Testosterone decline associated with increased mortality risk

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Men experiencing a pronounced, age-related decline in testosterone level are more likely to die of any cause during a 15-year period vs. men who have testosterone levels in the 10th to 90th percentile, according to findings reported in the European Journal of Endocrinology.

Stine A. Holmboe, MSc, a doctoral student in the department of growth and reproduction at the University of Copenhagen, Denmark, and colleagues analyzed data from 1,167 men aged 30 to 60 years participating in the Danish Monitoring Trends and Determinants of Cardiovascular Disease (MONICA1) study, conducted between November 1982 and February 1984, as well as the follow-up examination 10 years later (MONICA10), conducted between 1993 and 1994. Researchers measured levels of testosterone, sex hormone-binding globulin and luteinizing hormone at baseline and follow-up, and then followed the cohort for up to 18 years (mean, 15.2 years) using data from national mortality registries. Researchers used Cox proportional hazard models, with age as the underlying time scale, to assess the association between intra-individual hormone changes and all-cause, CVD and cancer mortality.

During follow-up, 421 men (36.1%) died (106 cancer-related deaths; 119 CVD-related deaths). The estimated mean intra-individual percentage change in hormone levels per year for the cohort were –1.5% for total testosterone, 0.9% for SHBG, –1.9% for free testosterone and 1% for luteinizing hormone. When estimated cross-sectionally, however, mean percentage changes in hormone levels per year were –0.4% for total testosterone, 1.2% for SHBG, –1.1% for free testosterone and 1.1% for luteinizing hormone, according to researchers.

Researchers observed that men who experienced the most pronounced decline in total testosterone — men in the lowest 10th percentile — saw the greatest increased risk for all-cause mortality (HR = 1.6; 95% CI, 1.08-2.38) vs. the reference category. The risk corresponded with an annual total testosterone decline of at least –0.6 nmol/L.

Across tertiles of SHBG levels, researchers found no significant differences in all-cause mortality; however, there was a U-shaped trend observed, with increases in all-cause mortality for those with a change in SHBG levels below the 10th percentile (< –0.7 nmol/L per year) or above the 90th percentile (> 1.1 nmol/L per year) vs. the middle group.

Men with the most pronounced decline in free testosterone also saw an increased risk for all-cause mortality; however, this was significant only in the tertile model (HR = 1.45; 95% CI, 1.09-1.92), according to researchers. There were no disease-specific associations observed, and associations were independent of age, baseline hormone levels and lifestyle factors.

“A possible causal link between an increased tempo in age-related [testosterone] decline and subsequent health is unknown and remains to be investigated,” the researchers wrote. – by Regina Schaffer

Article Source: https://www.healio.com/endocrinology/reproduction-androgen-disorders/news/in-the-journals/%7Bb9ffabec-a385-4c19-b01b-4981f05e01d1%7D/testosterone-decline-associated-with-increased-mortality-risk

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The Benefits of High Cholesterol

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People with high cholesterol live the longest.

This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance.

Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers.

Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.

Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite.

But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis.

To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease.

This was the result of my search in the Medline database for studies addressing that question.

Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.

Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 and that almost all studies have found that high cholesterol is not a risk factor for women.

This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.

But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both.

This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.

High Cholesterol Protects Against Infection

Many studies have found that low cholesterol is in certain respects worse than high cholesterol.

For instance, in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.

Most gastrointestinal and respiratory diseases have an infectious origin.

Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection?

To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years.

At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.

This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered?

Isn´t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.

Written By: Uffe Ravnskov, MD, PhD

Article Source: https://www.functionalmedicineuniversity.com/public/924.cfm

 

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Exercise can boost brain power, prevent heart damage

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Looking for a magic elixir for health? There’s more evidence exercise may be it, improving thinking skills in older adults and protecting against heart damage in obese people, two separate studies published Monday show.

“Exercise has many, many benefits. … I don’t know that we fully understand why it has so many beneficial effects for so many organs and systems,” Dr. Roberta Florido, a cardiology fellow at the Johns Hopkins Hospital, told TODAY, as she listed some of the other known benefits, including improving depression, lowering blood pressure and strengthening muscles.

“We should do a better job of telling our patients to exercise,” she added.

In the first paper, published in the British Journal of Sports Medicine, researchers at the University of Canberra in Australia analyzed 39 previous studies looking into the effect of exercise on thinking skills in people over 50. That included things like memory, alertness and the ability to quickly process information.

They found physical activity improved all of those skills regardless of a person’s cognitive status.

The key was 45-60 minutes of moderate to vigorous exercise per session “on as many days of the week as feasible.” A combination of both aerobic exercise and resistance training worked best.

Each type of exercise seemed to have different effects on the factors responsible for the growth of new neurons and blood vessels in the brain, said co-author Joe Northey, a PhD student at the University of Canberra Research Institute for Sport and Exercise.

Tai chi was also helpful, though more evidence is needed to confirm this effect, the researchers note.

“Age is a risk factor no one can avoid when it comes to cognitive decline,” Northey said. “As our study shows, undertaking just a few days of moderate intensity aerobic and resistance training during the week is a simple and effective way to improve the way your brain functions.

Written By: A. Pawlowski

Article Source: http://www.today.com/health/exercise-can-boost-thinking-skills-protect-against-heart-damage-t110740

 

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Testosterone Replacement May Lower Cardiovascular Risks

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Testosterone replacement therapy (TRT) is associated with a lower risk of adverse cardiovascular (CV) events among men with testosterone deficiency, according to a new study.

Researchers led by T. Craig Cheetham, PharmD, MS, of the Southern California Permanente Medical Group, identified a retrospective cohort of 44,335 men aged 40 years and older with evidence of testosterone deficiency. The cohort included 8808 men who had ever been dispensed testosterone (ever-TRT group) and 35,527 men never dispensed testosterone (never-TRT group). The primary outcome was a composite of cardiovascular endpoints that included acute myocardial infarction (AMI), coronary revascularization, unstable angina, stroke, transient ischemic attack (TIA), and sudden cardiac death (SCD).

After a median follow-up of 3.2 years in the never-TRT group and 4.2 years in the ever-TRT group, the rates of the composite endpoint were significantly higher in the never-TRT than ever-TRT group (23.9 vs 16.9 per 1000 person-years), Dr Cheetham and colleagues reported online ahead of print in JAMA Internal Medicine. After adjusting for potential confounders, the ever-TRT group had a significant 33% lower risk of the primary outcome compared with the never-TRT group. The investigators found similar results when looking separately at combined cardiac events (AMI, SCD, unstable angina, coronary revascularization) and combined stroke events (stroke and TIA). The ever-TRT group had a significant 34% and 28% lower risk of cardiac events and stroke events compared with the never-TRT group, respectively.

“While these findings differ from those of recently published observational studies of TRT, they are consistent with other evidence of CV risk and the benefits of TRT in androgen-deficient men,” the investigators wrote.

Previous studies have found an association between low serum testosterone levels in aging men and an increased risk of coronary artery disease as well as an inverse relationship between serum testosterone and carotid intima thickness, Dr Cheetham’s team pointed out.

The never-TRT and ever TRT groups had a mean age of 59.8 and 58.4 years, respectively. In the never-TRT group, 13,824 men (38.9%) were aged 40 to 55 years, 10,902 (30.7%) were aged 56 to 65 years, and 10,801 (30.4%) were older than 65 years. In the ever-TRT group, 3746 men (42.5%) were aged 40 to 55, 2899 (32.9%) were aged 56 to 65 years, and 2163 (24.6%) were older than 65 years. The groups were similar with respect to race and ethnicity composition.

The researchers defined testosterone deficiency as a coded diagnosis and/or a morning serum total testosterone level below 300 ng/dL.

With regard to study limitations, the investigators noted that their criterion for identifying men with testosterone deficiency (a diagnosis or at least 1 morning testosterone measurement) does not meet the strict criteria established by the Endocrine Society. “Therefore some individuals in the study could be misclassified as being androgen-deficient.” In addition, as the study was observational in design, “unmeasured confounding may have had an influence on the results; unmeasured confounders could possibly influence clinicians to selectively use testosterone in healthier patients.”

In an accompanying editorial, Eric Orwoll, MD, of Oregon Health & Sciences University in Portland, commented that while the study by Dr Cheetham’s group “provides reassuring data concerning the effects of testosterone on cardiovascular health, convincing answers about this question—and other safety issues like prostate health—remain elusive and will require large, prospective randomized trials.

“At this point, clinicians and their patients should remain aware that the cardiovascular risks and benefits of testosterone replacement in older hypogonadal men have not been adequately resolved.”

Reference

1. Cheetham TC, An JJ, Jacobsen SJ et al. Assocation of testosterone replacement therapy with cardiovascular outcomes among men with androgen deficiency. JAMA Intern Med 2017; published online ahead of print. doi: 10.1001/jamainternmed.2016.9546

Jody A. Charnow, Editor

Article Source: http://www.renalandurologynews.com/hypogonadism/testosterone-deficiency-treated-trt-may-reduce-cardiovascular-events/article/639486/

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What causes heart disease

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As 2016 draws to an end, I believe that a change is in the air. The dietary guidelines, or perhaps I should call them the ‘dietary misguidedlines’, are under a sustained attack. This, finally, may actually result in success. We will be able move on from believing that fat, or saturated fat, in the diet is responsible for cardiovascular disease or, indeed, any form of disease.

But where to then? The current dogma is that saturated fat in the diet raises cholesterol levels and this, in turn, leads to cardiovascular disease. However, as many of you may have spotted earlier this year, in the Minnesota Coronary Experiment (MCE), substituting saturated fat with polyunsaturated fat was effective at lowering cholesterol levels. However, it had absolutely no effect on deaths for heart disease, and greatly increased the overall risk of death.

The summary of this trial was, as follows:

  • It involved 9423 women and men aged 20-97
  • A cholesterol lowering diet was used, replacing saturated fat with linoleic acid (from corn oil and corn oil polyunsaturated margarine).
  • The low saturated fat group had a significant reduction in serum cholesterol compared with controls.
  • There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts.
  • For every 0.78mmol/l reduction in serum cholesterol [Around a 20% reduction], there was a 22% higher risk of death [This is about a 30% reduction in cholesterol level]

Big deal, you might think. This is just one trial, so what difference does it make. However, this was no ordinary trial. It was absolutely pivotal for four main reasons:

  • It was the largest controlled trials of its kind ever done. That is, substituting saturated with polyunsaturated fats.
  • It was done by Ancel Keys (who started the entire diet-heart hypothesis in the first place)
  • It was finished, before the main clinical nutritional guidelines were developed
  • It was not published at the time, for reasons that have never been explained, by anyone.

As the authors of the re-analysis note.

Whatever the explanation for key MCE data not being published, there is growing recognition that incomplete publication of negative or inconclusive results can contribute to skewed research priorities and public health initiatives. Recovery of unpublished data can alter the balance of evidence and, in some instances, can lead to reversal of established policy or clinical practice positions.” 1

Which is a polite way of saying that a bunch of liars hid the results. Almost certainly because the results contradicted their self-promoted message that saturated fats are unhealthy. It is clear that these researchers, in particular Ancel Keys, did this quite deliberately, and then continued to promote their own dietary dogma.

I think it is almost impossible to overestimate the long-term impact of the non-publication of this trial.

  • For want of a nail the shoe was lost.
  • For want of a shoe the horse was lost.
  • For want of a horse the rider was lost.
  • For want of a rider the message was lost.
  • For want of a message the battle was lost.
  • For want of a battle the kingdom was lost.
  • And all for the want of a horseshoe nail.

Here is my updated version

  • For want of the MCE trial evidence the McGovern hearings were lost
  • For want of the hearings the guidelines were lost
  • For want of the guidelines the message was lost
  • For want of the message battle was lost
  • For want of the battle saturated fat was lost
  • All for the want of the MCE trial data.

The McGovern hearings which set the entire direction of nutritional thinking, and guidelines, took place in 1977. The MCE trial ran from 1968 to 1973. Had the data from this study been made available, the dietary guidelines in the US, the UK and the rest of the world (In their current form, demonising saturated fat) simply could not have been written.

If those guidelines had not been written, then the entire world of cardiovascular research would almost certainly have gone off in a different direction. The role of LDL in causing CVD would have been consigned to the dustbin history. Goldstein and Brown wouldn’t have done their research on Familial Hypercholesterolaemia, statins would never have been developed, and we not have been forced to endure fifty years of the damaging, destructive diet-heart/cholesterol hypothesis.

The fact that the diet-heart/cholesterol hypothesis is complete nonsense, has been clear as day to many people for many years. In 1977 George Mann, a co-director of the Framingham Study, writing in the New England Journal of Medicine called it ‘the greatest scam in the history of medicine.’ In my view, anyone with a moderately functioning brain, can easily see that it is nonsense.

So, if not fat and cholesterol, what does cause cardiovascular disease, and more importantly, what can be done to prevent it, or at least delay it? At last (some of you are thinking) I will state what I believe to be one of the most important things you can do to reduce the risk.

Returning to the central process of cardiovascular disease (CVD), for a moment. If you are going to reduce the risk of cardiovascular disease, you must do, at least, one of three things:

  • Protect the endothelium (lining of blood vessels) from harm
  • Reduce the risk of blood clots forming – especially over areas of endothelial damage
  • Reduce the size and tenacity (difficulty of being broken down) of the blood clots that develop

If you can do all three, you will reduce your risk of dying of a heart attack, or stroke, to virtually zero.

What protects the endothelium?

There are many things that that can do this, but the number one agent that protects the endothelium is nitric oxide (NO). Thus, anything that stimulates NO synthesis will be protective against CVD. Which brings us to sunshine and vitamin D.

  • Sunlight on the skin directly stimulates NO synthesis, which has been shown to reduce blood pressure, improve arterial elasticity, and a whole host of other beneficial things for your cardiovascular system, not least a reduction in blood clot formation.
  • Sunlight on the skin also creates vitamin D, which has significant impact on NO synthesis in endothelial cells, alongside many other actions. It also prevents cancer, so you get a double benefit.

Therefore, my first direct piece of direct advice for those who want to prevent heart disease, is to sunbathe. In the winter when the sun is not shining take vitamin D supplementation. Alternatively, go on holiday to somewhere sunny. Or get a UVB sunbed, and use it.

My only note of warning here is to say, don’t burn, it is painful and you don’t need to.

By the way, don’t worry about skin cancer. Sun exposure protects against all forms of cancer to a far greater degree than it may cause any specific cancer. To give you reassurance on this point, here is a Medscape article, quoting from a long-term Swedish study on sun exposure:

‘Nonsmokers who stayed out of the sun had a life expectancy similar to smokers who soaked up the most rays, according to researchers who studied nearly 30,000 Swedish women over 20 years.

This indicates that avoiding the sun “is a risk factor for death of a similar magnitude as smoking,” write the authors of the article, published March 21 in the Journal of Internal Medicine. Compared with those with the highest sun exposure, life expectancy for those who avoided sun dropped by 0.6 to 2.1 years.

Pelle Lindqvist, MD, of Karolinska University Hospital in Huddinge, Sweden, and colleagues found that women who seek out the sun were generally at lower risk for cardiovascular disease (CVD) and noncancer/non-CVD diseases such as diabetes, multiple sclerosis, and pulmonary diseases, than those who avoided sun exposure.

And one of the strengths of the study was that results were dose-specific — sunshine benefits went up with amount of exposure. The researchers acknowledge that longer life expectancy for sunbathers seems paradoxical to the common thinking that sun exposure increases risk for skin cancer.

“We did find an increased risk of…skin cancer. However, the skin cancers that occurred in those exposing themselves to the sun had better prognosis,” Dr Lindqvist said.”2

In short, avoiding the sun is a bad for you as smoking. In my opinion ordering people to avoid the sun, is possibly the single most dangerous and damaging piece of health prevention advice there has ever been. The sun has been up there, shining down, for over four billion years. Only very recently have we hidden from it. If you believe in evolution, you must also believe that sunshine provides significant health benefits. It cannot be otherwise.

Written By: Dr. Malcolm Kendrick

Article Source: https://drmalcolmkendrick.org/2016/12/24/what-causes-heart-disease-part-xxiii/

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Low DHEA Predicts Coronary Heart Disease

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Men with low blood levels of DHEA may be at increased risk of developing coronary heart disease events.

The most abundant steroid in the human body, dehydroepiandrosterone (DHEA) is involved in the manufacture of testosterone, estrogen, progesterone, and corticosterone.  Claes Ohlsson, from Sahlgrenska Academy (Sweden), and colleagues monitored 2,614 men, ages 69 to 80 years, who resided in 3 Swedish communities, for five years, during which DHEA levels were assessed. The findings demonstrated that the lower the DHEA level at the study start, the greater the risk of coronary heart disease events during the five-year follow-up.  The study authors report that: “Low serum levels of DHEA and its sulfate predict an increased risk of [coronary heart disease], but not [cerebrovascular disease], events in elderly men.”

Article Source: http://www.worldhealth.net/news/low-dhea-predicts-coronary-heart-disease/

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Heart and bone damage from low vitamin D tied to declines in sex hormones

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Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone.

In a national study in 1010 men, to be presented Nov. 15 at the American Heart Association’s (AHA) annual Scientific Sessions in Orlando, researchers say the new findings build on previous studies showing that deficiencies in vitamin D and low levels of estrogen, found naturally in differing amounts in men and women, were independent risk factors for hardened and narrowed arteries and weakened bones. Vitamin D is an essential part to keeping the body healthy, and can be obtained from fortified foods, such as milk and cereals, and by exposure to sunlight.

“Our results confirm a long-suspected link and suggest that vitamin D supplements, which are already prescribed to treat osteoporosis, may also be useful in preventing heart disease,” says lead study investigator and cardiologist Erin Michos, M.D., M.H.S.

“All three steroid hormones – vitamin D, estrogen and testosterone – are produced from cholesterol, whose blood levels are known to influence arterial and bone health,” says Michos, an assistant professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute. “Our study gives us a much better understanding of how the three work in concert to affect cardiovascular and bone health.”

Michos says the overall biological relationship continues to puzzle scientists because studies of the long-term effects of adding estrogen in the form of hormone replacement therapy in women failed to show fewer deaths from heart disease. Indeed, results showed that in some women, an actual increase in heart disease and stroke rates occurred, although, bone fractures declined.

The Hopkins team’s latest data were provided by analyzing blood samples from a subset of men participating in a study on cancer. That study was part of a larger, ongoing national health survey involving both men and women and was designed to compare the risk of diseases between those with the lowest blood levels of vitamin D to those with higher amounts. An unhealthy deficiency, experts say, is considered blood levels of 20 nanograms per milliliter or lower.

The men in the study had their hormone levels measured for both chemical forms of testosterone and estrogen found in blood, when each is either unattached or circulating freely, and when each is attached to a separate protein, known as sex hormone binding globulin, or SHBG for short.

Initial results showed no link between vitamin D deficiency and depressed blood levels of either hormone. And despite finding a harmful relationship between depressed testosterone levels and rates of heart disease, stroke, and high blood pressure, as well as osteopenia in men, researchers found that it was independent of deficiencies in vitamin D.

However, when researchers compared ratios of estrogen to SHBG levels, they found that rates of both diseases, especially osteopenia, the early stage of osteoporosis, were higher when both estrogen and vitamin D levels were depressed.

For every single unit decrease in ratios of estrogen to SHBG (both in nanomoles per liter), men low in vitamin D showed an 89 percent increase in osteopenia, but men with sufficient vitamin D levels had a less worrisome 64 percent jump.

Using the same measure of estrogen levels, men low in vitamin D were also at heightened risk of cardiovascular diseases, at 12 percent, compared to men with adequate levels of the vitamin, at 1 percent, numbers that researchers say are still statistically significant.

“These results reinforce the message of how important proper quantities of vitamin D are to good bone health, and that a man’s risk of developing osteoporosis and heart disease is heavily weighted on the complex and combined interaction of how any such vitamin deficits interact with both their sex hormones, in particular, estrogen,” Michos says.

Michos and her team next plan to analyze blood samples from women to see if the same results from men hold true.

Michos recommends that men and women boost their vitamin D levels by eating diets rich in fatty fish, such as cod, sardines and mackerel, consuming fortified dairy products, taking vitamin supplements, and in warmer weather briefly exposing skin to the sun’s vitamin-D producing ultraviolet light.

She points out that clinical trials are under way to determine whether or not vitamin D supplements can prevent incidents of or deaths from heart attack, stroke and other signs of cardiovascular disease.

The U.S. Institute of Medicine suggests that an adequate daily intake of vitamin D is between 200 and 400 international units, but Michos feels this is inadequate to achieve optimal nutrient blood levels (above 30 nanograms per milliliter). Previous results from the same nationwide survey showed that 41 percent of men and 53 percent of women are technically deficient in the nutrient, with vitamin D levels below 28 nanograms per milliliter.

###

Funding for this study was provided by the Hormone Demonstration Project, a part of the Maryland Cigarette Restitution Fund Research Grant Program at the Johns Hopkins University. Additional support was provided by the American College of Cardiology Foundation and a Clinician Scientist Award at the Johns Hopkins University.

Besides Michos, other researchers at Johns Hopkins involved in this study were Jared Reis, Ph.D.; and Meredith Shields and Elizabeth Platz, Ph.D., Sc.D., at the University’s School of Public Health; and Sabine Rohrmann, now at the German Cancer Research Center in Heidelberg. Another investigator in this research was Nader Rifai, Ph.D., at Children’s Hospital Boston and Harvard Medical School.

(Presentation title: The association of cardiovascular disease and osteopenia may be mediated through a vitamin D-sex steroid hormone interaction, results from the Third National Health and Nutrition Examination Survey, NHANES-III.)

Article Source: https://www.eurekalert.org/pub_releases/2009-11/jhmi-hab111109.php

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