Updated clinical vitamin D guidelines

Michael Holick, MD, Ph.D., told me in a phone interview nearly a year ago that vitamin D insufficiency and deficiency was "one of the most common medical conditions" and has implications on the health of bones, the heart, the immune system, and likely every cell in the body.

Dr. Holick added, "If a normal adult isn’t taking at least 1,500 to 2,000 IU from supplement and diet—and you can’t really get it from your diet—then we know you’re vitamin D deficient."

Now, The Endocrine Society has released new clinical practice guidelines intended to help curtail widespread vitamin D deficiency with extra focus on care for populations who are most at risk.

The guidelines follow on the coattails of last November's updated vitamin D recommendations by the Institute of Medicine (IOM), which several experts have condemned as conservative and inadequate. In response, a "Task Force," led by Dr. Holick, reexamined the evidence and compiled new recommendations to provide a more therapeutic emphasis.

The guidelines call for screening populations at risk for vitamin D deficiency and correcting deficiencies with supplementation at levels high enough to maximize effects on calcium, bone and muscle metabolism.

The Task Force recommends maintaining blood concentrations of 25(OH)2D (the active circulating form of vitamin D) consistently above 30 ng/mL. Circulating blood levels below 30 ng/mL are regarded as "insufficient" and below 20 ng/mL as "deficient".

To assist at-risk individuals with meeting blood levels above 30 ng/mL of circulating vitamin D, the Task Force issued new dietary intake recommendations that differ significantly from those given by the IOM:

• Infants ages 0-1: 400-1,000 IU/day
• Children ages 1-18: 600-1,000 IU/day
• Adults ages 18+: 1,500-2,000 IU/day
• Pregnant or nursing women under 18: 600-1,000 IU/day
• Pregnant or nursing women 18+: 1,500-2,000 IU/day
• Obese children and adults: at least 2-3 times the recommendation for their age group
• Children and adults on anticonvulsants, antifungals and AIDS medications: at least 2-3 times the recommendation for their age group

The Task Force also increased Tolerable Upper Limits for vitamin D to substantially higher levels than what the IOM recommended last fall.

Depression and telomeres

Reference: Wolkowitz et al. 2011 March.

People who suffer from major depression have a higher risk of age-related illness and earlier mortality (1 &2). Researchers from University of California, San Francisco (UCSF), investigated (1) telomere length in depressed individuals versus matched controls and assessed other biological factors associated with telomere shortening.

Led by Nobel laureate Elizabeth Blackburn, Ph.D., the team of researchers published their findings in the March issue of PLos One. Their hypothesis was that not all depressed subjects would show shortened telomeres equally because of a large variance in depressive episodes over a lifetime. However, they predicted that those who suffered from depression for long durations would have shorter telomeres due to longer exposure to oxidative stress and inflammation induced by psychological stress.

The scientists recruited 18 subjects diagnosed with Major Depressive Disorder (MDD), excluding those with psychosis or bipolar histories, as well as those with Post-Traumatic Stress Disorder to eliminate confounding variables due to interferences with stress hormone regulation. Results from depressed individuals were compared to those of the matched control group.

Fitness, hunter-gatherer style

Aché man hunting. Credit: Wiki

“So the bottom line is that foragers are often in good shape and they look it. They sprint, jog, climb, carry, jump, etc all day long but are not specialists.”

The quote above is excerpted from a description given by anthropologist Kim Hill (whose work I've previously written about here) of his experience observing the behaviors of the Aché of Paraguay and the Hiwi of Venezuela. The ASU professor, who has been living and studying the tribes for more than 30 years, recently had his work highlighted in a commentary published in Progress in Cardiovascular Diseases.

The article, whose lead author was James O'Keefe, MD, examines the daily physical activity patterns among hunter gatherers and fossil hominins. According to the authors, ancestral hunter-gatherers expended as much as five times more amounts of energy on physical activity than the average modern sedentary adult.

Based on data from Cordain's earlier work and that of colleagues, the article proposes a cross-training exercise regimen, as opposed to specialized trainings of Olympic athletes, intended to mimic the way of life that is required of a typical hunter gatherer. The "prescription for organic fitness" includes 14 essential features, which the authors suggest "appear to be ideal for developing and maintaining fitness and general health while reducing risk of injury."

How Neandertals Lived, Hunted, and Ate

This Discovery Channel series "Neanderthal" presents a wonderful re-enactment of how Neandertals lived in small groups, how they hunted together, and how they ate.

I was especially taken by how much we know about the way they used tools to butcher meat, scraped animal hides (by holding the hides in their teeth and face as a tool to spread the stress around the skull) for use in making clothing (shown in Part 1).

It's amazing that we know so much about these ancient peoples -- how strong they were, how intelligent, how adaptive, as said in the documentary.

The scientific techniques mentioned that lend to our understanding of Neandertals are studies on fossilized feces, worn-out teeth from scraping animal hides, and bone fractures that reveal injuries that led to illness or death.

Those daily extra cups of joe not linked to hypertension

An extra shot of espresso can surely help wake you up in the morning, but what does it mean for your blood pressure? It is well known that coffee's caffeine content can raise blood pressure temporarily, especially in people who have hypertension. Could habitually drinking high amounts have long-term effects on blood pressure too?

Java lovers will rejoice in a large study's findings that more cups daily isn't associated with increased risk of hypertension. The study, published in American Journal of Clinical Nutrition on March 30, was a systematic review and meta-analysis that examined six prospective cohort studies.

Diagnosing Darwin's multiple gastrointestinal diseases

Charles Darwin (Credit: Wikimedia)

Throughout most of Charles Darwin's adult life, the famed author of On the Origin of Species struggled with repeated episodes of severe abdominal pain, nausea and vomiting that could last for hours at a time, often occurring about three hours after breakfast, and thought to have been brought on by times of emotional stress.

England's physicians of the time could not properly diagnose the syndrome of cyclic vomiting, although they tried by suggesting its etiology was anything to do with allergies, gout, and mental overwork. But what of an assessment of Darwin's symptoms by modern physicians of today?

On Friday, May 6, modern physicians gathered to discuss Darwin's lifelong illness at the 18th Historical Clinicopathological Conference sponsored by University of Maryland Health Care System. The conference previously has examined and provided modern medical diagnoses of other prominent historical figures such as Abraham Lincoln and Edgar Allan Poe. The scientists chose Darwin for this year's conference to commemorate the naturalist's 200th birthday.

At the conference, the medical researchers determined that the nature of Darwin's sickness may be explained by multiple gastrointestinal illnesses he might of contracted while traveling to remote areas of South America, the Pacific, Far East, and Africa. A transmission of parasites, for example, may have led to what would become chronic "Chagas disease" and "peptic ulcer disease," further explaining the onset of Darwin's cardiac symptoms and eventual heart disease.

Getting off the death chair

My stand-up desk

As bipedal apes, our bodies are meant for walking and running, which may have even been a catalyst for eventually bringing about the means of evolving larger brains.

Physical activity is strongly linked to brain performance. The exercise boosts blood flow in the brain and improves our memory and cognitive function. Exercise acts like a trigger for the brain saying, "It's time to be alert, find food, survive." Exercise may even fuel brain power by increasing neurogenesis and also guard against the harmful effects of stress.

Yet now we sit, and sit, and sit. Until the sitting kills us.

This article in the New York Times magazine gives a pretty good description of just what really happens when you sit in that death chair with quotes from Marc Hamilton, an inactivity researcher at the Pennington Biomedical Research Center:

This is your body on chairs: Electrical activity in the muscles drops — “the muscles go as silent as those of a dead horse,” Hamilton says — leading to a cascade of harmful metabolic effects. Your calorie-burning rate immediately plunges to about one per minute, a third of what it would be if you got up and walked. Insulin effectiveness drops within a single day, and the risk of developing Type 2 diabetes rises. So does the risk of being obese. The enzymes responsible for breaking down lipids and triglycerides — for “vacuuming up fat out of the bloodstream,” as Hamilton puts it — plunge, which in turn causes the levels of good (HDL) cholesterol to fall.

Isn't that enough to scare the "sit" out of you? If not, this infographic will do the trick.

Safe weight loss for seniors through diet and exercise

In the United States, the number of obese older adults has reached disturbing heights—now affecting approximately 20 percent of those ages 65 and older—and is only expected to rise as more Baby Boomers become senior citizens.

Weight loss through calories reduction or exercise are generally good for most people as an intervention in obesity, although the appropriateness of these methods has historically been a matter of controversy in older, obese adults.

A major concern with weight loss is the accompanying loss of lean tissue, which can accelerate existing sarcopenia (age-related loss of muscle and strength), and result in reduction of bone mineral density that could worsen frailty. This could lead to greater risk of bone fractures and broken hips. Studies have yet to provide sufficient evidence, one way or another, as to whether or not weight loss provides a true enhancement to quality of life.

Printing organs for transplants

Advances in medicine are allowing us to live longer than ever, but with our older age comes a greater risk that our organs will fail us. In fact, the shortage of organs available for transplant increases by the day, according to Anthony Atala who spoke at TEDMED.

In his talk, posted in March, Atala presents developments in regenerative medicine including new devices that use the same technology of scanners, fax, copy machines and printers. Instead of using ink in their cartridges, they simply use cells.

On stage, Atala shows us how one of these devices works, actually printing a kidney in as little as seven hours. It's mind bending.

I feel as though I'd like to show this video to every person I know. This is our future medicine. This technology will no doubt keep us living longer than ever. One day, like salamanders, we will be growing our own organs whenever needed -- kidneys, livers, lungs, etc.

Can you even imagine? Eat and drink whatever you like, ruin your liver and kidneys, then have new ones printed in all but a few hours, and you're as good as new?

It's almost sickening.

News that "Nutcracker Man didn't eat nuts" isn't exactly news

Photosimulation montages of "Nutcracker Man's" dental microwear. Reference: Ungar et al. PLoS One 2008. 

Because of a huge jaw and large, flat molars, Paranthrapus boisei was nicknamed Nutcracker Man and thought to have eaten a diet comprised largely of hard nuts and seeds.

But, it turns out, the hominin species who in evolutionary terms has been likened to our great uncle was more likely to have eaten soft fruits, leaves and grass, according to carbon stable isotope data just published in PNAS by Thure Cerling and his team from University of Utah.

See more about Cerling's paper on John Hawks's blog.

A big deal has been made of this new paper and rightly so, but reporters should also note that the findings are a confirmation of what was already supposed based on dental microwear (shown above) almost exactly three years ago.

On 30 April 2008, Peter Ungar and colleagues at University of Arkansas also told us Nutcracker Man didn't eat nuts in a study in PLoS One (and featured by @9brandon in Wired Science here) citing wear and tear on the hominin's teeth that looked nothing like that of what would've been produced by hard foods.

Michael Ruse on "Origins of Human Evolution"

Michael Ruse

Why were the great Greek philosophers (including Plato and Aristotle) firmly set against the idea of natural origins? Why were they so adamant that natural origins were impossible? According to Michael Ruse, a philosopher of biology at Florida State University, the reason is the problem of "final causes."

Aristotle, for example, "could not see how something like this could come about through blind law," said Ruse in a lecture given at Arizona State University’s Origins Project Science and Culture Festival on April 7, 2011.

This is why, for good scientific reason, said Ruse, they turned their back and rejected the idea of natural origins.

What was the big move? Robert Boyle particularly put his finger on it, said Ruse, we’ve changed the thinking of the world as an organism, to the world as a clock. This was a new metaphor for the world—the world is at some level a machine.

Resveratrol Improves Insulin Sensitivity in Humans

Low-dose supplementation of resveratrol daily may reduce oxidative stress and improve the body's sensitivity to insulin, a study from University of Pecs in Hungary suggests.

In a double-blind, placebo-controlled study published in the British Journal of Nutrition, Hungarian researchers report observations that people with type 2 diabetes who take 5 milligrams of resveratrol twice daily improved their sensitivity to insulin after only our weeks.

"The present study shows for the first time that resveratrol improves insulin sensitivity, which might be due to a resveratrol-induced decrease in oxidative stress that leads to more efficient insulin signaling via the Akt pathway," the authors concluded.

The Akt pathway is a pathway involved in cellular uptake of glucose in response to insulin—it induces glucose transport, particularly into muscle cells. When working properly, insulin stimulates cells to take in glucose from the blood stream, thereby lowering circulating glucose levels and providing carbohydrate for the cells for energy production.

In this study, the researchers randomized 19 Caucasian male participants with type II diabetes into two groups. The intervention group received 5 milligrams of resveratrol, twice daily for four weeks. The control group received a placebo twice daily.

By the fourth week, the intervention group showed significantly reduced oxidative stress and increased levels of phosphroylated Akt, indicating improved insulin sensitivity. Similar studies also documented a glucose-lowering effect of resveratrol in diabetic rodents.

Resveratrol, a naturally occurring compound found in grapes and other foods, is also famed because of evidence as an anti-aging bioactive and an aid in weight management.

Reference

Brasnyo P, Molnar GA, Mohas M et al. Resveratrol improves insulin sensitivity, reduces oxidative stress and activates the Akt pathway in type 2 diabetic patients. Br J Nutr 2011;1-7.

Calcium: U.S. adults still not getting enough

A new study suggests most U.S. adults continue to fail to get enough of the mineral through diet and supplementation to meet recommended levels.

University of Connecticut and Yale University researchers examined data from National Health and Nutrition Examination Survey collected from 9,475 adults between 2003 and 2006. They found that, although dietary calcium intake was reported highest in older age groups, the amounts remained insufficient to meet adequate intake standards for age groups 50 years and older.

These inadequate intakes come despite the fact that more than half of individuals ages 19 and older were taking a calcium supplement, according to the authors. For men, supplementation increased from 34 percent in the 19 – 30 age group to 54 percent in the 81 and older age group. The percentage of women taking supplements rose from 42 percent to 64 percent across the same range of age groups.

"Adequate lifelong calcium intake is essential to optimizing bone health," remind the study authors, who published their findings in the May 2011 issue of Journal of American Dietetic Association. They also recommend "new approaches to increasing the frequency and level of calcium supplement use to enhance calcium density in diets."

Calcium is the most abundant mineral in the body, primarily found in the bones and teeth. As bones develop, calcium, along with other minerals, crystallizes on the collagen matrix of the bone, making it denser and giving it strength and rigidity. The body loses calcium continuously, and if this loss is not replaced through diet, the body will remove calcium from the bones to perform necessary functions such as regulation of muscle contraction. This removal causes bones to become soft and brittle, making them prone to fractures.

Adequate calcium intake is necessary for strong and healthy bones. The current recommended intake of calcium is between 1,000 mg and 1,300 mg per day. Good sources (more than 300 mg per serving) of calcium include dairy products such as low-fat milk, cheese, and yogurt. Dark green vegetables such as broccoli, kale, and spinach can also add about 90 milligrams of this mineral to daily intake. In addition, calcium-fortified foods (orange juice and breakfast cereals) and dietary supplements can also help fill gaps.
Other important factors in optimizing bone health include engaging in weight-bearing exercise and obtaining recommended amounts of vitamins D and K2 daily.

Reference: Mangano KM, Walsh SJ, Insogna KL, Kenny AM, Kerstetter JE. Calcium Intake in the United States from Dietary and Supplemental Sources across Adult Age Groups: New Estimates from the National Health and Nutrition Examination Survey 2003-2006. J Am Diet Assoc 2011;111:687-95.

Thoughts:

Time and time again, studies have shown that calcium when combined with vitamin D are effective in increasing bone density. However, there's been a lot of back and forth in the calcium world around the topic of supplements, particularly their efficacy and safety. A critical piece lacking in the conversation is of absorption since calcium is one mineral that depends on a few factors -- vitamin D, doses that oversaturate absorption, too much absorbed at once.

The best approach for obtaining calcium is perhaps to consume it as we would have back in the time of our hunter-gatherers ancestors before the agricultural revolution and pastoralism, which is by getting a little here and a little there when we only obtained it from the leaves of plants. That's not to say that we should only get it from plant leaves, but that we should get it in smaller amounts in sustained fashion over the course of a day.

Wake up, Neo-evolution

What would you change about your own naturally evolved, naturally flawed body? Would you choose genetics to avoid diseases like Alzheimer's, diabetes, and cancer? Would you enhance your brain to increase memory and to boost creativity? Would you choose more fast-twitch muscle fibers to run faster or longer? Would you live longer?

These are the questions that Harvey Fineberg, president of the Institute of Medicine, discusses in this new TED talk given in March that was posted only this month. Fineberg says that a new era of neo-evolution -- in which we, as humans, could guide the selection of traits that would define the course of humanity -- is upon us, and he called it "exciting," but "frightening."

I want to answer all of his questions with a "Yes, sign me up!" Who is insane enough to reject a world with an absence of disease, of aging, of dying and death?

Apparently, there are quite a few people. Hava Tirosh-Samuelson, professor of history at Arizona State University, is one of them. Earlier this month, at ASU's Origins Project Science and Culture Festival Tirosh-Samuelson was speaking about a completely different topic when she suddenly surprised us with a few critical words of the "so-called trans-humanist movement."

In a nutshell, her argument is that we still haven't a clue of what humanity is to begin with, so reason suggests against trying to define what it should be in the future. Naturally, after her talk, I decided to ask Tirosh-Samuelson a few questions about her views.

Health at Telomere's Length

A health checkup could soon incorporate a telomere measurement to estimate a person's biological age as a superior indicator of age-related degeneration and vulnerability to disease than chronological age, reports Mitch Leslie in an article entitled, "Are Telomere Tests Ready for Prime Time," published in Science magazine today.

The article reports that two companies have announced plans to start performing tests for the general public this year: Life Length of Madrid has already began offering the tests to patients and Telome Health, of Menlo Park, Calif., will begin to make them available to clinicians sometime later this year.

Already, medical researchers have employed telomere measurement for predicting illness and tailoring treatments to save lives, yet the article reports that skepticism exists about how effective telomere tests will be in predicting disease or determining lifespan in a clinical setting.

"By curtailing self-renewal, worn-down telomeres might promote the senescence of our bodies—although how much has been controversial," writes Leslie.

On one side of the issue is Telome Health co-founder Elizabeth H. Blackburn, a cell biologist at University of California, San Francisco (UCSF), who is quoted as saying "Telomeres are an integrative indicator of health."

Carol W. Greider, a former graduate student in Blackburn's lab and a molecular biologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, disagrees saying, “Do I think it’s useful to have a bunch of companies offering to measure telomere length so people can find out how old they are? No.”

In 2009, Blackburn and Greider were awarded the Nobel Prize in Physiology or Medicine, along with Jack W. Szostack, for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase.

Telomeres are comprised of non-coding, repetitive sequences of coiled DNA that serve as protective caps at the end of chromosomes, preserving their integrity and keeping them from fraying and sticking to each other.

Shortened telomeres are linked with a greater chance of developing cardiovascular disease, diabetes, Alzheimer's disease, and other chronic diseases. In the last few years, studies have also showed that the rate of telomere shortening can be strongly affected by diet and lifestyle.

According to the article, among factors that affect telomeres harshly are smoking, drinking heavily, obesity, and chronic psychological stress. On the other hand, meditation, exercise, a healthy diet, and higher blood levels in omega-3 fatty acids offer a buffer to help maintain longer telomeres.

The enzyme telomerase, which plays a role in helping to maintain telomere length, is a recognized target of pharmaceutical-nutraceutical companies for producing possible therapies in the future.

Stress Awareness Month and the baboon inside you

I love to read about Robert Sapolsky's baboons. They give me a kind of peace -- the kind received when you succeed in letting go of a stressful situation by thinking, "we're all just a bunch of baboons."

What you get from Sapolsky's books, apart from its enjoyable wittiness, is a unique snapshot on how baboons are affected by stress, which is more or less the same way that we are affected by stress. Only, while baboons are stressed occasionally -- by a more dominant baboon or to escape a predator, for example -- we humans have built ourselves an environment where we're stressed chronically.

What African Americans should know about vitamin D and heart health

A while back, I was talking with a friend of mine. He was a giant of a black man and we spoke about his  blood pressure woes and his weight issues. So I asked him about his diet, his habits, and all that. He told me all about it: How he ate all the right foods, how he was trying to avoid the wrong ones, and how he recently started walking on his treadmill.

I said to him, "What do you do all day?"

He said, "I'm in the office all day."

"What do you do at lunchtime?"

"I usually have a protein shake or eat a salad with some chicken."

That's good, I tell him. But I want you to do one more thing. It's easy. While or after you eat, take a walk. Outside. In the parking lot. Once or twice a week.

OK, he says. "But why outside?"

I said, "Sunlight and vitamin D." Then, I told him a story we should all be familiar with by now, which went something like this:

Darker skin is a result of greater production of a pigment called melanin that rewards skin with a natural protection against ultraviolet light. Ultraviolet light would otherwise burn skin, destroy the body's stores of nutrients like folic acid that are needed for refurbishing DNA, increase risk of neural tube defects among other reproductive problems, and also raise risk of skin cancer.

So, in short, melanin is a good thing. Near the equator, with strong UVB rays aplenty to compensate slower vitamin D production, darker skin offers an evolutionary advantage that would only serve to sustain naked humans. But, as often is the case, reward comes with recompense. The downside of higher amounts of melanin is that the pigment interferes with the skin's ability to absorb enough UVB rays to activate Vitamin D's pre-cursor into a full-fledged hormone.
As is well-documented, humans at higher latitudes with dark skin would never have survived over the generations without shedding the extra melanin and opting for a lighter color. Lighter color would afford more UVB absorbed, more D created, stronger bones and, as evidence emerges to show, better cardiovascular health. During summer months, lighter-skinned humans who had migrated to higher latitudes collected vitamin D in fat as they gained weight, then released it into the bloodstream when they shed weight during sunlight-lacking winter months.


On the other hand, when darker-skinned humans live in a Northern latitudes of the United States -- as African Americans do -- you can bet that problems will arise.

Then, I gave him some details about asking his doctor for a 25-hydroxyvitamin D test.

A couple of weeks later, I spotted him outside walking around a parking lot. He tells me, "Thanks so much, David. I had no idea about vitamin D. Plus, my doctor says the walking and the vitamin D are helping my heart."

While attending Experimental Biology (#eb2011) over the weekend, one of the presentations had me thinking about my friend. And that was Richard Harris, Ph.D., of Georgia Health Sciences University in Augusta, presenting a study on vitamin D supplementation in African Americans.


What Dr. Harris and his fellow Georgia researchers found was that vitamin D supplementation in overweight African American adults in a single dose of 60,000 IU every for four weeks every 16 weeks improved blood vessel endothelial function – the equivalent of 2,000 IU since vitamin D has a half life of about three weeks.

It was notable that they used overweight adults, since extra weight can increase blood volume, raise blood pressure, resulting in rigid, inflamed vessels. Details are that the researchers used an inflatable cuff to increase blood flow in the brachial arteries of each of the participants, then an ultrasound to measure flow-mediated dilation.

What exactly vitamin D was able to do is what Dr. Harris calls the "million-dollar question," according to this press release. But it's likely that the hormone acted directly on endothelial cells, on a receptor perhaps, that helps dilate blood vessels when needed. The more dilation, the easier it is for blood to flow through vessels.

This study is great news, especially for this population at higher risk for cardiovascular disease factors like higher blood pressure. However, there is still too little vitamin D deficiency awareness.

Here's what I say, Why not teach African Americans why they have a greater need for vitamin D from an evolutionary perspective?

In the case of my friend, it really helped put things in perspective. There's an easy solution for this mess, which is to take a walk around the block for a few minutes when UVB rays are out (mostly just in summer months) or, simply, by just taking a vitamin D supplement as they did in the summer. Lots of benefits to come from such an easy habit of getting D daily like better blood pressure along with better bone health.

Another thing is that the Institute of Medicine's recommended daily intakes of vitamin D (although they are based as if there were no sun-produced D at all) just make little sense when they don't treat all adults the same, not bringing high-risk groups into consideration. Until more research is available and the IOM can build on current guidelines by raising them for high-risk groups, African Americans should take health into their own hands by getting tested to make sure they keep 25-hydroxyvitamin D in healthy ranges continually.   

Fusing aging theories: Telomere shortening causes mitochondrial dysfunction

New research is adding insight and linking three theories of aging—one that suggests telomere shortening governs lifespan, and two others that suggest dysfunctional mitochondria or oxidative stress leads to aging.

At Harvard-affiliated Dana-Farber Cancer Institute, scientists have gathered data suggesting telomere shortening is the cause of mitochondrial dysfunction and diminished antioxidant defenses. Together, they decrease the body’s energy and diminish organ function, both characteristic of old age.

As telomeres—protective caps at the end of cell chromosomes—shorten with age and begin to fray, cells activate the p53 gene, which signals an “emergency shutdown” chain of events that turns off normal cell growth and division and compromise antioxidant defenses. Going one step further, data from the carefully orchestrated mouse study, published in Nature, show that the p53 gene also represses PGC1-alpha and PGC1-beta. These PCGs are considered the master regulators of metabolism and mitochondrial function.

Repressing PCGs increases the number of dysfunctional mitochondria (with mutated mitochondrial DNA) and leads to a decrease in functional mitochondria distributed throughout in muscles and organs. The dysfunctional mitochondria in aged tissues leak greater amounts of reactive oxygen species and the lack of functional mitochondria hinders normal energy production from cell respiration (the body’s main producer of ATP energy).

“What we have found is the core pathway of aging connecting several age-related biological processes previously viewed as independent from each other,” said Ronald A. DePinho, M.D., a cancer geneticist and senior author of the paper, in a press release.

“Because telomere dysfunction weakens defenses against damage by free radicals, or reactive oxygen species,” Dr. DePinho said, “we think this exposes telomeres to an accelerated rate of damage which cannot be repaired and thereby results in even more organ deterioration. In effect, it sets in motion a death spiral.”

In an article also published in the same issue Nature, Daniel P. Kelly, M.D., scientific director and professor at Burnham Institute for Medical Research-Lake Nona, Orlando, Florida, said that the “intriguing study… unveils a potentially unifying mechanism for cellular ageing.”

Mitigating the Toll of Aging

The new study further supports current thinking that the best defense against aging is to reduce the adverse affects of overproduction of free radicals produced from dysfunctional mitochondria, which cause additional oxidative stress.

Dr. DePinho said, “The findings bear strong relevance to human aging, as this core pathway can be directly linked to virtually all known genes involved in aging, as well as current targeted therapies designed to mitigate the toll of aging on health.”

Those current targeted therapies include boosting the human body’s antioxidant defenses by eating a healthy diet, reducing calories (by around 25 percent), and supplementing with antioxidant vitamins C and E, as well as with green tea, CoQ10 and resveratrol. These practices not only help to protect against oxidative stress, thereby protecting against telomere shortening, but also help boost generation of new, healthy mitochondria.

When we asked telomere biologist Bill Andrews, Ph.D., to comment on the new study, he answered that it was “tremendous news,” as it supports the need for more research into management of telomeres by activating the genetic expression of the enzyme telomerase, which re-lengthens telomeres.

Dr. Andrews wrote, “It’s the best support ever for the fact that telomere elongation’s role in aging far exceeds the roles played by mitochondria and oxidative stress.” In effect, telomere shortening is the root cause of the others.

Mitochondria become dysfunctional when telomeres shorten and fray, a new study suggests. In an article to be published in a forthcoming issue of IsaNews magazine, Dr. Andrews writes, “Mitochondrial dysfunction causes aging—but telomere shortening has turned out to be the primary cause of mitochondrial dysfunction. And humans’ natural defenses against oxidative stress are really quite exceptional (for example, our cells produce ten times more superoxide dismutase, a potent natural antioxidant, than mice)—until telomere shortening begins to degrade those defenses inside our bodies.”

He added that while “anti-aging therapies of years past merely treated the symptoms of aging. New research is devoted to identifying a new class of therapies that treat aging at its root cause, and hold great promise of one day allowing us to feel young and healthy at 120 years of age and beyond.”

An earlier study, of which Dr. DePinho was also the senior author, gives testimony to the benefits of telomerase, as found in mice that were genetically engineered to produce the enzyme. The study found that when the telomerase was restored in the mice, their age-related symptoms disappeared and several organs including the brain were rejuvenated.

References:

Kelly DP. Cell biology: Ageing theories unified. Nature 2011;470:342-3.

Sahin E, Colla S, Liesa M et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011;470:359-65.

Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature 2010;464:520-8.

Jaskelioff M, Muller FL, Paik JH et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature 2011;469:102-6.

Potassium iodide: Why you should avoid it

Ever since the news of Japan's nuclear crisis, there have been several claims made over the Internet that have panicked people in the U.S. about potential exposure to radiation (one culprit is this viral e-mail), which has led to me being the recipient of questions about whether or not people should be taking potassium iodide supplements to avoid absorption to radioactive iodine.

Should you take potassium iodide pills? My answer has been an unequivocal, "No, it's not necessary. There is little risk of any level of radiation exposure to worry about anywhere else other than in Japan near the reactors. If you're worried about getting cancer, try thinking more about losing weight, eating more dietary fiber, and eating more fruits and vegetables."

In the process of answering questions, I did find myself interested in learning more about radiation and health. By far the best, most in-depth article I've read on "How Radiation Threatens Health" is this one written by Nina Bai and published by Scientific American. Bai's article gives readers an excellent understanding on the typical radiation levels that people are currently exposed to (0.2 to 0.3 milliSieverts), how much they are exposed to by a typical CT scan (1 milliSievert) and what kinds of levels people should really be worried about—the kind of levels that lead to symptoms of radiation sickness ("a whole body dose of 3 sieverts, that is, 3,000 times the recommended public dose limit per year") and the kind that kills people within weeks (5 to 10 sieverts).

Yes, there are concerns over low-dose radiation over time, but as Bai's article points out, the increase of cancer risk is small and basically comes out to about an increase of eight potential cancer cases per 10,000 people. And, the point is that even if any radiation made it over the ocean and to the U.S. (which is unlikely) it would be at levels too low to cause concern.

As for potassium iodide (KI) supplements (not addressed in Bai's article), there is cause for concern because I keep reading that these are "flying off the shelves" in various articles.

The way KI works is by flooding iodine into the thyroid gland to become trapped by the thyroid's receptors, which blocks the uptake and accumulation of radioiodine that could lead to possible thyroid diseases or cancer. This is particularly important in children who are more at risk for radioiodine-induced cancer (as is what happened with the Chernobyl incident because of radioiodine0contaminated milk). The doses for preventing radioidine uptake are high: 50 to 100 milligrams for adults. If exposure is pretty certain, then supplementation with these pills make sense.

But consider that the Upper Limit for adults is 1.1 milligram per day. These pharmacologic doses could be potentially detrimental since excessive iodine can actually lead to hyper- or hypothyroidism and have been known to increase risk of thyroid cancers. Taking these doses should not be considered a safe precautionary measure, as marketed. There is a risk!

My concern is this: that the irresponsible Internet claims are leading people to actually take the high doses of the KI and that retail outlets selling them (like this one with 130 milligram per tablet!) are doing so without giving people any sense of what the risks are when taking high amounts.

Vitamin K2: Building bones while beating back arterial calcification

Vitamin K2's time to shine has come—move over vitamin D! Once only known for its role as a "koagulation" factor in blood clotting, vitamin K2 is emerging as another fundamental anti-aging nutrient. While vitamins D and E have garnered the majority of interest in the last decade, the impact of vitamin K2 on aging bones and hearts demands that we give it equal attention.

Whereas most vitamin and mineral supplements use vitamin K in its form of K1 (phylloquinone sourced from plants) because it is easily available and cheap, it is the natural form of K2 (menaquinone sourced from friendly bacteria) that is the most biologically active and shown to enhance both bone formation and vascular health.

The full compilation of recent research underscores the idea that K1 and K2 should be appreciated as separate nutrients with distinct physiological actions and benefits. K1 is the more familiar vitamin known for its key role in directing blood-clotting in the body and the one given as a shot at birth (a common practice in many countries to curtail hemorrhage incidents in newborns.) The picture for K2 seems to be a bit more varied and is key in regulating calcium balance.

Vitamin K2 acts by activating the bone-building hormone (carboxylating osteocalcin) to clear calcium from the arteries and use it in bone mineralization. It effectively removes calcium that would otherwise end up deposited in arterial plaques. Since protecting arteries and soft tissues from calcification is one of the most important ways to stave off the ravages of aging on the body, consuming enough vitamin K2 daily is key for a long, healthy life.

Getting Enough K2

Because vitamin K2 is synthesized by friendly bacteria in the intestine, nutrition scientists have long assumed that that deficiencies were rare. However, new data are showing that intestinally synthesized vitamin K is not absorbed as easily as previously thought. Vitamin K also preferentially accumulates in the liver where it does have a clotting factor role.

In fact, once overlooked because "time to clot" was the test for vitamin K status, it is here where we are now seeing new signs of vitamin K deficiency previously only seen with vitamin D deficiency—fragile, brittle bones and increased fractures—even with adequate calcium and vitamin D.

Most people in North America should increase amounts consumed daily. The evidence finds that only with much higher intake do bone cells get their share and the same holds true for removal of calcium in arteries.

People can obtain enough vitamin K2 by eating plenty of fermented foods such as cheese, sauerkraut, and natto (a traditional Japanese soy-based food). Supplementation is another viable option as achieved with a quality multivitamin.

Regardless of how one gets it, it’s important not to underestimate value of this underdiscussed nutrient and to understand that most people are not getting enough. Consuming sufficient amounts of K2 along with a healthy diet will increase odds of a healthier life with clear arteries and stronger bones.

Sources

McCann and Ames. Vitamin K, an example of triage theory: is micronutrients inadequacy linked to diseases of aging?. Am J Clin Nutr 90:889-907, 2009.
Vitamin K2. Monograph. Alternative Medicine Review 14(3):284-293, 2009.
Koitaya. Et al. Effect of low dose vitamin K2 (MK-4) supplementation on bioindices in postmenopausal Japanese women. J Nutr Sci Vitaminol. 55:15-21, 2009.
Gast, et al. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovas Dis 19:504-510, 2009.
Shea, et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr 89: 1799-1807, 2009.
Shea MK, Booth SL Update on the role of vitamin K in skeletal health. Nutr Rev 66(10):549-57, 2008.