(HealthDay News) -- Vitamin D deficiency is a common problem that can lead to a number of serious health conditions, but it can be prevented, says one expert.
People get vitamin D from sun exposure, diet and supplements. Yet vitamin D deficiency is all too common.
In utero and in childhood, not getting enough vitamin D can cause growth retardation, skeletal deformities and increase the risk of future hip fractures. In adults, too little vitamin D can lead to or exacerbate osteopenia, osteoporosis, muscle weakness, fractures, common cancers, autoimmune diseases, infectious diseases and cardiovascular diseases.
In the July 19 issue of the New England Journal of Medicine, Michael Holick, director of the General Clinical Research Center at Boston University School of Medicine and director of the Bone Healthcare Clinic at Boston Medical Center, published an overview of his work on vitamin D.
According to Holick, it has been estimated that one billion people in the world are vitamin D deficient or insufficient.
Without vitamin D, only 10 percent to 15 percent of dietary calcium and about 60 percent of phosphorus is absorbed by the body. This can have a direct effect on bone mineral density.
There is evidence that people who live at higher latitudes -- where the angle of the sun's rays is not sufficient to produce adequate amounts of vitamin D in the skin -- are more likely to develop and die of Hodgkin's lymphoma, colon, pancreatic, prostate, ovarian, breast and other cancers.
And there is an association between low levels of vitamin D and increased risk for type 1 diabetes, multiple sclerosis, Crohn's disease, hypertension and cardiovascular disease.
Holick says that the current recommended adequate intake for vitamin D needs to be increased to 800 to 1,000 international units (IU) of vitamin D3 per day.
"However, one can not obtain these amounts from most dietary sources unless one is eating oily fish frequently. Thus, sensible sun exposure (or UVB radiation) and/or supplements are required to satisfy the body's vitamin D requirement," Holick said in a prepared statement.
Holick added, "The goal of this paper is to make physicians aware of the medical problems associated with vitamin D deficiency. Physicians will then be able to impart this knowledge to their patients so they, too, will know how to recognize, treat and most importantly, maintain adequate levels of this important vitamin."
More information
The National Institutes of Health Office of Dietary Supplements has more about vitamin D.
Kamis, 19 Juli 2007
Senin, 16 Juli 2007
Patch Helps Heart Grow New Cells
(HealthDay News) -- A special patch placed on a damaged area of the heart regenerates cardiac cells after heart attack and improves heart function, a new study finds.
Success with the patch in rats may lead the way to new methods of repairing damaged human hearts and possibly spare some patients the need for a heart transplant, according to researchers reporting in the July 15 online edition of Nature Medicine.
"Normally, adult human hearts do not regenerate because the heart doesn't make more cardiomyocytes (heart muscle cells) after injury," explained lead researcher Dr. Bernhard Kuhn, from the Department of Cardiology at Children's Hospital Boston. "It would be desirable to induce the heart to make new cardiomyocytes after injury."
To that end, Kuhn's team created a patch that contains a compound called periostin, which helps cardiomyocytes divide and multiply. "If you do that over a number of cycles, you do get an increase in cardiomyocytes," he said. "So, the cardiomyocytes you have lost are replaced."
Periostin is a natural component of tissue surrounding cells. It comes from the skin lying around bone and helps stimulate cells to divide.
During a heart attack, cardiac cells die from lack of blood and oxygen. This damage prevents the heart from working normally. Typically, lost or damaged cardiac tissue cannot regrow.
In their experiments, Kuhn's team made patches from a material called Gelfoam and soaked the patches with periostin. They placed the patches on the damaged heart muscle of rats in which they had induced a heart attack.
After 12 weeks, the rats treated with the periostin patch experienced a 16 percent improvement in their heart's cardiac pumping ability. They also had less scarring of heart tissue, a reduction in the size of the damaged area of the heart, and more blood vessels feeding the area. In contrast, rats that received a patch without periostin showed no change in their heart function.
The hearts of rats treated with periostin showed a 100-fold increase in the number of heart cells and an average of 6 million more heart cells, far outnumbering the amount of dying cells.
The advantage of this technique is that it doesn't require new cells, such as stem cells, to coax the growth of new heart cells. Stem cells might also migrate to other parts of the body, with unknown consequences, Kuhn said. The patch is "also not gene-based, so it's not gene therapy," he said.
It is possible that this same technique could be used in people who have severe heart disease, Kuhn said. Although the technique might not restore heart function back to normal, there could be significant improvement, he said.
"At this point, the only biologically proven myocardial [heart] replacement therapy is heart transplant," Kuhn said. "But with this method, if you were on a transplant list, you may be able to come off it," he said. "This could be a revolutionary approach to treating heart failure."
One expert was impressed by the findings.
"The work is important in at least two ways: It helps improve our understanding of the molecular pathways regulating cell cycle reentry in adult cardiomyocytes, and it can form a basis for novel heart therapies based on the mobilization of [the heart's own] cells," said Gordana Vunjak-Novakovic, a professor of biomedical engineering at Columbia University Medical Center in New York City and co-director of the Tissue Engineering Resource Center at the U.S. National Institutes of Health.
"It will be interesting to see the extensions of this work to human cells and other cell types, including cardiogenic stem cells that could also be affected by periostin," Vunjak-Novakovic said.
Another expert echoed those sentiments.
"This research nicely demonstrates that periostin induced cardiomyocytes' reentry into the cell cycle," said Dr. Gregg C. Fonarow, director of the Ahmanson-UCLA Cardiomyopathy Center at the University of California Los Angeles.
Rather than needing to introduce brand new cells into the damaged heart, it may be possible to induce existing cardiomyocytes to grow and thus regenerate normal functioning heart muscle, said Fonarow, who is also professor of clinical medicine at UCLA.
"The ability to enhance cardiac regeneration holds great promise as novel treatment strategies for [heart attack] complicated by left ventricular dysfunction and for chronic heart failure," he said.
But rat studies can only tell scientists so much, Fonarow added. "Additional studies with adult human cardiomyocytes, and ultimately clinical trials, are needed," he said.
More information
To learn more about how the heart works, head to the American Heart Association.
Success with the patch in rats may lead the way to new methods of repairing damaged human hearts and possibly spare some patients the need for a heart transplant, according to researchers reporting in the July 15 online edition of Nature Medicine.
"Normally, adult human hearts do not regenerate because the heart doesn't make more cardiomyocytes (heart muscle cells) after injury," explained lead researcher Dr. Bernhard Kuhn, from the Department of Cardiology at Children's Hospital Boston. "It would be desirable to induce the heart to make new cardiomyocytes after injury."
To that end, Kuhn's team created a patch that contains a compound called periostin, which helps cardiomyocytes divide and multiply. "If you do that over a number of cycles, you do get an increase in cardiomyocytes," he said. "So, the cardiomyocytes you have lost are replaced."
Periostin is a natural component of tissue surrounding cells. It comes from the skin lying around bone and helps stimulate cells to divide.
During a heart attack, cardiac cells die from lack of blood and oxygen. This damage prevents the heart from working normally. Typically, lost or damaged cardiac tissue cannot regrow.
In their experiments, Kuhn's team made patches from a material called Gelfoam and soaked the patches with periostin. They placed the patches on the damaged heart muscle of rats in which they had induced a heart attack.
After 12 weeks, the rats treated with the periostin patch experienced a 16 percent improvement in their heart's cardiac pumping ability. They also had less scarring of heart tissue, a reduction in the size of the damaged area of the heart, and more blood vessels feeding the area. In contrast, rats that received a patch without periostin showed no change in their heart function.
The hearts of rats treated with periostin showed a 100-fold increase in the number of heart cells and an average of 6 million more heart cells, far outnumbering the amount of dying cells.
The advantage of this technique is that it doesn't require new cells, such as stem cells, to coax the growth of new heart cells. Stem cells might also migrate to other parts of the body, with unknown consequences, Kuhn said. The patch is "also not gene-based, so it's not gene therapy," he said.
It is possible that this same technique could be used in people who have severe heart disease, Kuhn said. Although the technique might not restore heart function back to normal, there could be significant improvement, he said.
"At this point, the only biologically proven myocardial [heart] replacement therapy is heart transplant," Kuhn said. "But with this method, if you were on a transplant list, you may be able to come off it," he said. "This could be a revolutionary approach to treating heart failure."
One expert was impressed by the findings.
"The work is important in at least two ways: It helps improve our understanding of the molecular pathways regulating cell cycle reentry in adult cardiomyocytes, and it can form a basis for novel heart therapies based on the mobilization of [the heart's own] cells," said Gordana Vunjak-Novakovic, a professor of biomedical engineering at Columbia University Medical Center in New York City and co-director of the Tissue Engineering Resource Center at the U.S. National Institutes of Health.
"It will be interesting to see the extensions of this work to human cells and other cell types, including cardiogenic stem cells that could also be affected by periostin," Vunjak-Novakovic said.
Another expert echoed those sentiments.
"This research nicely demonstrates that periostin induced cardiomyocytes' reentry into the cell cycle," said Dr. Gregg C. Fonarow, director of the Ahmanson-UCLA Cardiomyopathy Center at the University of California Los Angeles.
Rather than needing to introduce brand new cells into the damaged heart, it may be possible to induce existing cardiomyocytes to grow and thus regenerate normal functioning heart muscle, said Fonarow, who is also professor of clinical medicine at UCLA.
"The ability to enhance cardiac regeneration holds great promise as novel treatment strategies for [heart attack] complicated by left ventricular dysfunction and for chronic heart failure," he said.
But rat studies can only tell scientists so much, Fonarow added. "Additional studies with adult human cardiomyocytes, and ultimately clinical trials, are needed," he said.
More information
To learn more about how the heart works, head to the American Heart Association.
Kamis, 12 Juli 2007
Reevaluating Hormone Replacement Therapy
(HealthDay News) -- Five years after the results of the Women's Health Initiative sounded the supposed death knell for hormone replacement therapy, experts gathered Wednesday to reassess those results and discuss the fine-tuning and evaluation that has taken place since.
"The science has evolved substantially in the past five years," Dr. JoAnn Manson, chief of the division of preventive medicine at Brigham and Women's Hospital in Boston, said at a press conference sponsored by the Society for Women's Health Research. "There's been mounting evidence that a woman's age and amount of time since onset of menopause may influence the effect of hormone therapy."
The Society for Women's Health Research is a nonprofit organization but has received funds from companies such as Amgen, Cytyc, Eli Lilly, Ethicon and Wyeth.
The original Women's Health Initiative (WHI) was halted when U.S. researchers found an increased risk of adverse events which, depending on whether the woman was taking estrogen alone or estrogen plus progestin, included heart attack, stroke, breast cancer and blood clots.
Manson was one of the principal investigators on the WHI trial.
The average age of women enrolled in the WHI was 63, or about 12 years past menopause.
And the trial was designed not to look at how well hormone therapy combated menopausal symptoms such as hot flashes, but whether it could play a role in chronic disease prevention.
"The WHI was designed to evaluate the balance of benefits and risks of hormone therapy in generally healthy postmenopausal women when used for chronic disease prevention," Manson said. "At the time WHI was started in the early 1990s, it was becoming increasingly common in clinical practice to use hormone therapy in older women who were at high risk of cardiovascular disease, or who already had a diagnosis of cardiovascular disease, in order to prevent future cardiovascular events."
Since then, it has become increasingly clear that hormone therapy has different benefits and risks, depending on the age of the woman.
Just last week, Manson and her colleagues reported in the New England Journal of Medicine that women in their 50s who take estrogen therapy have lower levels of dangerous calcium deposits in their arteries, suggesting they're at reduced risk for heart disease.
But in older women, hormone therapy appears to increase the risk of cardiovascular problems and blood clots, a phenomenon confirmed by a study in this week's British Medical Journal.
And researchers have speculated that a decline in the incidence of breast cancer in recent years is due to a decline in the use of hormone therapy after the WHI results were announced. But a cause-and-effect link is not at all clear.
"I think it's possible that declining use of hormone therapy has contributed at least a little to a decreased incidence rate, but there could be other explanations," Manson said. "There's some suggestion that the decline in breast cancer may have begun as early as 1999, which was well before there was decreasing use of hormone therapy. And there is also some evidence that mammogram screening has decreased over the past several years and that this could contribute to lower rates of detection and diagnosis of breast cancer."
That being said, combined estrogen and progestin has been linked to a risk of breast cancer after four to five years of use. It's not clear if estrogen has a similar risk.
There was some evidence in the WHI study that combination hormone therapy reduced the risk of colon cancer, but the evidence isn't enough to recommend hormones as a preventive strategy, Manson said.
Similarly, while estrogen reduces the risk of fracture and enhances bone density, this benefit would require long-term treatment. Other medications are available and should be tried first, Manson said.
Overall, the bulk of the research today, five years after the WHI, should serve to reassure younger women who may need hormone therapy to alleviate menopausal symptoms.
"The most important reason to go on hormone therapy is for menopausal symptoms," said Dr. Nieca Goldberg, medical director of the Women's Health Program at New York University Medical Center and associate professor of medicine at New York University School of Medicine.
"Younger women who need to go on hormone therapy for this reason can relax. But hormone therapy should never be given to women with cardiovascular disease."
Manson added: "I don't think that hormone therapy should be started or continued for the express purpose of preventing cardiac disease or other chronic diseases, because there are known risks. However, this is very different from the situation in a recently menopausal woman who has moderate to severe hot flashes and night sweats which interfere with sleep and quality of life. Hormone therapy is known to be the most effective treatment for menopausal symptoms.
It's still a very appropriate short-term treatment, but we still recommend using the lowest effective dose for the shortest duration of time necessary."
More information
Visit the U.S. National Library of Medicine for more on hormone replacement therapy.
"The science has evolved substantially in the past five years," Dr. JoAnn Manson, chief of the division of preventive medicine at Brigham and Women's Hospital in Boston, said at a press conference sponsored by the Society for Women's Health Research. "There's been mounting evidence that a woman's age and amount of time since onset of menopause may influence the effect of hormone therapy."
The Society for Women's Health Research is a nonprofit organization but has received funds from companies such as Amgen, Cytyc, Eli Lilly, Ethicon and Wyeth.
The original Women's Health Initiative (WHI) was halted when U.S. researchers found an increased risk of adverse events which, depending on whether the woman was taking estrogen alone or estrogen plus progestin, included heart attack, stroke, breast cancer and blood clots.
Manson was one of the principal investigators on the WHI trial.
The average age of women enrolled in the WHI was 63, or about 12 years past menopause.
And the trial was designed not to look at how well hormone therapy combated menopausal symptoms such as hot flashes, but whether it could play a role in chronic disease prevention.
"The WHI was designed to evaluate the balance of benefits and risks of hormone therapy in generally healthy postmenopausal women when used for chronic disease prevention," Manson said. "At the time WHI was started in the early 1990s, it was becoming increasingly common in clinical practice to use hormone therapy in older women who were at high risk of cardiovascular disease, or who already had a diagnosis of cardiovascular disease, in order to prevent future cardiovascular events."
Since then, it has become increasingly clear that hormone therapy has different benefits and risks, depending on the age of the woman.
Just last week, Manson and her colleagues reported in the New England Journal of Medicine that women in their 50s who take estrogen therapy have lower levels of dangerous calcium deposits in their arteries, suggesting they're at reduced risk for heart disease.
But in older women, hormone therapy appears to increase the risk of cardiovascular problems and blood clots, a phenomenon confirmed by a study in this week's British Medical Journal.
And researchers have speculated that a decline in the incidence of breast cancer in recent years is due to a decline in the use of hormone therapy after the WHI results were announced. But a cause-and-effect link is not at all clear.
"I think it's possible that declining use of hormone therapy has contributed at least a little to a decreased incidence rate, but there could be other explanations," Manson said. "There's some suggestion that the decline in breast cancer may have begun as early as 1999, which was well before there was decreasing use of hormone therapy. And there is also some evidence that mammogram screening has decreased over the past several years and that this could contribute to lower rates of detection and diagnosis of breast cancer."
That being said, combined estrogen and progestin has been linked to a risk of breast cancer after four to five years of use. It's not clear if estrogen has a similar risk.
There was some evidence in the WHI study that combination hormone therapy reduced the risk of colon cancer, but the evidence isn't enough to recommend hormones as a preventive strategy, Manson said.
Similarly, while estrogen reduces the risk of fracture and enhances bone density, this benefit would require long-term treatment. Other medications are available and should be tried first, Manson said.
Overall, the bulk of the research today, five years after the WHI, should serve to reassure younger women who may need hormone therapy to alleviate menopausal symptoms.
"The most important reason to go on hormone therapy is for menopausal symptoms," said Dr. Nieca Goldberg, medical director of the Women's Health Program at New York University Medical Center and associate professor of medicine at New York University School of Medicine.
"Younger women who need to go on hormone therapy for this reason can relax. But hormone therapy should never be given to women with cardiovascular disease."
Manson added: "I don't think that hormone therapy should be started or continued for the express purpose of preventing cardiac disease or other chronic diseases, because there are known risks. However, this is very different from the situation in a recently menopausal woman who has moderate to severe hot flashes and night sweats which interfere with sleep and quality of life. Hormone therapy is known to be the most effective treatment for menopausal symptoms.
It's still a very appropriate short-term treatment, but we still recommend using the lowest effective dose for the shortest duration of time necessary."
More information
Visit the U.S. National Library of Medicine for more on hormone replacement therapy.
Langganan:
Postingan (Atom)
