In fact, as Dr. Klionsky wrote in a paper published online in Trends in Cell Biology, this cannibalism may extend our lifespan. Increasing our body?s ability to self-destruct may, paradoxically, let us live longer. ?All of a sudden, researchers in different fields are seeing a connection.?

When proteins and other molecules go bad, they can start to gum up the intricate chemical reactions on which a cell?s survival depends. The cell recognizes defective parts and tags them for destruction. Experiments on flies show the harm that can occur when cells cannot clear away the old and bring in the new. Flies that are genetically engineered with defective lysosomes start to accumulate abnormal clumps of proteins in their cells. The clumps build up especially in their neurons, which start to die as a result.

As mitochondria get old, they cast off charged molecules that can wreak havoc in a cell and lead to mutations. By gobbling up defective mitochondria, lysosomes may make cells less likely to damage their DNA.

Unfortunately, as we get older, our cells lose their cannibalistic prowess. The decline of autophagy may be an important factor in aging. Unable to clear away the cellular garbage, our bodies start to fail.

If this hypothesis turns out to be right, then it may be possible to slow the aging process by raising autophagy. It has long been known, for example, that animals that are put on a strict low-calorie diet can live much longer than animals that eat all they can. Recent research has shown that caloric restriction raises autophagy in animals and keeps it high. The animals seem to be responding to their low-calorie diet by feeding on their own cells, as they do during famines. In the process, their cells may also be clearing away more defective molecules, so that the animals age more slowly.

Our cells build two kinds of recycling factories. One kind, known as the proteasome, is a tiny cluster of proteins. It slurps up individual proteins like a child sucking a piece of spaghetti. Once inside the proteasome, the protein is chopped up into its building blocks.

For bigger demolition jobs, our cells rely on a bigger factory: a giant bubble packed with toxic enzymes, known as a lysosome. The Belgian biochemist Christian de Duve discovered lysosomes in 1955, for which he later won the Nobel Prize. Lysosomes can destroy big structures, like mitochondria, the sausage-shaped sacs in cells that generate fuel. To devour a mitochondrion, a cell first swaddles it in a shroudlike membrane, which is then transported to a lysosome. The shroud merges seamlessly into the lysosome, which then rips the mitochondrion apart. Its remains are spit back out through channels on the lysosome?s surface.

Lysosomes are versatile garbage disposals. In addition to taking in shrouded material, they can also pull in individual proteins through special portals on their surface. Lysosomes can even extend a mouthlike projection from their membrane and chew off pieces of a cell.

The shredded debris that streams out of the lysosomes is not useless waste. A cell uses the material to build new molecules, gradually recreating itself from old parts. ?Every three days, you basically have a new heart,? said Dr. Ana Maria Cuervo, a molecular biologist at Albert Einstein College of Medicine.

This self-destruction may seem like a reckless waste of time and energy. Yet it is essential for our survival, and in many different ways. Proteasomes destroy certain proteins quickly, allowing them to survive for only about half an hour. That speed allows cells to keep tight control over the concentrations of the proteins. By tweaking the rate of destruction, it can swiftly raise or lower the number of any kind of protein.

Lysosomes, which eat more slowly than proteasomes, serve different roles that are no less essential. They allow cells to continue to build new molecules even when they are not getting a steady supply of raw ingredients from the food we eat. Lysosomes also devour oily droplets and stores of starch, releasing energy that cells can use to power the construction of new molecules.

?If you don?t have a snack between lunch and dinner,? Dr. Cuervo said, ?you?re going to have to activate your lysosomes to get nutrients.?

Lysosomes become even more active if dinner never comes, and a short-term hunger turns to long-term starvation. Cells respond to famine by making only a small number of crucial molecules and using lysosomes to destroy the rest. ?When times are good, make everything,? Dr. Klionsky said. ?When times are lean, focus on what you need. You can get rid of everything else.?

This strategy for survival, known as autophagy (?eating oneself?), evolved in our ancestors over two billion years ago. Today, all animals rely on it to endure famines, as do plants, fungi and single-cell protozoa.

Autophagy?s great antiquity has helped scientists discover the genes that make it possible in humans. Rather than study starving people, they introduced mutations into yeast and then observed which strains could no longer survive without food. In many cases, the scientists discovered, the mutations that made yeast vulnerable struck genes that are involved in autophagy. They were then able to find nearly identical versions of those genes in the human genome.

The protection humans get from lysosomes is essential not just during famines. It is also vital just after birth. When babies emerge from their mothers, they need huge amounts of energy so that they can start to run their bodies on their own. But this demand comes at precisely the moment that babies stop getting food through their umbilical cord. Japanese scientists have found that lysosomes in mice kick into high gear as soon as they are born. After a day or two, as they start to nurse, the rate of autophagy drops back to normal.

When the scientists engineered mice so they could not use their lysosomes at birth, the newborn mice almost immediately died of starvation.

Some scientists are investigating how to manipulate autophagy directly. Dr. Cuervo and her colleagues, for example, have observed that in the livers of old mice, lysosomes produce fewer portals on their surface for taking in defective proteins. So they engineeredmice to produce lysosomes with more portals. They found that the altered lysosomes of the old experimental mice could clear away more defective proteins. This change allowed the livers to work better.

?These mice were like 80-year-old people, but their livers were functioning as if they were 20,? Dr. Cuervo said. ?We were very happy about that.?

Andrea Ballabio, the scientific director of Telethon Institute of Genetics and Medicine in Naples, Italy, and his colleagues have found another way to raise autophagy. By studying the activity of genes that build lysosomes, they discovered that at least 68 of the genes are switched on by a single master protein, known as TFEB.

When Dr. Ballabio and his colleagues engineered cells to make extra TFEB, the cells made more lysosomes. And each of those lysosomes became more efficient.

Researchers at Mayo Clinic increased normal mouse lifespan by up to 35% by removing senescent cells that accumulate with age and negatively impact health. The results, which appear today in Nature, demonstrate that clearance of senescent cells preserves tissue and organ function and extends lifespan without observed adverse effects.

“Cellular senescence is a biological mechanism that functions as an ’emergency brake’ used by damaged cells to stop dividing,” says Jan van Deursen, Ph.D., Chair of Biochemistry and Molecular biology at Mayo Clinic, and senior author of the paper. “While halting cell division of these old or damaged cells is important, it has been theorized that once the ’emergency brake’ has been pulled, these cells are no longer necessary.”

The immune system sweeps out the senescent cells on a regular basis, but over time becomes less effective. Senescent cells produce factors that damage adjacent cells and cause chronic inflammation, which is closely associated with frailty and age-related diseases.

Mayo Clinic researchers used a transgene that allowed for the drug-induced elimination of senescent cells from normal mice. Upon administration of a compound called AP20187, removal of senescent cells delayed the formation of tumors and reduced age-related deterioration of several organs. Median lifespan of treated mice was extended by 17 to 35 percent. They also demonstrated a healthier appearance and a reduced amount of inflammation in fat, muscle and kidney tissue.

“Senescent cells that accumulate with aging are largely bad, do bad things to your organs and tissues, and therefore shorten your life but also the healthy phase of your life,” says Dr. van Deursen. “And since you can eliminate the cells without negative side effects, it seems like therapies that will mimic our findings or our genetic model that we used to eliminate the cells like drugs or other compounds that can eliminate senescent cells would be useful for therapies against age-related disabilities or diseases or conditions.”

Darren Baker, Ph.D., a molecular biologist at Mayo Clinic, and first author on the study is also optimistic about the potential implications of the study for humans.

“The advantage of targeting senescent cells is that clearance of just 60-70 percent can have significant therapeutic effects,” says Dr. Baker. “If translatable, because senescent cells do not proliferate rapidly, a drug could efficiently and quickly eliminate enough of them to have profound impacts on health span and lifespan.”

Research Study:

Darren J. Baker, Bennett G. Childs, Matej Durik, Melinde E. Wijers, Cynthia J. Sieben, Jian Zhong, Rachel A. Saltness, Karthik B. Jeganathan, Grace Casaclang Verzosa, Abdulmohammad Pezeshki, Khashayarsha Khazaie, Jordan D. Miller, Jan M. van Deursen. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature, 2016; DOI: 10.1038/nature16932