Medical News

Anti-Aging Supplement Is A Fountain Of Hope For Would-Be Mothers

Monday, August 12, 2013
According to the American Pregnancy Association, six million women a year deal with infertility. Now, a Tel Aviv University study is giving new hope to women who want to conceive - in the form of a pill they can find on their drugstore shelves right now. 

Prof. Adrian Shulman of Tel Aviv University's Sackler Faculty of Medicine and the Meir Medical Center has found a statistical connection between the over-the-counter vitamin supplement DHEA, used to counter the effects of aging, and successful pregnancy rates in women undergoing treatment for infertility. 

In the first controlled study on the effects of the supplement, Prof. Shulman found that women being treated for infertility who also received supplements of DHEA were three times more likely to conceive than women being treated without the additional drug. The results were recently published in AYALA, the journal of the Israeli Fertility Association. 

A natural supplement to fertility treatments 

After hearing anecdotal evidence from his patients and the medical community on the benefits of combining fertility treatments with DHEA, a supplement marketed as an anti-aging drug around the world, Prof. Shulman decided to put this old wives' tale to the statistical test. 

He and his fellow researchers conducted a study in which a control group of women received treatment for poor ovulation, and another group received the same treatment with the addition of the DHEA supplement. The latter group took 75mg of the supplement daily for 40 days before starting fertility treatments, and continued for up to five months. 

Not only were women who combined infertility treatment with DHEA more likely to conceive, the researchers discovered, they were also more likely to experience a healthy pregnancy and delivery. 

"In the DHEA group, there was a 23% live birth rate as opposed to a 4% rate in the control group," explains Shulman. "More than that, of the pregnancies in the DHEA group, all but one ended in healthy deliveries." 

Making grade-A eggs? 

Shulman believes that women who are finding little success with their current fertility treatments could look to DHEA to improve their chances of conceiving. "We recommend that women try this DHEA treatment, in conjunction with fertility treatments, for four to five months," says Prof. Shulman. It could also be used as a regular "vitamin" for women who have already conceived and are pregnant, but more research would need to be done on the compound to determine its effects, says Prof. Shulman. 

DHEA, for 5-Dehydroepiandrosterone (5-DHEA), is a naturally-occurring steroid found in the brain, which plays an important biological role in humans and other mammals. Produced in the adrenal glands, it is also synthesized in the brain. The pharmaceutical version of this molecule is known as Prastera, Prasterone, Fidelin and Fluasterone, and identical generics are widely available over the counter in the United States without a prescription. Women interested in using DHEA to conceive, however, should consult their practitioner first, suggests Prof. Shulman, a gynecologist and director of the IVF Unit of the Obstetric and Gynecology Department at Meir Medical Center. 

While studies on the effects of DHEA are far from complete - his test group only included around 20 women - Prof. Shulman hopes that further research will unlock the secrets of why the supplement aids in successful conception in women with an otherwise poor response to fertility treatments. "We need to look into what the drug actually does to make the body more fertile," he says. "It could be affecting components such as the quality of the eggs or the follicles." 


Source: American Friends of Tel Aviv University


Copyright: Medical News Today 

Anti-Aging Hormone Klotho May Prevent Complications In Chronic Kidney Disease

Monday, August 12, 2013
Low levels of the anti-aging hormone Klotho may serve as an early warning sign of the presence of kidney disease and its deadly cardiovascular complications, according to findings by UT Southwestern Medical Center researchers.

Using mice, investigators found that soft-tissue calcification, a common and serious side effect of chronic kidney disease (CKD), improves when Klotho hormone levels are restored. The study is available online in the Journal of the American Society of Nephrology.

The essential Klotho protein, which is produced by the kidneys, often plummets in CKD. This may explain why supplementing Klotho levels helps counteract a major side-effect associated with the disease, said Dr. Orson Moe, director of the Charles & Jane Pak Center for Mineral Metabolism and Clinical Research at UT Southwestern and the senior author of the study.

Mice with chronic kidney disease exhibit low levels of Klotho in their kidneys, blood and urine, indicating that CKD is a state of systemic Klotho deficiency, Dr. Moe said. In the study, researchers also tested urine from 53 human participants, including 40 CKD patients, and found that they also had low levels of the essential protein.

"It can be a vicious cycle, where CKD begets low Klotho and low Klotho accelerates CKD," Dr. Moe said. "Chronic kidney disease appears to go hand-in-hand with chronic Klotho deficiency. Animal studies have shown that a dangerous consequence of inadequate Klotho is soft-tissue calcification, which can interfere with normal organ function."

In the current study, UT Southwestern researchers decreased Klotho levels in mice by genetically engineering them to produce inadequate levels of the protein. Restoring adequate Klotho levels to the rodents with CKD markedly improved renal function and blood chemistry and reduced vascular calcification.

In contrast, mice with CKD that were genetically engineered to have abnormally low levels of Klotho had worse kidney function and severe calcification. The beneficial effect of proper Klotho levels on vascular calcification goes beyond the hormone's effect on kidney function, suggesting a direct protective effect of Klotho on the vasculature, Dr. Moe said.

According to the research, Klotho lessens vascular calcification by enhancing the urine's phosphate excretions (essential for building and repairing bones and teeth, helping nerve function and making muscles contract, but it can be toxic when levels are high); and preserving kidney fluid filtration. Most importantly, Klotho also appears to inhibit vascular smooth-muscle phosphate uptake and calcification, a complication of CKD that can significantly increase risk of death.

"We tested three hypotheses," Dr. Moe said. "The first was that CKD is a state of Klotho deficiency; the second, that Klotho is an early marker of CKD; and the third, that Klotho deficiency contributes to vascular calcification and Klotho replacement ameliorates CKD via multiple mechanisms. The data we collected seem to bear out all three."

The study's findings also suggest that Klotho replacement therapy may eventually prove to be effective in battling CKD as well as in preventing and reversing its complications.

"It is our hope that this and future research will ultimately lead to better ways to retard the progression of CKD and avoid the dire consequences associated with the disease," Dr. Moe said.

Other UT Southwestern researchers involved in the study were Dr. Ming-Chang Hu, instructor of internal medicine and lead author; Dr. Makoto Kuro-o, associate professor of pathology who discovered Klotho more than a decade ago; Mingjun Shi, research associate in internal medicine; Dr. Jianning Zhang, research scientist in internal medicine; Dr. Henry Quinones, assistant professor of internal medicine; and Carolyn Griffith, senior research nurse in mineral metabolism.

Primary funding for the study was provided by the Simmons Family Foundation. Other support was given by the National Institutes of Health, the George M. O'Brien Kidney Research Core Center at UT Southwestern, the American Heart Association, the Eisai Research Fund, Ellison Medical Foundation, Ted Nash Long Life Foundation, and the Charles & Jane Pak Center for Mineral Metabolism and Clinical Research.

Source: UT Southwestern Medical Center 

Can Where You Live Make You Older? Or Younger? Yes! New RealAge Report Identifies The Cities Where People Age Fastest And Slowest

Monday, August 12, 2013
Want to live a longer life? Move to Salt Lake City. Or San Francisco, or Austin. 

Those three cities lead RealAge's top 10 list of the "youngest" cities in America-metropolitan areas with such healthy lifestyles that on average their residents are physically at least two years younger than their chronological age, and many are years younger than that. RealAge analyzed data from the largest 50 metropolitan areas to compile the rankings. 

A passion for fitness and a loathing for smoking are key factors in Salt Lake City's number one ranking. At the other extreme, residents of Knoxville, Greensboro/Winston-Salem, and Nashville are aging faster than they should. (Get an infographic of the 10 youngest and oldest cities here.) 

What are the 10 metro areas where you have the best odds of staying young? 

1. Salt Lake City, Utah 
2. San Francisco/Oakland/San Jose, Calif. 
3. Austin, Texas 
4. Denver, Colo. 
5. Boston, Mass. 
6. Washington, DC/Baltimore, Md. 
7. San Diego, Calif. 
8. Raleigh-Durham/Chapel Hill, N.C. 
9. Minneapolis/St. Paul, Minn. 
10. Seattle/Tacoma/Bremerton, Wash. 

Which metro areas are likely to make you old before your time? 

1. Knoxville, Tenn. 
2. Greensboro/Winston-Salem/High Point, N.C. 
3. Nashville, Tenn. 
4. Saginaw/Bay City/Midland, Mich. 
5. Cincinnati, Ohio 
6. Tampa/St. Petersburg, Fla. 
7. Oklahoma City, Okla. 
8. Las Vegas, Nev. 
9. Jacksonville, Fla. 
10. Tulsa, Okla. 

"Each city's ranking is more than just a number," says Keith Roach, MD, Chief Medical Officer of RealAge and a co-creator of its test. "It's a unique assessment of the healthy lifestyles, or lack of them, in each metro area-of how people live there, what they're doing right and what they need to change. If you live in one of the 10 oldest cities, take this as the alarm on your body's aging clock going off! It's never too late for a fresh start." 

Note that half of the 10 youngest cities are in the Western U.S., from Denver to Seattle. 

"Maybe it's the weather, maybe it's the mountains, but Western cities have adopted active lifestyles that can slow down the aging process," says Dr. Roach. 

Behind the Rankings 

To compile the rankings, RealAge analyzed data for America's 50 largest metropolitan areas generated by its landmark online assessment, the RealAge Test, taken by over 27 million people. This is the first time the company has analyzed aggregated results on a city-by-city basis. 

A random sample of 1,000 RealAge members was drawn from each city. The sample data was adjusted for age differences, so a metropolitan area that's a magnet for retirees wasn't penalized, and a city jammed with university students didn't benefit. 

The Test uses a powerful algorithm that combines the latest scientific studies with lifestyle, genetics, and medical history to calculate your RealAge-how old your body thinks you are. 

What Makes a City Younger or Older 

While multiple lifestyle factors are involved, here are four big ones that help people in Boston (the 5th youngest city), for example, stay younger and healthier than those in Cincinnati (the 5th oldest): 

1. Getting the right amount of sleep. Six of the 10 youngest cities are among those with stellar sleep habits. And (surprise) New York isn't the city that never sleeps-the Big Apple ranks second in ZZZ's; Austin is first. Sleeping six to nine hours a night can make your RealAge as much as 3 years younger. 

2. Stubbing out cigarettes for good. Four of the five fastest-aging cities have the highest percentage of smokers. 

3. Not sitting around. Six of the 10 youngest cities are among the most physically active in the country. A daily 30-minute walk can make your RealAge up to 3.5 years younger. 

4. Controlling your blood pressure. Five of the 10 fastest-aging cities-Knoxville, Cincinnati, Oklahoma City, Jacksonville, and Tulsa-are among the worst for high blood pressure. Nothing ages you faster. Who has the lowest BP? Residents of Minneapolis-St. Paul, the 9th youngest city. 

Source: 
RealAge 

Chronic Depression Linked To Accelerated Immune Cell Aging

Monday, August 12, 2013
Certain cases of major depression are associated with premature aging of immune cells, which may make people more susceptible to other serious illness, according to findings from a new UCSF-led study. 

The findings indicate that accelerated cell aging does not occur in all depressed individuals, but is dependent upon how long someone is depressed, particularly if that depression goes untreated. The study was published online in March 2011 by the journal PLoS One. 

"There's a lot more to depression than feeling blue," said first author Owen Wolkowitz, MD, a professor of psychiatry at UCSF. "As if feeling depressed is not bad enough, we are finding that long-term depression may be associated with damage to cells in the body, and this may predispose patients to certain physical diseases." 

Previously considered a mental illness affecting only the brain, major depressive disorder, or MDD, now is believed to be tied to significant physical damage outside the brain, explained Wolkowitz. For example, depressed individuals are more likely to develop the diseases of advanced age, including diabetes, heart disease, osteoporosis, stroke and dementia. 

In probing the links between depression and physical disease, the research team explored aging of the immune system as measured by the shortening of telomeres in immune cells taken from the blood. 

Telomeres are tiny units of DNA-protein complexes that seal off and protect the ends of chromosomes and act as a biological clock controlling a cell's life. Telomere shortening predicts earlier onset of several major age-related diseases and earlier mortality, and may serve as one index of human longevity. 

The researchers compared the length of telomeres in 18 individuals with MDD not currently receiving antidepressant medications to the length of telomeres in 17 healthy controls. Overall, telomeres of the depressed group did not differ from those of the healthy group; however, individuals with nine or more years of untreated chronic depression showed significant telomere shortening, even after accounting for chronological age. The degree of shortening in this subset of the depressed group corresponded to about seven years of "accelerated cell aging." 

Telomere shortening also was associated with higher levels of inflammation and oxidativestress in patients, both linked to cell damage and premature aging. Oxidative stress is an imbalance between destructive "free radical" molecules and the body's ability to neutralize them with antioxidants. The authors suggest that telomere shortening in very chronic depression may reflect an individual's cumulative exposure to biochemical stressors that promote cell death and increase the likelihood of physical disease. 

"While this finding itself might seem depressing, there is yet good news: many lifestyle factors like exercise and aspects of diet have been linked to longer telomeres," said co-author Elissa Epel, PhD, an associate professor in the UCSF Department of Psychiatry. "So while our personal history matters, it is possible that what we do today may matter even more, in terms of protecting our telomeres." 

Epel and co-author Elizabeth Blackburn, PhD, UCSF professor of biochemistry and biophysics, pioneered research on the impact of psychological stress on several biological markers of cell aging. Blackburn shared the 2009 Nobel Prize in Physiology or Medicine for her telomere research and co-discovery of the cellular enzyme telomerase. Telomerase helps repair and restore telomeres, protecting cells from damage related to premature aging. 

In related work, the research team recently reported in the journal Molecular Psychiatry, available here, that individuals with MDD show increased activity of the telomerase enzyme. Depressed individuals with the lowest telomerase activity before antidepressant treatment, and those with the greatest increase in activity during treatment, showed the strongest antidepressant responses. These findings suggest that the seemingly paradoxical increase of telomerase in untreated depressed individuals indicates their bodies are attempting to compensate for the damage to their telomeres. Increases during treatment, on the other hand, may represent true improvement in depression. 

"We speculate that telomerase may provide a biological marker for antidepressant responses," Wolkowitz said. "Once we better understand these systems, we will be in a stronger position to treat depression and possibly prevent some of its associated physical illnesses." 

As a next step, UCSF researchers plan to replicate these preliminary findings in a larger sample of depressed individuals in order to explain why certain people develop shortened telomeres and physical disease, and how that process can be combated. Depressed individuals not taking antidepressants are currently being enrolled for this ongoing study, and interested participants may visit mood@ucsf.edu. mood@ucsf.edu Additional UCSF co-authors are Synthia Mellon, PhD; Jue Lin, PhD; Victor Reus, MD; Rebecca Rosser; Heather Burke, PhD; Eve Kupferman, PhD; Mariana Compagnone, MD; and J. Craig Nelson, MD. Co-authors from other institutions are Firdaus Dhabhar, PhD, of Stanford and Yali Su, PhD, of Kronos Science Laboratory. 

The studies were funded by the National Institute of Mental Health, the O'Shaughnessy Foundation, the Bernard and Barbro Osher Foundation, and UCSF. Additionally, Blackburn, Epel and Lin are co-founders of a new company called Telome Health, Inc., which is developing applications of telomere biology to identify disease risk and to improve wellness. 

Source: 
Kate Vidinsky
University of California - San Francisco

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