or Immediate Release
Thursday, March 1, 2012
Contact:
Robert Bock or Marianne Glass Miller
301-496-5133
Vitamin D shrinks fibroid tumors in rats
NIH-funded study suggests possible treatment for common condition

Treatment with vitamin D reduced the size of uterine fibroids in laboratory rats predisposed to developing the benign tumors, reported researchers funded by the National Institutes of Health.

Uterine fibroids are the most common noncancerous tumors in women of childbearing age. Fibroids grow within and around the wall of the uterus. Thirty percent of women 25 to 44 years of age report fibroid-related symptoms, such as lower back pain, heavy vaginal bleeding or painful menstrual periods. Uterine fibroids also are associated with infertility and such pregnancy complications as miscarriage or preterm labor. Other than surgical removal of the uterus, there are few treatment options for women experiencing severe fibroid-related symptoms and about 200,000 U.S. women undergo the procedure each year. A recent analysis by NIH scientists estimated that the economic cost of fibroids to the United States, in terms of health care expenses and lost productivity, may exceed $34 billion a year.

Fibroids are three to four times more common in African-American women than in white women. Moreover, African-American women are roughly 10 times more likely to be deficient in vitamin D than are white women. In previous research, the study authors found that vitamin D inhibited the growth of human fibroid cells in laboratory cultures.

“The study results provide a promising new lead in the search for a non-surgical treatment for fibroids that doesn’t affect fertility,” said Louis De Paolo, Ph.D., chief of the Reproductive Sciences Branch of the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development, which funded the study.

First author Sunil K. Halder, Ph.D., of Meharry Medical College in Nashville conducted the research with Meharry colleagues Chakradhari Sharan, Ph.D., and Ayman Al-Hendy, M.D., Ph.D., and with Kevin G. Osteen, Ph.D., of Vanderbilt University Medical Center, also in Nashville. The findings appeared online in the journal Biology of Reproduction.

For the current study, the researchers tested the vitamin D treatment on a strain of rats genetically predisposed to developing fibroid tumors. After examining the animals and confirming the presence of fibroids in 12 of them, the researchers divided the rats into two groups of six each: those that would receive vitamin D and those that would not.

In the first group, small pumps implanted under the skin delivered a continuous dose of vitamin D for three weeks. The researchers then examined the animals in both groups. Fibroids increased in size in the untreated rats, but, in the rats receiving vitamin D, the tumors had shrunk dramatically. On average, uterine fibroids in the group receiving vitamin D were 75 percent smaller than those in the untreated group.

The amount of vitamin D the rats received each day was equivalent to a human dose of roughly 1,400 international units. The recommended amount of vitamin D for teens and adults age 70 and under is 600 units daily, although up to 4,000 units is considered safe for children over age 9, adults, and for pregnant and breastfeeding females.

“Additional research is needed to confirm vitamin D as a potential treatment for women with uterine fibroids,” said Dr. Al-Hendy. “But it is also an essential nutrient for the health of muscle, bone and the immune system, and it is important for everyone to receive an adequate amount of the vitamin.”

Fatty fish such as salmon, mackerel and tuna are the best natural sources of the vitamin. Very few foods naturally contain vitamin D. Fortified milk and other fortified foods provide an additional source of the vitamin. Vitamin D is also produced when ultraviolet rays from sunlight strike the skin.

About the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD): The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute’s website at http://www.nichd.nih.gov/.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.


EMBARGOED UNTIL: March 7, 2005 at 4:45 p.m. ET
Contact: Bill Seiler [email protected]
Ellen Beth Levitt [email protected] 410-328-8919
UNIVERSITY OF MARYLAND SCHOOL OF MEDICINE STUDY SHOWS LAUGHTER HELPS BLOOD VESSELS FUNCTION BETTER

Volunteers were shown funny and disturbing movies to test the effect of emotions on blood vessels

Read more: http://www.umm.edu/news/releases/laughter2.htm#ixzz1oTXpfaII

Using laughter-provoking movies to gauge the effect of emotions on cardiovascular health, researchers at the University of Maryland School of Medicine in Baltimore have shown for the first time that laughter is linked to healthy function of blood vessels. Laughter appears to cause the tissue that forms the inner lining of blood vessels, the endothelium, to dilate or expand in order to increase blood flow.

When the same group of study volunteers was shown a movie that produced mental stress, their blood vessel lining developed a potentially unhealthy response called vasoconstriction, reducing blood flow. That finding confirms previous studies, which suggested there was a link between mental stress and the narrowing of blood vessels.

The results of the study, conducted at the University of Maryland Medical Center, were presented at the Scientific Session of the American College of Cardiology on March 7, 2005, in Orlando, Florida.

The endothelium has a powerful effect on blood vessel tone and regulates blood flow, adjusts coagulation and blood thickening, and secretes chemicals and other substances in response to wounds, infections or irritation. It also plays an important role in the development of cardiovascular disease.

“The endothelium is the first line in the development of atherosclerosis or hardening of the arteries, so, given the results of our study, it is conceivable that laughing may be important to maintain a healthy endothelium, and reduce the risk of cardiovascular disease,” says principal investigator Michael Miller, M.D., director of preventive cardiology at the University of Maryland Medical Center and associate professor of medicine at the University of Maryland School of Medicine. “At the very least, laughter offsets the impact of mental stress, which is harmful to the endothelium.”

The study included a group of 20 non-smoking, healthy volunteers, equally divided between men and women, whose average age was 33. The participants had normal blood pressure, cholesterol and blood glucose levels. Each volunteer was shown part of two movies at the extreme ends of the emotional spectrum. They were randomized to first watch either a movie that would cause mental stress, such as the opening scene of “Saving Private Ryan” (DreamWorks, 1998), or a segment of a movie that would cause laughter, such as “King Pin” (MGM, 1996). A minimum of 48 hours later, they were shown a movie intended to produce the opposite emotional extreme.

Prior to seeing a movie, the volunteers fasted overnight and were given a baseline blood vessel reactivity test to measure what is known as flow-mediated vasodilation. For that test, blood flow in the brachial artery in the arm was restricted by a blood pressure cuff and released. An ultrasound device then measured how well the blood vessel responded to the sudden increase in flow.

Volunteers watched a 15-minute segment of the movie while lying down in a temperature-controlled room. After the movie was shown, the brachial artery was constricted for five minutes and then released. Again, ultrasound images were acquired. Changes in blood vessel reactivity after the volunteers watched a movie lasted for at least 30 to 45 minutes. A total of 160 blood vessel measurements were performed before and after the laughter and mental stress phases of the study.

There were no differences in the baseline measurements of blood vessel dilation in either the mental stress or laughter phases. But there were striking contrasts after the movies were seen. Brachial artery flow was reduced in 14 of the 20 volunteers following the movie clips that caused mental stress. In contrast, beneficial blood vessel relaxation or vasodilation was increased in 19 of the 20 volunteers after they watched the movie segments that generated laughter. Overall, average blood flow increased 22 percent during laughter, and decreased 35 percent during mental stress.

Several volunteers had already seen “Saving Private Ryan,” says Dr. Miller, but even so, some of them were among the 14 with reduced blood flow.

“The magnitude of change we saw in the endothelium is similar to the benefit we might see with aerobic activity, but without the aches, pains and muscle tension associated with exercise,” says Dr. Miller. “We don’t recommend that you laugh and not exercise, but we do recommend that you try to laugh on a regular basis. Thirty minutes of exercise three times a week, and 15 minutes of laughter on a daily basis is probably good for the vascular system.”

Dr. Miller says this study was not able to determine the source of laughter’s benefit. “Does it come from the movement of the diaphragm muscles as you chuckle or guffaw, or does it come from a chemical release triggered by laughter, such as endorphins?” he asks. Dr. Miller says a compound called nitric oxide is known to play a role in the dilation of the endothelium. “Perhaps mental stress leads to a breakdown in nitric oxide or inhibits a stimulus to produce nitric oxide that results in vasoconstriction,” says Dr. Miller.

The current study builds on earlier research Dr. Miller conducted on the potential benefits of laughter, reported in 2000, which suggested that laughter may be good for the heart. In that study, answers to questionnaires helped determine whether people were prone to laughter and ascertain their levels of hostility and anger. Three hundred volunteers participated in the study. Half of them had suffered a heart attack or had undergone coronary artery bypass surgery; the other half did not have heart disease. People with heart disease responded with less humor to everyday life situations than those with a normal cardiovascular system.

Dr. Miller says certain factors in the earlier study may have affected the results. For example, he says it may be that people who have already had a coronary event are not as laughter-prone as those who do not have heart disease.

He says the current study sought to eliminate that uncertainty by using volunteers whose cardiovascular system was healthy. The results of the brachial artery blood flow measurements, which are precise and objective, appear to make the connection between laughter and cardiovascular health even stronger, according to Dr. Miller.

Other researchers in the study included Charles Mangano, R.D.M.S; Young Park, M.D.; Radha Goel, M.D.; Gary Plotnick, M.D. and Robert A. Vogel, M.D., all from the University of Maryland School of Medicine. The study was supported by a grant from the National Institutes of Health and a Veterans Affairs Merit award to Dr. Miller.

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Read more: http://www.umm.edu/news/releases/laughter2.htm#ixzz1oTXwOhkb


Embargoed for Release
Wednesday, February 29, 2012
1 p.m. EST
Contact:
Daniel Stimson, NINDS
301-496-5751
Blockade of Learning and Memory Genes may Occur Early in Alzheimer’s Disease
NIH-funded research could lead to new therapy

A repression of gene activity in the brain appears to be an early event affecting people with Alzheimer’s disease, researchers funded by the National Institutes of Health have found. In mouse models of Alzheimer’s disease, this epigenetic blockade and its effects on memory were treatable.

“These findings provide a glimpse of the brain shutting down the ability to form new memories gene by gene in Alzheimer’s disease, and offer hope that we may be able to counteract this process,” said Roderick Corriveau, Ph.D., a program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research.

The study was led by Li-Huei Tsai, Ph.D., who is director of The Picower Institute for Learning and Memory at the Massachusetts Institute of Technology and an investigator at the Howard Hughes Medical Institute. It was published online February 29 in Nature.

Dr. Tsai and her team found that a protein called histone deacetylase 2 (HDAC2) accumulates in the brain early in the course of Alzheimer’s disease in mouse models and in people with the disease. HDAC2 is known to tighten up spools of DNA, effectively locking down the genes within and reducing their activity, or expression.

In the mice, the increase in HDAC2 appears to produce a blockade of genes involved in learning and memory. Preventing the build-up of HDAC2 protected the mice from memory loss.

Dr. Tsai and her team examined two mouse models of Alzheimer’s around the time that the mice begin to show signs of brain cell degeneration. They found that the mice had higher levels of HDAC2, but not other related HDAC proteins, specifically in the parts of the brain involved in learning and memory. This increase in HDAC2 was associated with a decrease in the expression of neuronal genes that HDAC2 is known to regulate.
Mouse model of Alzheimer’s disease elevated protein levels in the hippocampus.
In a mouse model of Alzheimer’s disease (right), HDAC2 levels in the hippocampus are higher than in the normal mouse hippocampus (left) Credit: Dr. Li-Huei Tsai, Massachusetts Institute of Technology

Use of a gene therapy approach to reduce the levels of HDAC2 prevented the blockade of gene expression. The treatment also prevented learning and memory impairments in the mice. It did not prevent neuronal death, but it did enhance neuroplasticity — the ability of neurons to form new connections.

Dr. Tsai and her team also examined HDAC2 levels in autopsied brain tissue from 19 people with Alzheimer’s at different stages of the disease, and from seven unaffected individuals. Even in its earliest stages, the disease was associated with higher HDAC2 levels in the learning and memory regions of the brain.

“We think that the blockade of gene expression plays a very important role in the cognitive decline associated with Alzheimer’s disease,” said Dr. Tsai. “The good news is that the blockade is potentially reversible.”

Alzheimer’s disease is the most common cause of dementia in older adults, and affects as many as 5.1 million Americans. In the most common type of Alzheimer’s disease, symptoms usually appear after age 65. A hallmark of the disease is the accumulation of a toxic protein fragment called beta-amyloid in brain cells, which is widely believed to be the initial trigger for neurodegeneration.

Dr. Tsai theorizes that HDAC2 is brought into play by beta-amyloid. Indeed, she and her team found that exposing mouse neurons to beta-amyloid caused them to produce more HDAC2.

“We think beta-amyloid triggers a cascade of damaging reactions. Once of these is to activate HDAC2, which in turn blocks the expression of genes needed for brain plasticity. Once this blockade is in place, it may have a more systemic, chronic effect on the brain,” she said.

Vaccines and other therapies aimed at reducing beta-amyloid are in clinical trials. Efforts to reduce HDAC2 may provide a complementary approach to treating Alzheimer’s, Dr. Tsai said. She has previously reported that HDAC inhibitor compounds can protect against signs of Alzheimer’s disease in mice. A problem with such compounds is that they inhibit not only HDAC2 but related HDAC proteins, leading to broad and potentially toxic effects. The new study supports the possibility of developing drugs more specifically targeted to HDAC2 and the pathology of Alzheimer’s disease, Dr. Tsai said. Her team is working to identify HDAC2-specific inhibitors that could be developed into drugs and moved into trials.

Dr. Tsai’s study was supported by NINDS and the National Institute on Aging through the NIH Common Fund Epigenomics Program. Additional support was provided through the NIH Blueprint for Neuroscience Research and its Neuroplasticity initiative.

NINDS (www.ninds.nih.gov) is the nation’s leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease — a burden borne by every age group, by every segment of society, by people all over the world.

NIA (www.nia.nih.gov) leads the federal government effort conducting and supporting research on aging and the health and well-being of older people. NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer’s Disease Education and Referral (ADEAR) Center at www.nia.nih.gov/Alzheimers.

The NIH Common Fund Epigenomics Program (http://commonfund.nih.gov/epigenomics/) aims to generate new research tools, technologies, datasets, and infrastructure to accelerate the understanding of how genome-wide chemical modifications to DNA regulate gene activity and what role these modifications play in health and disease.

The NIH Blueprint for Neuroscience Research (www.neuroscienceblueprint.nih.gov) is a cooperative effort among the NIH Office of the Director and the 15 NIH Institutes and Centers that support research on the nervous system. By pooling resources and expertise, the Blueprint supports transformative neuroscience research, and the development of new tools, training opportunities, and other resources to assist neuroscientists. For information about the Blueprint’s Neuroplasticity initiative, visit http://www.neuroscienceblueprint.nih.gov/blueprint_basics/BP_themes.htm.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

http://www.nih.gov/news/health/feb2012/ninds-29.htm


Discover the four important lessons I learned while losing weight. They can also help you on your journey to your goal weight.

4 Valuable Tips to Losing Weight Once and For All

Jacquie Cattanach

For years I struggled to lose weight. I couldn’t even begin to count the diets that I have encountered. In the end, I learned that none of those “get slim quick” plans could provide a trusted method for losing weight. Instead, it was these four lessons that helped me finally meet my weight loss goals. They’re basic and simple tips that I had always heard but never listened to. And when I finally paid attention and implemented them into my life, I found it much easier to drop my extra weight.
My problem was that I always struggled to stay motivated and stick with a program. But when I followed these four tips, I found myself approaching my target weight quicker than ever before.

The four tips consist of:

1. Set Small, Frequent Goals
Of all the tips I will share, this is the most important. Rather than setting your sites on one, big goal, focus on smaller goals that are easier to achieve. Don’t focus on your entire weight loss, but instead, set goals in five pound increments. Aim for a single day of healthy eating instead of cutting all junk food from your diet. Make it your goal to spend ten or fifteen minutes in the gym when you first get started instead of focusing on spending countless hours there. With each of these small goals you will feel accomplishments. And it might not sound like much, but getting to these check points will provide the boost of motivation you need to carry you through to the next one. When you are only focused on the big, far reaching goals, it is too easy to feel like you will never make it and give up.

2. Focus on Improvement Not Perfection
The fact is that you will never make it to every workout nor will you ever eat perfectly! Focus on improvement not perfection. Learn to make better choices and don’t beat yourself up when you have fallen “off the wagon”. And most importantly, don’t quit just because you’ve messed up. It’s human instinct to quit when we feel defeated. Fight against this instinct and get back on track.

3. Exercise For Your Health (not your weight)
You should exercise to feel good. I realize that we all want to look good too, but that will come. Give it time. Start out with a workout program that you enjoy and soon you will start to have more energy and also sleep much better. As you learn to enjoy exercise, you will find it hard to go back to being inactive. My exercise of choice is running and, although I didn’t enjoy it in the beginning, I really love it now. Running is great for burning calories. A couple of years ago I bought a Garmin Forerunner GPS. It’s kind of like having your own personal trainer. My favorite feature is where it tells me how many calories I’ve burned. This is such a motivator for me that I actually get pumped to go for a run and burn more calories. Once you get used to feeling great, you will be less likely to slip into unhealthy habits, and at that point, you’ll be well on your way to reaching your weight loss goals.

4. Partner With a Friend
Recruit a friend – this tip will help you stay motivated, no matter what. It’s not usually too difficult to find a friend who also wants to lose weight and get healthier. And it’s all too easy to indulge with unhealthy foods or to miss workouts if you are on the journey alone. But if you have a partner to compare your progress with, you will keep each other encouraged and will be more likely to stay on track. A healthy competitive spirit will probably develop, too, making you push yourself just a bit harder than you would if you were all on your own.
Losing weight isn’t easy, but it doesn’t have to be difficult, either. Adopt these four tips and put them to use in your life and you’ll find it rather easy to make progress towards your goals. You will look back over the years of effort you put into shedding pounds and wonder why it was so difficult. With these tips, you can succeed.

Jacquie struggled with her weight for years. She found that what worked best for her was combining common sense with regular exercise. Now, as an avid runner, Jacquie believes in maintaining a healthy lifestyle and she attributes running as one of the key factors in helping her sustain her goal weight. On her blog – Online Running Gear dot com, she tries to stay current with the newest trends in fitness by researching and writing detailed, informative reviews on products she recommends such as the P90X Reviews and the Forerunner 305 Review.