Rejuvenating “Old” Blood Reverses Aging

Master Circuit Discovered that Controls Aging – Tweaking it Doubled Lifespan

Epigenetic Fountain of Youth Set to Extend Life Span by up to 50 Years

What Your “Aging Pace” Says About Your Overall Health and Longevity

DNA methylation and aging

Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells

We’re Just Three Decades Away from Immortality, says Leading Scientist

Is Your Life Expectancy Down to Your DNA?

Vitamin D Deficiency Triples Risk of an Early Death

　

Rejuvenating “Old” Blood Reverses Aging

Over a century ago, early doctors performed experiments joining two living organisms together surgically so they share the same blood supply. Yes, it sounds Frankenstein-esque, and these experiments did fall out of favor for a time, but have recently been revived for research into the subject of aging.

The procedure is called parabiosis, which is Latin for “living beside.” We’ve written about it before, and in fact there was a lot of buzz about it several years ago. Some doctors enthused that it could lead to a fountain of youth.

Parabiosis-related therapies do not seem to be very popular at the moment, as far as I can gather from attending the meetings of the American Academy of Anti-Aging Medicine, a group consisting of thousands of doctors who focus on reversing the aging process.

But even though it may not be ready for prime time, there’s still something to it.

Recently, the pairing of a young mouse with an elderly mouse brought remarkable results. The elderly rodent, now getting a share of blood from the young mouse, was rejuvenated. The old mouse grew stronger, smarter and healthier.

Perhaps most exciting, the new research reveals that people can achieve similar youthful regeneration without the parabiosis procedure.

Let’s take a closer look…

In 2005, scientists at the University of California, Berkeley, discovered that parabiosis could reverse many of the signs of aging. In mouse experiments, they conjoined an old mouse with a young mouse and the old mouse experienced overall health improvements.

Animal rights advocates may be outraged at the cruelty of the experiment, and I can’t say I like it much myself. But let’s soldier on and see if we can learn anything…

Other studies followed confirming that after parabiosis old mice had better health and repair of tissues such as cartilage, muscle, skin, and even major organs such as the liver, brain, and kidneys. Even skeletal structures such as bones and the spinal cord were in better repair.

Then, scientists decided to try a new technique. Instead of parabiosis, they merely transfused young blood into elderly mice. They found the procedure rejuvenated muscle and liver tissues, but the transfusion of young blood did not have the same effect of regenerating brain tissues.

Parabiosis was clearly superior for rejuvenation purposes, and the scientific community was keen to establish what factors in the blood of the young animals brought this about.

Professor Irina Conboy, lead author of the original laboratory experiment, explained, “There are two main interpretations… The first is that…rejuvenation was due to young blood and young proteins or factors that become diminished with aging.

“But an equally possible alternative is that, with age, you have an elevation of certain proteins in the blood that become detrimental, and these were removed or neutralized by the young partners.”

Rejuvenating Old Blood in Mice
To test the second hypothesis, Prof. Conboy and her team recently took a group of old mice and replaced half of their plasma — the fluid portion of the blood, minus the blood cells — with saline and albumin protein. The latter was simply to replace the protein that’s lost when blood plasma is removed.

The procedure turned out to have the same or even stronger rejuvenation effects on the brain, liver and muscles than either parabiosisor transfusion. “As our science shows,” commented Prof. Conboy, “the second interpretation turns out to be correct. Young blood or factors are not needed for the rejuvenating effect; dilution of old blood is sufficient.”

Now that’s news.

The big question is whether this will work in humans.

It happens that a medical procedure is already well-established called therapeutic plasma exchange (TPE) or plasmapheresis that dilutes human blood. It’s used to remove pathogenic antibodies in the treatment of various autoimmune diseases such as multiple sclerosis (MS), myasthenia gravis and Guillain-Barre Syndrome.

Pressing the Molecular Reset Button in People
During TPE, a patient’s blood is removed and passed through a device that separates out and removes the plasma (which is discarded), and then the patient’s remaining red blood cells are mixed with a replacement fluid such as plasma or albumin protein and re-infused into the patient.

As part of their latest experiment, the researchers studied human blood samples collected both before and after TPE from four people aged 65 to 70.

They found a number of pro-inflammatory proteins that increase with age were lowered, while more beneficial proteins, such as those that promote vascularization (growth of new blood vessels), were greatly boosted. They described TPE as acting like a molecular reset button.

Michael Conboy, fellow author and husband of Prof. Irina Conboy, explained, “A few of these proteins are of particular interest…but I would warn against silver bullets. It is very unlikely that aging could be reversed by changes in any one protein.

“In our experiment we found that we can do one procedure that is relatively simple and FDA-approved, yet it simultaneously changed levels of numerous proteins in the right direction.”

Human trials are now in preparation to see if a modified form of TPE can improve the overall health of older people and treat age-associated diseases.

This is an exciting area of research indeed. I’ll keep you posted on any additional findings.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7288913/
https://news.berkeley.edu/2020/06/15/diluting-blood-plasma-rejuvenates-tissue-reverses-aging-in-mice/

　

Master Circuit Discovered that Controls Aging – Tweaking it Doubled Lifespan

Scientists have published a groundbreaking study which could unlock the secret to living for a century and beyond — all while avoiding illness and remaining healthy the entire time.

If you’re doubting the validity of such claims, I don’t blame you. It sounds too good to be true, but the research is the real deal.

Scientists discovered a “master circuit” that controls how yeast cells age. When they made some modifications in the circuit, the cells doubled their lifespan and remained healthy throughout.

If the same process takes place in human cells, it could mean a much longer and healthier life for all of us.

How long we live is determined by how our individual cells age. This in turn depends on both internal biochemical changes and environmental influences.

To see whether this cellular aging process happens at the same rate and from the same causes, molecular biologists and bioengineers from the University of California San Diego (USDC), carried out a series of experiments on the yeast, Saccharomyces cerevisiae, which has been used as a model for biological aging for decades.

They found that even though the cells had exactly the same genes and lived in the same environment, they could still age in strikingly different ways.

Two Routes to Aging
Exploring this more deeply, scientists found the cells aged in one of two ways.

About half aged through a gradual decline in an area within the nuclear DNA, where key proteins are synthesized. The other half aged due to dysfunction in the mitochondria, where energy is manufactured.

Cells embark on either of these “aging routes” early in their life cycle and continue to follow it until their life ends. The USDC team found these aging processes were guided by a master circuit within a cellular command center.

Lead researcher Nan Hao explains, “To understand how cells make these decisions, we identified the molecular processes underlying each aging route and the connections among them, revealing a molecular circuit that controls cell aging, analogous to electric circuits that control home appliances.”

Having made this discovery, the research team wondered whether they could manipulate this process to extend the life of the yeast cells.

Young or Old, Cells Remained Normal Throughout Life
Using a series of computer simulations, researchers reprogramed the master molecular circuit by tweaking its DNA. This allowed them to genetically engineer a novel aging route that doubled the lifespan of the yeast.

“In this new aging model,” explained Dr. Hao, “amazingly, throughout the entire lifespan, the cell cycle remains normal, meaning it’s the same as for a young cell. The cells were very, very healthy throughout their lifespan.

“Our study raises the possibility of rationally designing gene or chemical-based therapies to reprogram how human cells age, with a goal of effectively delaying human aging and extending human healthspan.”

The next stage of the research is to test their new aging model on cells and organisms more complex than yeast, and then to progress to human cells, to see if the same molecular circuit applies to them also. Dr. Hao calls this part of the testing the “easy part.”

What would happen after that is far more difficult. If the next phase of cellular testing proves positive, then researchers will undertake testing the DNA modifications on animals and eventually humans to make sure the interventions are safe and are not causing other diseases. That process will likely take many years.

https://ucsdnews.ucsd.edu/pressrelease/researchers-discover-two-paths-of-aging-and-new-insights-on-promoting-healthspan


Master Circuit Discovered that Controls Aging – Tweaking it Doubled Lifespan – Aging Defeated
https://agingdefeated.com/master-circuit-discovered-that-controls-aging-tweaking-it-doubled-lifespan/

　

Epigenetic Fountain of Youth Set to Extend Life Span by up to 50 Years

The lab mouse’s organs are failing. It lies hunched and motionless, just days from death. It has progeria, a disease of accelerated aging.

But the rodent is in for a surprise. Researchers give it an age-reversal cocktail, and before long, the mouse is active, energetic and full of life.

If you’re thinking this is too good to be true, that there must be a catch, you’re right…

　

A few days later the mouse is dead.

Oops!

But even in the face of this setback, scientists believe the technology that gave this mouse a new lease on life—at least temporarily— will be developed and safely applied to humans someday, allowing us to live much longer lives. Let’s take a look…

The age-reversal cocktail used in the mouse study sounds a lot like the fountain of youth.

“It completely rejuvenates,” explained Juan Carlos Izpisúa Belmonte from the Gene Expression Laboratory at the Salk Institute for Biological Studies in San Diego.

Dr. Izpisúa Belmonte reported that the age-reversal cocktail restored all of the cells and organs in the once dying mouse to their youthful state.

How?

Through a tool called epigenetic reprogramming, which resets the body’s epigenetic marks that control which genes are turned on and off within cells.

Epigenetic Reprogramming and Stem Cells
Dr. Izpisúa Belmonte’s work is based on a discovery made in 2006, which found that adding four proteins to human adult cells wipes out the epigenetic marks. If the marks are erased completely, the cell no longer knows what type of cell it is and reverts back to an embryonic state, giving the cell a fresh start.

These “embryonic” cells are called induced pluripotent stem cells (IPSCs) and can be turned into any other type of cell in the body. Even skin cells from centenarians can revert to an embryonic state when scientists apply epigenetic reprogramming. This technique isn’t brand new — in fact, it’s often used by labs to manufacture stem cells.

This reprogramming has also been demonstrated, not just in a Petri dish, but inside other laboratory mice. Some have lived and some have died.

Why Did the Rejuvenated Mouse Die?
The problem is that when you clear away the marks, the cell loses any identity or memory. While it might then grow into a functioning cell, it could just as easily remain dormant or become cancerous. The results are usually fatal. In the case of the lab mouse at the beginning of our article, it sprouted tumors.

However, the good news is that the scientists at the Gene Expression Lab have devised a way to temper the process. The cells of mice with progeria can be partially reprogrammed to not only reverse aging, but live longer.

Mice Live 30 Percent Longer
In their experiment using this new technique, mice gained strength, various organs saw functional improvement and no tumors formed. They also lived 30 percent longer.

“That was the benefit,” said Dr. Izpisúa Belmonte. “We don’t kill the mouse. We don’t generate tumors, but we have our rejuvenation.”

Solving the Root Cause of Aging
Dr. Izpisúa Belmonte believes this epigenetic reprogramming will extend human life span by 30 to 50 years, because aging as he describes it is “nothing other than molecular aberrations that occur at the cellular level.”

He points out how these aberrations come partly from changes that occur over time to the epigenetic marks. These changes cause cells to malfunction, leading the body to suffer the symptoms and illnesses of aging. Epigenetic reprogramming can reverse these alterations and successfully delay aging.

Many Unanswered Questions
While some scientists are positive about Dr. Izpisúa Belmonte’s findings, others are more cautious, pointing to a number of difficulties.

For one thing, a vast number of processes are involved in aging and it’s unlikely just one would be so powerful as to override all the others. It’s possible, but this hasn’t been demonstrated yet.

It’s also possible that epigenetic changes are merely signs of aging, not a major cause. Treatments may be no more than cosmetic, the equivalent of smoothing out wrinkles.

Mice with progeria are used in experiments because they only live three months, but progeria involves a single DNA mutation. Natural aging is far more complex. It isn’t known whether the technique will work in normal, healthy mice.

Although there are still many unanswered questions, Dr. Izpisúa Belmonte remains optimistic.

“I think the kid that will be living to 130 is already with us. He has already been born. I’m convinced.”

https://www.technologyreview.com/2019/08/08/65461/scientist-fountain-of-youth-epigenome/


Epigenetic Fountain of Youth Set to Extend Life Span by up to 50 Years – Aging Defeated
https://agingdefeated.com/epigenetic-fountain-of-youth-set-to-extend-life-span-by-up-to-50-years/

　

What Your “Aging Pace” Says About Your Overall Health and Longevity

A friend tells me that every few years she meets up with 50 or so of her school friends and swaps stories. Sadly, she notes, there are fewer folks to talk with at each reunion, but there’s something else she finds intriguing about these get-togethers.

All of the attendees at these shindigs are basically the same age, but their appearance and health status are all over the board.

Sure, there are some who’ve clearly had “some work done,” yet that can’t fully explain how many of her peers seem to be aging so much faster than others.

It turns out that she’s not alone in her curiosity about this paradox of aging. The latest research shows each of us has an “aging pace” that scientists believe can reveal much about our overall health and longevity.

Researcher Daniel Belsky, PhD, of Columbia University’s Mailman School of Public Health has long been intrigued by the idea of aging pace.

In 2015, Dr. Belsky authored a study published in the journal Proceedings of the National Academy of Sciences.1

He led a team of scientists who used a panel of 18 measures to evaluate 20-year-olds and 30-year-olds with an eye to determining how quickly they were aging.

These measures included blood pressure, lung function, body mass index, cholesterol, inflammation and characteristics of their DNA. Based on these results, researchers calculated the biological age for each volunteer.

When It Comes to Aging, Looks Do Matter
It turns out these markers were a good indicator of physiological age, and they were also good markers of a person’s age in years. Plus, they were quite similar to the biological effects of aging found in older people.

Unlike previous aging research, Dr. Belsky focused on younger populations. Interestingly, he found that the rate of biological aging was already highly variable in young adults who had not yet developed chronic disease.

Dubbed the “Pace of Aging,” the 2015 research revealed that by taking all of these factors into account, we can conclude that people of all ages who appear visibly older are generally biologically older as well when you look below the surface. And vice versa, those who appear younger than their years are generally biologically younger as well.

But Dr. Belsky went one step further…

He’s using his research findings to give scientists the ability to test treatments that might slow aging. This is an exciting new focus in medical research and could be a novel approach to preventing a number of chronic diseases.

For example, Dr. Belsky’s team of researchers developed a blood test that could be given at the start and end of a randomized controlled trial to determine if a given treatment had slowed participants’ pace of aging.

Blood Test Reveals Pace of Aging
Dr. Belsky’s team focused on DNA samples derived from white blood cells. Then they analyzed chemical tags on the DNA called methylation marks. DNA methylation marks change as we age, with some marks being added and others lost.

DNA methylation is an epigenetic process, which means it can change the way genes are expressed. Epigenetics is the study of environmental mechanisms – influences from outside the DNA — that switch genes on and off. These days, epigenetic factors are more and more frequently cited for their effects on the development of disease.2

Previous studies tried to measure aging by examining the DNA methylation differences between people of different chronological ages.

Dr. Belsky says there was one important limitation of this earlier approach.

“Individuals born in different years have grown up under different historical conditions, with a possibility of more exposure to childhood diseases, tobacco smoke, airborne lead, and less exposure to antibiotics and other medications, as well as lower quality nutrition, all of which affect DNA methylation,” Dr. Belsky explains.

He said an alternative approach is to study individuals who were all born the same year. Then researchers find methylation patterns that differentiate those who have been aging biologically faster or slower than their same-age peers.

Measure Methylation, Measure Pace of Aging
Knowing that this was just one of many future studies, the scientists came up with a blood-DNA-methylation measure that is sensitive to variations in biological aging among those born in the same year.

The measurement tool was based on an algorithm named “DunedinPoAm” for Dunedin (P)ace (o)f (A)ging in (m)ethylation.

According to the study, the DunedinPoAm offers a “unique measurement for intervention trials and natural experiment studies investigating how the rate of aging may be changed by behavioral or drug therapy, or by changes to the environment.”

Why is this study significant?

It has the potential to assist in the advancement of research into age-related chronic diseases and help sort out what specific behaviors can slow aging.

We already know that healthy lifestyle habits have a huge impact on the pace of aging, but I’m eager to learn more about how specific healthy lifestyle habits affect different disease processes, such as Alzheimer’s disease, cancer, cardiovascular disease and more.

I have no doubt important new studies are on the horizon using Dr. Belsky’s findings, and I hope that results will come sooner rather than later. I’ll be watching closely and will report back.

https://www.pnas.org/content/112/30/E4104
https://www.whatisepigenetics.com/what-is-epigenetics/

　

The strongest evidence that the age-related changes in DNA methylation play a role in aging comes from studies of anti-aging interventions (e.g., caloric restriction, dwarfism, and rapamycin treatment) in mice. These anti-aging interventions deaccelerate the epigenetic clocks and reverse/prevent 20 to 40% of the age-related changes in DNA methylation.

The role of DNA methylation in epigenetics of aging - PubMed
https://pubmed.ncbi.nlm.nih.gov/30419258/

　

Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells

https://pubmed.ncbi.nlm.nih.gov/23812591
Vitamin C has a stronger effect on regions that gain methylation in cultured ES cells compared to blastocysts, and in vivo are methylated only after implantation. In contrast, imprinted regions and intracisternal A particle retroelements, which are resistant to demethylation in the early embryo, are resistant to vitamin-C-induced DNA demethylation.

Cited by: 580
Publish Year: 2013
Author: Kathryn Blaschke, Kevin T. Ebata, Mohammad M. Kari

　

The role of DNA methylation in epigenetics of aging
https://pubmed.ncbi.nlm.nih.gov/30419258
The strongest evidence that the age-related changes in DNA methylation play a role in aging comes from studies of anti-aging interventions (e.g., caloric restriction, dwarfism, and rapamycin treatment) in mice. These anti-aging interventions deaccelerate the epigenetic clocks and reverse/prevent 20 to 40% of the age-related changes in DNA ...

Cited by: 27
Publish Year: 2019
Author: Archana Unnikrishnan, Willard M. Freeman, Jordan Jackson, Jonathan D. Wren, Hunter Porter, Arlan Ric...

Aging and DNA methylation | BMC Biology | Full Text
https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-015-0118-4
Jan 31, 2015 · The earliest studies, which related DNA methylation changes to the aging process, were investigating different organs and life stages of humpback salmon [] and found that 5-methylcytosine (5mC) levels during ontogenesis were significantly decreasing.Attesting to the evolutionary importance of DNA methylation, these results could be later extended to mammals [].

Cited by: 320
Publish Year: 2015
Author: Marc Jung, Gerd P Pfeifer

Aging and DNA methylation
https://pubmed.ncbi.nlm.nih.gov/25637097
In this Opinion article, we summarize how changes in DNA methylation occur during aging in mammals and discuss examples of how such events may contribute to the aging process. We explore mechanisms that could facilitate DNA methylation changes in a site-specific manner and highlight a model in which …

Cited by: 320
Publish Year: 2015
Author: Marc Jung, Gerd P Pfeifer


DNA methylation dynamics in aging: how far are we from ...
https://www.sciencedirect.com/science/article/pii/S0047637417302671
Sep 01, 2018 · 2.2. DNA methylation changes in cellular and disease models of aging. Aging is accompanied by a debilitating loss of cellular integrity and function, which induces age-related degeneration of tissues and organs, manifesting in age-related pathologies, such as sarcopenia, osteoporosis and neurodegeneration.

Cited by: 71
Publish Year: 2017
Author: Fabio Ciccarone, Stefano Tagliatesta, Paola Caiafa,

　

We’re Just Three Decades Away from Immortality, says Leading Scientist

There’s good news for anyone under the age of 40. You’re not going to die… at least that’s what Dr. Ian Pearson believes.

In fact, Dr. Pearson says that anyone who’s alive by the year 2050 will be able to “live forever,” thanks to new technologies. Let’s take a closer look at what science is doing to help people become immortal.

From scorpion oil to spiderweb elixir to drinking gold, there’s no shortage of concoctions humans have sampled in their search for the fountain of youth and the quest for eternal life. But of course, they’ve all fallen short.

Dr. Ian Pearson says that’s about to change.

He believes we are very close — just decades away — from achieving immortality. Dr. Pearson is a full time futurologist from England who has been on the same mission for nearly 30 years: tracking and predicting developments across a wide range of medical and environmental sciences, business and technology, as well as society and politics.

Immortality is no longer science fiction, in his view. It’s the result of huge strides in science, technology, robotics and artificial intelligence. Dr. Pearson believes that discoveries in these areas will give us three important ways to achieve immortality.

New Body Parts Printed Out
Dr. Pearson points first to biotechnologies that will allow us to replace badly functioning organs with new ones. This isn’t like organ donation of the past. Human donors won’t be needed.

Scientists internationally are investigating what it looks like to load 3D printers with human cells and create new organs.

Body parts could also be renewed continually by using genetic engineering and other technologies that prevent cells from aging, or that even reverse aging.

“No one wants to live forever at 95 years old,” Dr. Pearson says, “but if you could rejuvenate the body to 29 or 30, you might want to do that.”

We’re Just Three Decades Away from Immortality, says Leading Scientist – Aging Defeated
https://agingdefeated.com/were-just-three-decades-away-from-immortality-says-leading-scientist/

　

Is Your Life Expectancy Down to Your DNA?

I have quite a few relatives who made it into their late eighties or even their nineties. My brother and sister and I often say we hope we have their genes.

But recent research suggests genes may not matter all that much.

Consider British zoologist and painter Desmond Morris. Having looked at the lifespan of his recent ancestors, he became convinced he’d die at the age of 60.

Reasonably enough, he decided that life was too short to waste any time, and he became a prolific author and artist. In 1967, at the age of 39, he found fame after his book The Naked Ape sold 10 million copies worldwide. It made quite a splash.

Today, Dr. Morris is still painting and writing at the age of 92. So much for genetics predicting longevity!

In fact, Dr. Morris is not unique. The latest study — and largest of its kind — shows that genes have far less influence on lifespan than many believe.

Though it’s widely believed that long life runs in families for genetic reasons, experts now believe that the contribution DNA actually makes to your longevity is roughly 15 to 30 percent. But even this may be an overestimate.

Ancestry.com Reveals New Insight into Genes and Longevity
Dr. Graham Ruby, an analyst with the Silicon Valley longevity research company Calico, felt all previous research into a person’s lifespan and genetic background was incomplete. The only way to gain a deeper insight was to analyze more data.

So, Calico teamed up with Ancestry, the parent company of Ancestry.com, which boasts the world’s largest family history database. This allowed Dr. Ruby and his research team to analyze family tree structures for almost 440 million Americans, mostly of European descent, born throughout the whole of the 19th and early 20th centuries.

Now furnished with huge amounts of data on family ties, the team examined lifespan between family members and in-laws over generations.

For siblings and first cousins of the same gender, they found genes accounted for around 20 to 30 percent of longevity, falling to 15 percent or less for relatives of different genders. This was much the same as in previous research on lifespan.

Lifestyle Link Seen in Spouses
Also, as seen in some previous research, life expectancy for a husband and wife was very similar, even more so than between a brother and sister. The researchers believe this is because spouses share the same environment and many of the same lifestyle habits.

However, something unexpected cropped up.

The lifespan among siblings-in-law and first cousins-in-law was also similar, yet they’re not blood relatives and they don’t live in the same household (at least, not usually). For example, your husband’s sister and your own sister are likely to have similar lifespans.

The same held true for even more remote relationships, such as aunts and uncles-in-law and first cousins once removed-in-law.

What factor could explain how, for instance, John’s sister’s husband’s brother could have a similar lifespan to John?

The Phenomena of “Assortative Mating”
Thanks to the massive dataset, the researchers detected a non-biological trend called assortative mating.

As explained by Dr. Ruby, “What assortative mating means here is that the factors that are important for lifespan tend to be very similar between mates. In other words, people tend to select partners with traits like their own.”

Choosing a partner is not a completely random event and usually goes against the old adage, “opposites attract.”

For instance, people with similar incomes, education and status may be more likely to marry each other. This influences lifespan and would explain similar longevity across non-family relations.

“There are a multitude of ways,” the authors wrote in the journal Genetics, “in which socioeconomic status is known to be transferred within families, and socioeconomic status is known to affect human lifespan.”

A researcher who doesn’t take assortative mating into account is likely to overestimate the impact of genetics.

When it is taken into account the impact of genetics shrinks to a mere seven percent or lower.

So, if you want to be a fit and active 92-year-old like Desmond Morris, you can largely disregard the genes you inherited. Focus instead on the choices you can control such as diet, supplements, exercise, environment and lifestyle.

https://www.genetics.org/content/210/3/1109
www.sciencedaily.com/releases/2018/11/181106104247.htm

Is Your Life Expectancy Down to Your DNA? – Aging Defeated
https://agingdefeated.com/is-your-life-expectancy-down-to-your-dna/

　

Vitamin D Deficiency Triples Risk of an Early Death

As long-time readers of this newsletter know, maintaining healthy vitamin D levels is critical to your good health. Brand-new research shows just how powerful vitamin D is, revealing that your very longevity might depend on healthy vitamin D levels.

But at the same time there’s lots of debate on what constitutes a “healthy” vitamin D level and just how much vitamin D you need to supplement with to achieve it. Let’s take a closer look at the research and what the experts say.

Vitamin D is a well-known factor in bone health, but it also plays many other important health roles throughout the entire body.

A recent review by researchers from Italy concluded that vitamin D is “a multi-dimensional predictor of ill health in the aging process.”

Meanwhile, The Buck Institute for Research on Aging, based in California, reports that “a wide variety of human age-related diseases are associated with vitamin D deficiency.” But that’s only the beginning…

Low Vitamin D Levels Triple Your Risk of Dying
In a brand-new large human study presented at a medical conference held in Spain last September, researchers at the Medical University of Vienna, Austria analyzed data from 78,581 patients with an average age of 51. Researchers monitored vitamin D levels from each of these patients for 10.5 years on average.

They compared a reading of 50 nmol/L, with those whose levels were low (10 nmol/L) and high (90 nmol/L).

Over the period of the study there were 11,877 deaths. The researchers found low levels (10nmol/L) were associated with a two to three-fold increase in the risk of death.

For example, for those aged 60 to 75 the risk of death doubled, for the 45 to 60 age group the risk of death nearly tripled at 2.9, and things weren’t much better for the under 45 set, with risk of death increasing over two-and-a-half times (2.7, to be exact).

As for patients with high blood vitamin D values at 90 nmol/L, they enjoyed a 30 to 40 percent lower risk of death from any cause. Again, the biggest effect was seen in the 45 to 60 age range.

Interestingly, for the over 75 group, no significant link between vitamin D levels and mortality was observed.

When it came to health problems, researchers observed the largest effect of too-low vitamin D levels in people with diabetes. Diabetics were at 4.4 times higher risk of death if they had levels below 50 nmol/L compared to those above it.

Now, some studies suggest vitamin D is only protective up to a certain level. Above this, a reverse effect takes hold and health risks increase instead of decrease. The current study does not bear this out. People with very high values (above 100 nmol/L) were not found to be at any increased risk of any health problems.

Researchers Conclude that RDAs are Too Low
The study found “a strong association” between deficiency and increased mortality which is more pronounced in younger and middle-aged groups. The researchers supported “supplementation to prevent premature mortality.”

Dr. RodrigMarculescu, who led the study, said that since many disease processes kick off early in life, supplementation should start at a young age.

He agrees with the recommendations of the hormone specialists at The Endocrine Society. This group broke ranks with the Institute of Medicine (IOM), which set the recommended daily amount at 600 IU from age 1 to 71, and 800 IU above 71.

I’ve said for years that this recommendation is absurdly, dangerously low.

The Vienna group suggests the range for children and teenagers should be 600 to 1000 IU while adults should get 1,500 to 2000 IU each day.

Dr. Michael Holick from Boston University School of Medicine, one of the world’s foremost authorities on vitamin D, states that deficiency of this vitamin is at epidemic proportions.

He issued a scathing rebuttal against the IOM vitamin D recommendations, saying their advice is inadequate and based on outdated science.

Dr. Holick advocates regular safe sun exposure and supplementing with 1000 to 2000 IU a day. He recommends maintaining blood levels of vitamin D at or above 75 nmol/L or 30 ng/mL, depending on the measurement used.

In the United States you more commonly see dosages expressed in ng/mL. Dr. Holick’s suggestion to aim for 30 is still pretty conservative. I’ve seen other authorities aim for 60 ng/mL as the ideal blood level for this vitamin.

In an interview, a doctor who has measured the D levels of hundreds of patients told us it’s extremely rare to see a patient with 60 ng/mL. Almost all of us are well below that.

Personally, I take 5,000 IU of vitamin D per day.

https://www.ncbi.nlm.nih.gov/pubmed/31590434
https://www.ncbi.nlm.nih.gov/pubmed/27783938
https://www.webmd.com/vitamins-and-supplements/news/20190920/low-vitamin-d-levels-shorter-life#2
The Vitamin D Solution by Michael Holick, Hudson Street Press 2010

Vitamin D Deficiency Triples Risk of an Early Death – Aging Defeated
https://agingdefeated.com/vitamin-d-deficiency-triples-risk-of-an-early-death/