Category Archives: Aging

Vitamin D’s anti-inflammatory properties

Get VITAMIN D SUPPLEMENTS Now At Amazon

Regular Vitamin D doses can tame inflammation linked to chromic diseases
Adequate time in the sun can supplement bolsters immune cell function
Vitamin D deficiency can lead to soft bones

VITAMIN D supplements can control inflammation associated with chronic conditions such as obesity, heart disease or diabetes.

This finding is based on a review by Curtin University scientists of 23 immune cell studies.

“We found evidence that vitamin D was able to indirectly quench reactive oxygen species, which are accepted as a major factor in the onset and development of chronic diseases including type 2 diabetes,” Professor Philip Newsholme says.

“In fact, inflammation may contribute to a multitude of diseases,” Prof Newsholme says

The results showed for the average person, if they were getting adequate levels of sun exposure or taking a vitamin D supplement, then their immune cell function would benefit.

People who had a good immune cell defence were more likely to have good overall health, according to the review.

Vitamin D deficiency can lead to soft bones or osteoporosis, with symptoms often not evident or ranging from muscle or joint pain, depression and fatigue. It can only be diagnosed via a blood test.

However, this can be avoided by taking the daily supplement or spending time in the sun.

“These kinds of diseases are associated from chronic inflammation and may well benefit from ensuring people have adequate amounts of vitamin D so that they can then supress any adverse levels of inflammation,” he says.

The researchers examined vitamin D in its active form being injected into human cells, focusing their attention on chronic conditions such as obesity and diabetes.

Prof Newsholme says the findings were exciting because it fed into longer term studies, in particular examining the effects of vitamin D levels in humans and its impact on metabolism.

“We believe vitamin D is important for regulation of immune cell metabolism and function, therefore may impact and reduce the onset of chronic inflammatory diseases related to ageing such as cardiovascular disease and diabetes,” he says.

He is now part of a clinical trial which takes blood samples from people and examines their vitamin D levels in winter, these participants are due to be tested again in February.

Early Celebrity Deaths Related To Stress and Overworking

Vote

When the medical journal Circulation printed a study last year about stress and depression being the cause of early deaths, it was generally overlooked by the public as being somewhat obvious and a given. What most people seem to forget is that the celebrities they love who die early are most likely the result of the stress their career puts on their bodies.

Seven researchers from the Department of Medicine at Columbia University wrote in their study Perfect Storm: Concurrent Stress and Depressive Symptoms Increase Risk of Myocardial Infarction or Death that patients with coronary heart disease are more at risk of early death if their mental state is also ill due to depression and stress. Considering one out of every four people that die in the United States every year suffer from coronary heart disease, this isn’t surprising at first, but when you also consider that stress affects the same number of adults, all you need to add to the mix for the “perfect storm” that leads to an early death is depression.

Depression is known to affect around 7% of American adults, although the definition of depression is often controversially discussed as being ambiguous to laymen. This study, however, assessed its 4487 participants based on showing signs of stress and signs of depression over a five year period, being categorized as either low stress/low depression or high stress/high depression, and the subjects with the most heart attacks happened to be the ones with high stress and high depression.

With the recent deaths of Prince and David Bowie, it might make sense to assume that Prince, known for being a workaholic, spiritually disrupted (for lack of a better explanation) and argumentative or “difficult” person, was prone to an early death despite being clean and sober — that is if he also had heart disease (reports are uncertain as this writing). Bowie, on the other hand, may have made it further if he hadn’t succumbed to liver cancer, most likely caused by a lifetime of alcohol and oral drug use (pills).

Of course this is just speculation, but it’s still may help to dispel the notion that celebrities, with all their millions and fan love, live longer, healthier lives then the rest of us..

We all age at different speeds – and scientists have worked out how to calculate it

Vote

A study has confirmed what many of us have been saying for years: age is nothing but a number. The researchers developed a method to determine the pace of ageing in individuals by looking at a range of biomarkers – including blood pressure and gum health. The study participants, all aged 38, varied widely in “biological age” and those ageing more quickly also looked older and reported more health problems.

The concept of biological age is often thought of as the proportion of an individual’s ultimate lifespan that has elapsed. In the context of this study, however, its measurement and meaning are slightly different. Examining 954 men and women in the Dunedin Birth Study Cohort, the researchers determined the biological ages of the participants to years above or below 38, which gave a range from 28 years to 61 years.

The only definition of ageing that really works is based on populations rather than individuals. Ageing is an increase in the likelihood of dying with increasing chronological age, as shown in this table. That is one reason why this work is significant; because it gives an idea of ageing in an individual.

According to population measures, in the absence of any other information, two people aged 65 have an equal risk of dying in the coming year. If one is destined to die from an undiagnosed cancer within two years and the other lives to 95, which individual is older? This is one reason the search for biomarkers of ageing is important, but the authors of this study give yet another reason.

Studying age-related diseases vs studying ageing

Age is the major risk factor for more than 75% of the mortality suffered by those aged over 64 (based on UK ONS 2013 mortality data), including cancers, circulatory and respiratory illness and neurodegeneration. The traditional view is that each of these many conditions have their own particular causes. This view has driven much research – and funding.

However, the view of biogerontologists, who study the biology of ageing, is that there are a few causes of ageing which substantially contribute to all of these age-related conditions. According to this view, if just a fraction of the billions spent on researching individual conditions were spent on finding and treating the basic causes of ageing, the payoffs could be huge, not least in terms of extended productive (tax-paying) lifespan and reduced healthcare costs.

This sort of basic research has been poorly funded in the past, but the logic of, and evidence for the biogerontologists’ view is beginning to be understood. Treatments to delay the onset of ageing and hence extend healthy lifespan in a majority of the population are likely to be found in the next 20 years.

Ageing alogorithm

They may already be being tested in animal models in a lab somewhere. But because humans are so long-lived, we can’t wait 40 or 50 years to see if it works. To test it in humans we need measures of biological age. To generate their estimates of biological age, the researchers used a previously described algorithm based on seven fairly common biomedical parameters.

They then produced a “pace of ageing” measure based on 18 parameters covering a range of organs and systems and known to change with age. Measures were taken at ages 26, 32 and 38. These included waist-hip ratio, lung and kidney function, blood pressure, cholesterol, even gum health. Study members with higher biological ages also showed a more rapid pace of ageing over the previous 12 years.

Study members with older biological ages and a faster pace of ageing looked older than others and reported more health problems. They also had poorer cognitive function, vascular health, grip strength, balance and motor ability.

Can the wrinkles on your face actually reveal your pace of ageing?
Goodluz/Shutterstock

Pace of ageing was scaled so that the mean was one year of physiological change per chronological year, with a range of 0-3 years of change per chronological year. It is frightening to think that the study member with a biological age of 61 may physiologically age 18 years within the next six chronological years, taking him (most likely a man, as men typically die earlier than women) to near his mean population life expectancy (around 80-years-old). According to the model this 38-year-old person may die within six or seven years.

Advances in anti-ageing therapies and in estimating biological age raise big questions for society, both at an individual level and in the public and private sectors. We should not be frightened of them, but we should start talking about these changes now, before they arrive.

David Clancy is Lecturer in Biomedical Science at Lancaster University.

This article was originally published on The Conversation.
Read the original article.

Officials Weigh Options To Hold Down Medicare Costs For Hospice

Vote

Medicare officials are considering changes in the hospice benefit to stop the federal government from paying twice for care given to dying patients. But patient advocates and hospice providers fear a new policy could make the often difficult decision to move into hospice care even tougher.

Patients are eligible for hospice care when doctors determine they have no more than six months to live. They agree to forgo curative treatment for their terminal illness and instead receive palliative or comfort care. However, they are also still allowed Medicare coverage for health problems not related to their terminal illness, including chronic health conditions, or for accidental injuries.

Medicare pays a set amount to the hospice provider for all treatment and services related to the terminal illness, including doctor’s visits, nursing home stays, hospitalization, medical equipment and drugs. If a patient needs treatment that hospice doesn’t provide because it is not related to the terminal illness — or the patient seeks care outside of hospice — Medicare pays the non-hospice providers. The problem is that sometimes Medicare pays for care outside the hospice benefit that it already paid hospice to cover.

To reduce the chances of these duplicative payments, Medicare officials have announced that they are examining whether to assume “virtually all” the care hospice patients receive should be covered under the hospice benefit.

Medicare has been paying millions of dollars in recent years to non-hospice providers for care for terminally ill patients under hospice care, according to government reports.

The Medicare Payment Advisory Commission (MedPAC), an independent organization that advised Congress, found that in 2012, Medicare paid $1 billion to hospitals, nursing homes, therapists and other providers for services for hospice patients unrelated to their terminal illness.

The commission did not estimate how much of that was incorrectly billed and should have been covered by hospices. Prescription drug plans received more than $33 million in 2009 for drugs that probably should have been covered by the hospice benefit, according to an investigation by the Department of Health and Human Services’ inspector general.

Hospice is growing rapidly among older Americans. Of those Medicare beneficiaries who died in 2013, nearly half used hospice, double the rate in 2000, MedPAC also found. Over the same time period, Medicare spending for hospice services grew five-fold, to $15 billion.

Medicare officials initially mentioned last year that they were exploring possible changes. Concerns about duplicative payments “strongly suggests that hospice services are being ‘unbundled,’ negating the hospice philosophy of comprehensive, holistic care and shifting the costs to other parts of Medicare, and creating additional cost-sharing burden to those vulnerable Medicare beneficiaries who are at end-of-life,” they wrote in regulationscontaining this year’s hospice payment rates and other program rules. Officials have not yet issued a formal proposal.

“There will always be exceptions for people who have terminal conditions and have other conditions that need to be attended to,” said Sean Cavanaugh, deputy administrator at the Centers for Medicare & Medicaid Services. “But the majority of their services would be provided through hospice.”

Seniors’ advocates are worried that putting all coverage under the hospice benefit will create obstacles for patients. Instead, Medicare should go after hospice providers who are shifting costs to other providers that Medicare expects hospice to cover, said Terry Berthelot, a senior attorney at the Center for Medicare Advocacy, who urged the government to protect hospice patients’ access to non-hospice care.

“The easiest thing for CMS to do is to say everything would be related to the terminal illness and then there would be no billing problems,” Berthelot said. But federal law, guarantees hospice patients Medicare coverage to control diabetes, blood pressure or other conditions not related to their terminal illness.

“If your blood sugar gets out of control, that could hasten your death,” she said. “But people shouldn’t be rushed off to die because they’ve elected the hospice benefit.”

Cavanaugh said the government is not trying to restrict drugs or other Medicare benefits for hospice patients.

“It’s more about getting the payment right,” he said. “The question is how to clearly circumscribe the benefit, to define what’s in the hospice benefit and what is not.”

That’s not always easy to figure out.

If a cancer patient in hospice slips on some ice and breaks her wrist, the injury could have happened because the cancer has attacked the bones, making them thin and brittle, said Dr. May Al-Abousi, medical director for hospice services at University Hospitals in Cleveland. Treatment for the injury would be covered by hospice. But the injury would not necessarily be part of the hospice benefit for someone with a terminal illness other than cancer, she said.

“Medicine has no cookbook, where we can apply all-or-none rules,” she said.

Sometimes a hospice provider may not even know when a patient has gone to the hospital and there’s usually no way the hospital knows the patient is in hospice unless the patient makes that clear, said Judi Lund Person, at the National Hospice and Palliative Care Organization, [http://www.nhpco.org/ ] which represents nearly 2,000 hospice companies.

“The emergency room physician should be aware that this is a hospice patient with lung cancer as opposed to an 85-year-old male who fell at Denny’s,” she said.

Patients and their families may be afraid to volunteer that information, said Dr. Al-Abousi. “A lot of people get scared when they hear the “H” word,” she said. “They think once they sign that paper for Medicare, nothing else is going to be covered.”

Your Environment Can Be Making You Look Old

Vote

You are the inspiration for Ageless Beauty Secrets. Every time I sit down to write an issue I think about you. I want to answer the questions that are on your mind. And I rely on you to let me know what you’re thinking.So when you spoke, I listened.In our recent survey, many readers told me they want to look beautiful. But they don’t want superficial fixes or a lot of fluff.Most said they wanted cutting-edge, anti-aging beauty advice. They want to turn back the clock and look more youthful, be more energetic, with more confidence to go along with it.But maybe you’re not sure it’s possible to reverse the changes that come with aging. That’s something I often hear when I speak about anti-aging science to audiences.The biggest skeptics are the powers that be at the FDA. They don’t want me discussing this with you at all. They don’t even want me to say “anti-aging.”

Some people even make the mistake of thinking anti-aging is about extending life. That’s a noble goal, but it’s not my view of anti-aging.

I want you to look, feel and act young and vibrant. Anti-aging is about being able to enjoy life for however long you’re alive.

I’m talking about extending your “youthspan.”

This science is exciting. Anti-aging medicine is one of the hottest areas of scientific research. It’s so new most people don’t even know it’s a medical specialty. And I’m proud to say I’m one of the nation’s first board-certified anti-aging physicians.

Every day I look for ways to use this cutting-edge anti-aging research to help my patients look, feel, and act younger.

And that’s exactly what I’m going to help you do in future issues of Ageless Beauty Secrets.

Now, some people think anti-aging won’t work because of genetics. They think you’re genetically programmed to age like your mother, or live to a certain age, and that’s it.

But we exceed our genetic limitations all the time. Genes are only a predisposition. They’re not your fate. You control how they get turned on or off. Your diet, sleep habits, stress levels, exercise, environmental toxins and other lifestyle choices activate chemical switches that regulate your genes.

All of those choices can increase or decrease your risk of disease. And it’s no different when it comes to beauty and aging.

I see many women in their 20s who look like they’re 40 or older. You might think the problem is sun damage. But the truth is most people these days are afraid of sunshine. They cover up and slather on sunscreen.

But other things in your environment can be making you look old. Chemicals in the air make you vulnerable to skin damage. Smog sucks moisture out of your skin. And we are all swimming in a sea of artificial chemical hormones that muck up your endocrine system. It all takes a toll.

But it doesn’t have to be that way.

I travel over 20,000 miles every year. And when I visit third world countries, I see women who look decades younger than they really are. It’s not their genes. It’s that they aren’t constantly assaulted by a toxic environment.

How can you reverse the damage?

Makeup and superficial creams just mask the problem. Anti-aging science has a completely different approach. Timeless beauty isn’t about what you put on your body … It’s about what’s going on deep down at the cellular level.

Anti-aging science holds the key to reversing the signs of aging because it works at the level of your cells… your DNA …and your stem cells. It holds the secret to lasting beauty from the inside out.

And in every future issue of Ageless Beauty Secrets, I’ll show you how to apply the latest in anti-aging technology to keep you looking young and radiant.

You’ll discover how you can:

Slow down – and even reverse – signs of aging by changing the DNA of your skin cells.
Activate your stem cells to regenerate your skin.

Use the latest scientific breakthroughs to protect your skin from free radical damage, sunspots and even cancer.

Optimize your body’s natural defenses to tighten skin, improve tone, and prevent fine lines and wrinkles.

Regenerate and heal your skin, hair and nails with little-known nutrients that help you look younger naturally.

I guarantee that Ageless Beauty Secrets will not be like any other newsletter…

In every issue I’ll give you science-based information that very few people know about. You’ll learn what ingredients to look for in your beauty products and what to avoid.

You won’t see this information in magazines or on TV. Sometimes it’s not even in the science journals yet. You see, I’ve trekked into the deep jungles of Brazil, up the mountains of Peru, and through the islands of Jamaica and Bali. I’ve discovered rare and potent essential oils, antioxidants, and vitamins derived from exotic plants growing in these remote areas. You’ll be the first to know about these discoveries, too.

I promise I’ll keep it brief, clear, and easy to understand. And I’ll tell you exactly how you can use this information right now to look young and radiant for life.

It won’t take long before you see a real difference in the way you look and feel.

And please…if you have a question about looking and feeling younger, I want to hear from you.

To Your Good Health,

Al Sears, MD

Accidental Discovery Could Turn Cancer Cells Into Cancer-Attacking Immune Cells

Vote

Unexpected results are sort of the point of lab experiments. Laboratory studies reveal the unforeseen and if they didn’t, there would seldom be a reason to perform lab studies. It can be problematic when scientists don’t get the results they wanted or thought to expect but other times new data can be the result of the unexpected, and lead to discoveries no one thought to check for in the beginning. Some famous discoveries happened on total accident throughout scientific history. The latest unintentional discovery might make one of the most aggressive types of cancer more treatable than ever before.

Scientists at Stanford recently discovered a way to force leukemia cells to become mature immune cells do something amazing. The researchers were actually trying to stabilize cancer cells so they could keep them alive longer in order to study them. The method of keeping the cells alive allowed the cells to develop into immune cells that may one day help the immune system attack cancerous tumor cells!

You can read the study in full at Proceedings of the National Academy of Sciences.

Acute lymphocytic leukemia (ALL) is the name for a particularly rapidly-progressing cancer where the immature cells that should differentiate and become white blood cells or lymphocytes instead become cancerous. ALL has several classifications based on which kind of lymphocyte (B cell or T cell) the mutated cancer cell originated from.

The scientists were simply investigating a common type of lymphoblastic leukemia, an acute cancer called precursor B cell ALL, aka B-ALL. B-ALL starts as a rogue B cell mutating away from usefulness during an early part of its maturation. The immature cells can’t fully differentiate and become the B cells they were otherwise destined to be. The flawed B cells lack the transcription factors required for normal development. Transcription factors are basically proteins that attach themselves to sections of DNA and are then supposed to switch designated genes on or off, depending on the type of transcription factor. Did you follow that? It’s a bit technical for the layman but most of us understand DNA. Transcription factors are basically a DNA reader than helps the cell decide which part of your DNA it should use to become a specific type of cell.

So, when a transcription factor messes up and activates the wrong section of DNA or doesn’t activate the correct section, it can cause mutations where the cell doesn’t develop or develops poorly. B-ALL is one of the most nasty types of cancer and the prognosis for victims is not good. The Stanford U team wanted to study this villain but had trouble keeping the cancer cells alive outside of the victims body.

Lead researcher Ravi Majeti reported in the lab’s news release: “We were throwing everything at the cells to help them survive.”

One of the techniques they used to attempt to keep the cancer cells from dying involved exposure to a certain transcription factor. The exposed cells began to grow and change shape, and the new morphology was a type of white blood cell called a macrophage, normally responsible for attacking damaged, mutated cells or foreign material.

The team recognized the cancerous cells behaved the same as macrophages in various ways such as surrounding and engulfing bacteria. Most notably, the pseudomacrophages from the cancer cells of mice added back into the cancerous mouse did not behave as a cancer cell, and the mice who did not have cancer did not develop cancer after being exposed.

The Stanford researchers believe the newly converted cells are no longer cancerous. Furthermore, they might even help the body’s immune system regroup and attack other, still cancerous cells. It could work because macrophages normally collect DNA tags from abnormal cells they encounter and also mark foreign material so that other cells in the immune system know what to attack. Since the false macrophages were originally cancerous cells, they will, in theory, already possess the correct signals that recognize the same kind of cancer.

Now that this principle has been identified as a possible method of treating one cancer, it might open the door to helping the immune system combat other cancers.

Related Cosmoso article: Pre-Darwinian Theory of Heredity Wasn’t Too Far Off

Jonathan Howard
Jonathan is a freelance writer living in Brooklyn, NY

Anti-Aging Studies Reveal Longer Lives on the Horizon

Vote

OF MICE AND DIRT

At this very moment, there is a mouse who although appears a bit dogged and raggedy is actually quite animated and bears a wild spirit as he sniffs, scrambles, and snoops about his cage at the University of Texas Health Science Center at San Antonio. Though next to his younger siblings he appears on the runtier end of the litter, unlike them he boasts a coat of black fur lustrous enough to land him a spot on a Pantene commercial. Our said mouse’s name is Mouse UT2598 and he is 3 years old, which translates into the centennial years when it comes to a human life span, as mice typically live to around 4 years old, if they are lucky.

For the sake of this article, let’s call this mouse Mighty. So, what gives Mighty his punk-ass edge? It’s called rapamycin, a compound which is gradually revealing to scientists its ability to slow the aging process along with the havoc it can cause on certain cells. Mighty’s heart and liver are functioning as if he were an adolescent, and his tendons are far more resilient with the elasticity of a 3 year-old mouse. Evidence also reveals that his organs are damaged markedly less than is considered standard at his age, leading to the theory that Mighty may be spared the effects of cancer for quite some time longer than mice not involved in the experiments taking place at the University of Texas. In fact, place him in a line-up alongside other mice his age and the distinctions are absolutely extraordinary.

The experiment involving Mighty and rapamycin is just one of many when it comes to investigation into the aging process. Research all over the globe entails experiments with a plethora of agents, not just rapamycin, some of which are already being used to treat a number of human conditions. Scientists are assembling the puzzle by employing tactics like manipulating genes, too. Essentially, they are all in a race for the big cheese: finding ways to extend longevity and ultimately trap the aging process and curb – if not cure (or even reverse) – it altogether.

As it stands, aging is the single most potent ingredient when it comes to recipes needed for age-related diseases that eventually shorten our lives like cancer, heart conditions, Alzheimer’s and other degenerative brain ailments, and others. While the main components typically associated with heart disease are high cholesterol, obesity and high blood pressure, simply celebrating an 80th birthday can be the factor that tips the scale towards contracting a fatal heart condition – even if that 80 year-old resisted a single nibble of his birthday cake. That being said, scientists are beginning to treat aging as a disease in and of itself, one which may be sensitive to treatment as simple as a doctor’s prescription.

Let’s get back to Mighty and his happy pill. Rapamycin has its origin in dirt. That is, soil samples which were collected in 1964 on a voyage to Easter Island eventually became the foundation for developing the antibiotic, and researchers have found that mice who were given the drug were prone to longer lives (about 20% longer) than mice who did not ingest the medication. What makes rapamycin particularly interesting is that it functions in a variety of species including yeast, worms and flies – and it works even when started late in life. Thus, if studies involving the drug are successful and actually lead to human treatment, it could potentially offer benefits to those starting it in their 60s or even 80s.

HOW DOES RAPAMYCIN WORK?

Rapamycin essentially hinders the operation of a gene that both people and mice possess. It is a gene called mTOR which gives the “Okay To Go” to cells for absorbing and expending energy. In the case that there is an abundance of cell-chow, mTOR gets busy directing cells to take in nutrients and start growing. When food is in short supply, the gene retracts as a turtle would into its shell until the next opportunity to feast arises. Scientists have discovered that when cells are active and “eating”, they age substantially, chiefly due to the fact that they are working their cell-butts off to process food while belching out toxic free radicals at the same time. Thus, the mission is to metaphorically slip that cell a “mickey” and keep it mellowed out without putting it at risk of starving itself – and that’s just what rapamycin is allegedly capable of doing. But – and there’s always a but when it comes to this sort of thing – rapamycin is far from being the long-searched-for fountain of youth. In studies like that starring our friend Mighty, rapamycin has resulted in a body that is 30% smaller than average while mTor-manipulated mice developed cataracts and proved more susceptible to diabetes. The study also showed that males are inclined to progressively lose testicular functioning – not exactly a perk when it comes to a pill that may help you live longer.

Another disadvantage of rapamycin was revealed when humans who were administered the drug after kidney transplants in order to decrease the risk of rejection showed signs of higher susceptibility to diabetes. Despite this, scientists feel positive when it comes to their abilities to whip up a tantalizing cocktail when it comes to adjusting doses and arriving at the ideal blend to increase the pros when it comes to longevity rather than the cons of any possible risks.

GENETIC SOLUTIONS – AND COMPLICATIONS

For some researchers, the passcode for achieving longevity lies in our genes, particularly when it comes to telomeres which are essentially timekeepers of a cell’s life. When a cell divides, it automatically xeroxes its chromosomes’ DNA and telomeres carry the responsibility of cueing when to halt that copying process. Every cell division triggers squiggles of DNA to essentially tie themselves into a knot at the end of a thread (or chromosome) and eventually vanish for good. Certain factors can cause telomeres to shorten cell lives at different rates (like exposure to UV light), making them a perfect target for further research regarding the scavenger hunt for anti-aging formulas.

Healthy human bodies typically maintain a perfect waltz between telomeres and telomerase (an enzyme that handles the lengthening or shortening of DNA strands) so that telomerase can lengthens telomeres just enough that an ideal amount of lost DNA can be retrieved back. But in individuals with telomere-syndrome, ailments like bone problems, liver failure and immune disorders can occur. Discovering how to tame malfunctioning telomeres can lead to correcting their misbehavior and coming up with aging-combatant formulas.

Just over a decade ago, a scientist and her collaborator, Dr. Mary Armanios and Carol Greider (the co-discoverer of telomerase) respectively, worked together in a lab at Johns Hopkins University and met a student with a blood disorder that necessitated blood transfusions on the regular. The boy was in his 20s and already had a full head of startlingly gray hair, signs of which began showing when he was only 9 years old. Curiouser and curiouser, Armanios and Greider learned that all of his paternal relatives had died at staggeringly young ages including his grandmother who died of osteoporosis in her 60s, his father who died at 59 while waiting for a liver transplant, and his aunt and uncle who both died of pneumonia in their 60s. What’s more, the boy himself had suffered from various infections that landed him in the hospital multiple times a year – and he eventually died of a staph infection at 31. It turned out that all of the family members had a severe form of telomere malfunction known as dyskeratosis congenita.

To date, Armanio feels strongly that she will learn a lot by tinkering with telomeres, including how they can be engineered to halt aging-related ailments. Similar interest lingers at Stanford University where Helen Blau and her co-researchers have splashed cells with the precise amount of genetic matter to encourage the lengthening of telomeres. In her study, cells ceased to divide indefinitely and on the contrary started to deteriorate at a normal pace, sparking hope in Blau and her team that the cells might be used for testing in the bodies of people with dyskeratosis congenita. If the cells can target the abnormally rapid growing cells entailed in the disease, they might also be used to create techniques for turning back time on normal human aging cells.

SIAMESE-MICE (YES, YOU READ THAT CORRECTLY)

There exists promises of age-defiance in another quite odd experiment taking place at the Harvard Stem Cell Institute. There, researchers have pinned their hopes on the cousins of our friend Mighty – but in a very unusual way. To conduct their work, scientists conjoin two mice, Siamese-twin style, so that they share the same blood system. Via this most bizarre procedure, it’s been discovered that among of a pair of harnessed mice, the older one presents more new nerve-cell growth in their brains than the younger one. The elders were also brawnier, and boasted a reversal of the heart-enlargening process that typically goes hand-in-hand with aging.

The mysterious component that appears to be the cause of these findings is a protein called GD11 which is normally aplenty in young animal blood and meager in older blood. Naturally, the team at Stanford is clawing away at this amazing discovery in hopes of unearthing an answer to the question of whether or not people who live longer have higher levels of GD11, or whether people with little amounts of the protein prove more liable to develop age-related diseases like heart complication, muscle atrophy and cognitive deterioration.

DOES LONGEVITY HAVE ITS ROOTS TO GREEK MYTH?

At the University of California, San Francisco, another experiment is taking place under the auspices of neurobiologist Dena Dubai and involves a hormone called called klotho. Klotho received its nomenclature after the Greek fate responsible for spinning the thread of life for mortals. Klotho is known for extending the lives of animals by 30% when in increased levels. Approximately 1 in 5 humans carry enough of the protein to tack on an extra 3 or 4 years to their lives and although it is not a passport to the land of immortality, it is certainly a bigfoot-sized step towards that mystical destination.

MORE BIRTHDAYS ON THE HORIZON

On that note, it is important to keep in mind that most – if not all – research is not fixed on the objective of creating neverending lifetimes, rather extending healthy lives a bit longer. While toying around with components like telomeres, klotho, and GD11 offer promising results, it is not as easy as simply whipping up the perfect recipe and stocking up Rite-Aid shelves. Further manipulation of longevity genes could involve some big league moves like gene therapy and cell transplants and of course first solving all of the questions that pop up with each answer a scientist reaches. While these riddles are the culprit for bringing researchers back to the drawing board again and again, the general outlook for battling the effects of aging is remarkably upbeat. Scientists seem to bear a spirited momentum certain to bring about some serious headway in the not-too-distant future.

Janice Bevilacqua