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

In the United States an increasing number of doctors are already using autologous stem cells in their practice. The stem cells are harvested from the adipose tissue (fat) or blood from bone marrow of the patient and then injected the same day into another part of the body. For instance many doctors inject joints like knees, hips and various parts of the spine. You can learn more about this or locate a physician at www.getprolo.com. The stem cells can also be injected intravenously into the cardiovascular system.

A Japanese researcher, Nobel laureate Shinya Yamanaka, collected genes from mature adult skin tissue and reprogrammed them to become pluripotent, which is a stem cell characteristic that means a cell is able to differentiate into multiple types of cells. This conversion process, referred to as induced pluripotent stem cells (iPSCs), means that we can take adult cells from a person with a particular disease, turn them into iPSCs, and then induce the iPSCs to turn into different types of body cells. Yamanaka?s iPSC findings show how scientists can essentially ?make any cell turn into any other type of cell and in effect move through wormholes in developmental time? to produce such things as a pancreas from skin tissue.? As a result, ?the petri dish becomes an avatar of the patient? whereby medicines can be identified “that will improve the condition of cells in the patient without having to take cells out of the petri dish and put them back in the patient.”

While harvesting “stem cells” from a patient’s blood from bone marrow or fat from liposuction has great value today neither of these procedures provides pluripotent stem cells needed for diverse tissue differentiation in a laboratory. Rather, these procedures produce mesenchymal cells, which work well for cardiovascular and orthopedic conditions because these tissues are the end organ targets for mesenchymal cells. However, they do not work well for other germ cell layer target organs, such as those produced from endoderm (incl., pancreas, liver, lungs) and ectoderm (incl., nervous system, skin).

Fortunately, there is a lesser known but more viable means for obtaining real pluripotent stem cells that merely involves a blood draw. In 2005, a study published in Minerva Biotechnologica identified stem cells in the blood. In other follow-up studies, scientists showed that such cells could, in fact, be used to regenerate not only heart tissue, but brain, lung, and pancreas as well.

In 2010, a clinical protocol was developed for harvesting, concentrating, reconstituting, and administering pluripotent stem cells obtained from autologous blood. Today the use of stem cells for clinical applications is in its infancy. Physicians still have much to learn about how to more effectively utilize pluripotent stem cells in their practice for the benefit of their patients. Such knowledge includes not only using the most appropriate source for harvesting real stem cells but in improving the means of attracting those stem cells to where they are needed and facilitating their differentiation. As more physicians implement the use of pluripotent stem cells in their practice, such as those obtained from autologous blood, we can begin accumulating the objective data needed to validate stem cells in the present and advance stem cell science into the future.

A hormone that extends lifespan in mice by 40% is produced by specialized cells in the thymus gland, according to a new study by Yale School of Medicine researchers. The team also found that increasing the levels of this hormone, called FGF21, protects against the loss of immune function that comes with age.

Published online in the Proceedings of the National Academy of Sciences on Jan. 11, the study’s findings have future implications for improving immune function in the elderly, for obesity, and for illnesses such as cancer and type-2 diabetes.

When functioning normally, the thymus produces new T cells for the immune system, but with age, the thymus becomes fatty and loses its ability to produce new T cells. This loss of new T cells in the body is one cause of increased risk of infections and certain cancers in the elderly.

Led by Vishwa Deep Dixit, professor of comparative medicine and immunobiology at Yale School of Medicine, the researchers studied transgenic mice with elevated levels of FGF21. The team knocked out the gene’s function and studied the impact of decreasing levels of FGF21 on the immune system. They found that increasing the levels of FGF21 in old mice protected the thymus from age-related fatty degeneration and increased the ability of the thymus to produce new T cells, while FGF21 deficiency accelerated the degeneration of the thymus in old mice.

“We found that FGF21 levels in thymic epithelial cells is several fold higher than in the liver therefore FGF21 acts within the thymus to promote T cell production,” said Dixit.

“Elevating the levels of FGF21 in the elderly or in cancer patients who undergo bone marrow transplantation may be an additional strategy to increase T cell production, and thus bolster immune function,” said Dixit.

Dixit added that FGF21 is produced in the liver as an endocrine hormone. Its levels increase when calories are restricted to allow fats to be burned when glucose levels are low. FGF21 is a metabolic hormone that improves insulin sensitivity and also induces weight loss.

Dixit said further studies will focus on understanding how FGF21 protects the thymus from aging, and whether elevating FGF21 pharmacologically can extend the human healthspan and lower the incidence of disease caused by age-related loss of immune function.

“We will also look to developing a way to mimic calorie restriction to enhance immune function without actually reducing caloric intake.”

Journal Source:

Yun-Hee Youm, Tamas L. Horvath, David J. Mangelsdorf, Steven A. Kliewer, Vishwa Deep Dixit. Prolongevity hormone FGF21 protects against immune senescence by delaying age-related thymic involution. Proceedings of the National Academy of Sciences, 2016; 201514511 DOI: 10.1073/pnas.1514511113

Summary:

Liver-derived metabolic hormone fibroblast growth factor 21 (FGF21) improves insulin sensitivity and extends lifespan in mice. Aging also compromises the adaptive immune system by reducing T-cell production from the thymus. In this paper, we describe a new immunological function of FGF21 as a regulator of T-cell production from thymus in aging. The overexpression of FGF21 prevents thymic lipoatrophy, which protects the mice from age-induced loss of na?ve T cells. FGF21 expression in thymic epithelial cells and signaling in thymic stromal cells support thymic function in aging. Loss of FGF21 in mice increases lethality postirradiation and delays the reconstitution of thymus. Hence, we highlight FGF21 as an immunometabolic regulator that can be harnessed to delay immune senescence.

Abstract:

Age-related thymic degeneration is associated with loss of na?ve T cells, restriction of peripheral T-cell diversity, and reduced healthspan due to lower immune competence. The mechanistic basis of age-related thymic demise is unclear, but prior evidence suggests that caloric restriction (CR) can slow thymic aging by maintaining thymic epithelial cell integrity and reducing the generation of intrathymic lipid. Here we show that the prolongevity ketogenic hormone fibroblast growth factor 21 (FGF21), a member of the endocrine FGF subfamily, is expressed in thymic stromal cells along with FGF receptors and its obligate coreceptor, ?Klotho. We found that FGF21 expression in thymus declines with age and is induced by CR. Genetic gain of FGF21 function in mice protects against age-related thymic involution with an increase in earliest thymocyte progenitors and cortical thymic epithelial cells. Importantly, FGF21 overexpression reduced intrathymic lipid, increased perithymic brown adipose tissue, and elevated thymic T-cell export and na?ve T-cell frequencies in old mice. Conversely, loss of FGF21 function in middle-aged mice accelerated thymic aging, increased lethality, and delayed T-cell reconstitution postirradiation and hematopoietic stem cell transplantation (HSCT). Collectively, FGF21 integrates metabolic and immune systems to prevent thymic injury.

Acoustics experts have created a new class of sound wave — the first in more than half a century in a breakthrough they hope could lead to a revolution in stem cell therapy.

The team at RMIT University in Melbourne, Australia, combined two different types of acoustic sound waves called bulk waves and surface waves to create a new hybrid: “surface reflected bulk waves.”

The first new class of sound wave discovered in decades, the powerful waves are gentle enough to use in biomedical devices to manipulate highly fragile stem cells without causing damage or affecting their integrity, opening new possibilities in stem cell treatment.

Dr Amgad Rezk, from RMIT’s Micro/Nano Research Laboratory, said the team was already using the discovery to dramatically improve the efficiency of an innovative new “nebuliser” that could deliver vaccines and other drugs directly to the lung.

“We have used the new sound waves to slash the time required for inhaling vaccines through the nebuliser device, from 30 minutes to as little as 30 seconds,” Rezk said.

“But our work also opens up the possibility of using stem cells more efficiently for treating lung disease, enabling us to nebulise stem cells straight into a specific site within the lung to repair damaged tissue.

“This is a real game changer for stem cell treatment in the lungs.”

The researchers are using the “surface reflected bulk waves” in a breakthrough device, dubbed HYDRA, which converts electricity passing through a piezoelectric chip into mechanical vibration, or sound waves, which in turn break liquid into a spray.

“It’s basically ‘yelling’ at the liquid so it vibrates, breaking it down into vapour,” Rezk said.

Bulk sound waves operate similar to a carpet being held at one end and shaken, resulting in the whole substrate vibrating as one entity. Surface sound waves on the other hand operate more like ocean waves rolling above a swimmer’s head.

“The combination of surface and bulk wave means they work in harmony and produce a much more powerful wave,” said Rezk, who co-authored the study with PhD researcher James Tan.

“As a result, instead of administering or nebulising medicine at around 0.2ml per minute, we did up to 5ml per minute. That’s a huge difference.”

The breakthrough HYDRA device is improving the effectiveness of a revolutionary new type of nebuliser developed at RMIT called Respite. Cheap, lightweight and portable, the advanced Respite nebuliser can deliver everything from precise drug doses to patients with asthma and cystic fibrosis, to insulin for diabetes patients, and needle-free vaccinations to infants.

In a study published Monday in the Proceedings of the National Academy of Sciences, the scientists tracked 1,000 people born in 1972-73 in the coastal city of Dunedin in New Zealand and calculated their “biological age” after their 38th birthdays based on a wide range of biomarkers. The measurements included:

?Kidneys, liver, lungs, metabolic and immune systems
?HDL cholesterol, cardiorespiratory fitness, lung function
?Length of the telomeres (protective caps at the end of chromosomes that have been found to shorten with age)
?Dental health like the condition of the gums
?Condition of the tiny blood vessels at the back of the eyes, (which are a proxy for the brain’s blood vessels)
?Cognitive function

They looked at the volunteers at age 26, 32 and 38 and found that while most of them aged at a normal pace — one year’s worth of physiological changes for each chronological year — some of them aged surprisingly slower or faster.

In fact, researchers calculated, the “biological ages” of the 38-year-olds ranged from 30 to nearly 60 years. From the report:

The fastest-aging study participants experienced two to three years of changes with the passage of a single calendar year. They tended to have worse balance and motor coordination and were physically weaker. Belsky and his colleagues said that these volunteers reported having more trouble with basic tasks like climbing stairs or carrying groceries.

Moreover, those who were aging fast also showed evidence of cognitive decline. Their IQ scores, which according to previous studies have been shown to remain relatively constant throughout a person’s life, were lower by age 38.

One particularly interesting finding of the study was that the people who were physiologically older looked older, at least according to Duke undergraduates who were asked to guess their ages from their pictures.

The study, which was funded in part by the National Institute on Aging, is significant because it looked at young adults. Most previous aging research is focused on the second half of the average person’s life, in the 50s, 60s, and 70s.

“Our findings indicate that aging processes can be quantified in people still young enough for prevention of age-related disease, opening a new door for antiaging therapies,” the researchers wrote. “The science of healthspan extension may be focused on the wrong end of the lifespan; rather than only studying old humans, geroscience should also study the young.”

Belsky said that in the future a person’s biological age could serve as a simple measure of a person’s health that may help patients better understand the battery of numbers they get from their doctors today.

“A single number would be much easier to process,” Belsky said.

He said the measurement could also help with assessing the health of a community. Right now we look at things like disease end points, new diagnoses, hospitalizations and death, but all are imperfect because they don’t give us a picture of the health of a whole person.