USPSTF recommends against hormone therapy

 

NEW YORK, 31 may 2012--- Women taking hormone replacement therapy face a complicated mix of possible benefits and risks, a new meta-analysis confirms.

The analysis, published Monday in the Annals of Internal Medicine, combines the results of nine previous clinical trials and found that women taking estrogen or a combination of estrogen and progestin lowered their risk of fracture, but increased their risks for a host of other complications, including strokes and gallbladder disease.
Taken together, estrogen and progestin also seemed to increase the risk of breast cancer and dementia -- although estrogen alone was tied to fewer breast cancer cases.
Based on the new analysis, the government-backed U.S. Preventive Services Task Force (USPSTF) issued preliminary recommendations on Tuesday that postmenopausal women not use hormone therapy to prevent certain chronic conditions.
The Women's Health Initiative study, sponsored by the U.S. National Institutes of Health, showed in 2002 that postmenopausal women taking combination hormone therapy had a higher risk of heart disease and certain cancers.
After that, the USPSTF recommended against the combined use of estrogen and progestin to prevent chronic conditions, and later did the same for estrogen alone in 2005. Their new recommendations do not change that.
The lead author of the new analysis done for the USPSTF said although women have heard a lot about the possible risks and benefits of hormone therapy, there hasn't been a clear message about hormone use.
"We looked at what we could find in this area and tried to find the most final results at this time," said Dr. Heidi Nelson, from Oregon Health & Science University in Portland.
The new recommendations, according to the USPSTF, are based on a "moderate to high certainty that the service has no benefit or that the harms outweigh the benefits."
Dr. Nelson and her team searched the medical literature and found nine randomized controlled trials that fit their standards and were published since 2002.
Four of the studies drew their conclusions from the two Women's Health Initiative trials on hormone therapy, which followed over 27,000 women. In those studies, one group took estrogen, another took estrogen and progestin and the other two took placebos.
Both trials were stopped short because the increased side effects tied to the drugs outweighed their benefits.
Overall, the researchers found women taking combined progestin and estrogen and women taking estrogen alone were 25 to 30% less likely to suffer a fracture during the studies compared to the women taking a placebo.
That worked out to about five fewer broken bones per every 1,000 women annually when they were on hormone therapy.
Women taking those hormones, however, had a 34% to 79% higher chance of having a stroke, gallbladder disease or urinary incontinence. Both combination and estrogen-only treatment were also tied to more cases of "probable" dementia.
And the risk of invasive breast cancer was 25% higher in the estrogen-plus-progestin group than in the comparison group not on hormonal therapy -- but 23 percent lower among those just on estrogen.
Finally, blood clots were about twice as common in women taking combined hormone therapy than in the placebo group.
"The biggest harms are still there," said Dr. Nelson, comparing the results to earlier findings. "We're talking about blood clots and stroke. Those things were there initially and those things have not changed."
The researchers note their conclusions are only based on a few trials, and although those trials followed a lot of women, many stopped taking the hormones during the trial. And the information is also limited to women between the ages of 60 and 69 years old.
The new USPSTF recommendations will be available for review and public comment on the panel's website until June 26.

SOURCE: http://bit.ly/KXHgHH

53 million Americans might have diabetes by 2025, according to new study

Population Health Management is an authoritative peer-reviewed journal published bimonthly in print and online that reflects the expanding scope of health care management and quality. Credit: (c) 2012 Mary Ann Liebert Inc., publishers

The Diabetes 2025 Model for the U.S. projects a continuous and dramatic increase in the diabetes epidemic and makes it possible to estimate the potential effects of society-wide changes in lifestyle and healthcare delivery systems. 

18 may 2012--Predictions for individual states and population subgroups are highlighted in an article published in Population Health Management, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Population Health Management website at http://www.liebertpub.com/pop.
"Diabetes is now a national security issue as it threatens all aspects of our nation's well-being," says Journal Editor-in-Chief David B. Nash, MD, MBA, Dean, Jefferson School of Population Health (Philadelphia, PA).
Based on their Diabetes 2025 Model, William Rowley, MD and Clement Bezold, PhD, Institute for Alternative Futures (Alexandria, VA), project that diabetes (mainly type 2 diabetes) will affect 53.1 million Americans by 2025, an increase of 64% from 2010. Their model can also be used to estimate the benefit of changes in lifestyle and specific interventions in reducing the burden of diabetes, according to the article "Creating Public Awareness: State 2025 Diabetes Forecasts."
Provided by Mary Ann Liebert, Inc.

Too many drugs for many older patients

Older patients are increasingly prescribed multiple drugs that, when combined, can lead to negative side effects and poor health outcomes.  A new Cochrane Library evidence review reveals that little is known about the best ways to avoid inappropriate prescribing of medications for seniors or how to maximize health benefits while minimizing prescriptions.

According to study author Susan M. Patterson, Ph.D., of Queen’s University in Belfast, U.K., inappropriate polypharmacy contributes to around one in 10 hospital admissions. While many patients appropriately take several drugs to treat the variety of medical problems that can arise with aging, she explains, some are inappropriately prescribed combinations of drugs intended to treat not only the original problem, but side effects from those treatments, and even side effects from side effect drugs.
“It becomes a prescribing cascade,” Patterson said. “Rather than review medications and stop the offending drug, doctors just prescribe an additional drug.”
Patterson and her colleagues gathered research on studies of interventions aiming to cut down on inappropriate drug combinations for aging patients.
One study examined the benefits of using electronic decision support, a computerized program that automatically reviews a doctor’s notes and suggests ways to avoid medical errors or improve care. Other studies researched the effectiveness of complex pharmaceutical care interventions that typically combined medication review, individual patient counseling, group patient education in the community and clinical case conferences.
Patterson and her colleagues reported that the interventions that appeared to work the best involved pharmacists as part of a multidisciplinary team working together to solve this problem.
However, she notes, it was impossible to judge from these studies whether these changes in care resulted in better patient outcomes. For example, only some of the studies reported a reduction in hospital admissions or adverse drug events. Additionally, the studies reviewed gave little insight on when to best implement interventions—for example, whether it’s more effective to counsel patients once when they’re discharged from the hospital, whenever they are prescribed new drugs, or at scheduled times of the year regardless of whether their care has changed.
“We don’t know enough about the process to say what a best scenario for reducing inappropriate polypharmacy should look like,” Patterson said. “That’s where we need further research.”
Bradley Flansbaum, D.O., director of hospitalist services at Lenox Hill Hospital in New York City, agrees. He notes that most doctors would say they’re more interested in how changes in prescribing affect patients’ quality of life, something that these studies didn’t fully examine. Rather than look at whether patients are experiencing problems such as headaches or constipation from the drugs they’re on, he says, the studies instead used a checklist to measure potentially dangerous interactions. “Not to say that a checklist isn’t important, but do you want a proxy of what you’d like to measure, or to know about the adverse event itself?” he said.

More information: Patterson SM, et al. Interventions to improve the appropriate use of polypharmacy for older people. Cochrane Database of Systematic Reviews 2012, Issue 5. Art. No.: CD008165. DOI: 10.1002/14651858.CD008165.pub2

Provided by Health Behavior News Service

Vitamin K2: New hope for Parkinson's patients?

Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven, succeeded in undoing the effect of one of the genetic defects that leads to Parkinson's using vitamin K2. His discovery gives hope to Parkinson's patients. This research was done in collaboration with colleagues from Northern Illinois University (US) and will be published this evening on the website of the authorative journal Science.

12 may 2012--"It appears from our research that administering vitamin K2 could possibly help patients with Parkinson's. However, more work needs to be done to understand this better," says Patrik Verstreken.

Malfunctioning power plants are at the basis of Parkinson's.
If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. They generate this energy by transporting electrons. In Parkinson's patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson's: lack of movement (akinesia), tremors and muscle stiffness.
The exact cause of this neurodegenerative disease is not known. In recent years, however, scientists have been able to describe several genetic defects (mutations) found in Parkinson's patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity. By studying these mutations, scientists hope to unravel the mechanisms underlying the disease process.

Paralyzed fruit flies
Fruit flies (Drosophila) are frequently used in lab experiments because of their short life spans and breeding cycles, among other things. Within two weeks of her emergence, every female is able to produce hundreds of offspring. By genetically modifying fruitflies, scientists can study the function of certain genes and proteins. Patrik Verstreken and his team used fruitflies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson's. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.
Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson's patients. Because of this they generated less intracellular energy – energy the insects needed to fly. When the flies were given vitamin K2, the energy production in their mitochondria was restored and the insects' ability to fly improved. The researchers were also able to determine that the energy production was restored because the vitamin K2 had improved electron transport in the mitochondria. This in turn led to improved energy production.

Conclusion
Vitamin K2 plays a role in the energy production of defective mitochondria. Because defective mitochondria are also found in Parkinson's patients with a PINK1 or Parkin mutation, vitamin K2 potentially offers hope for a new treatment for Parkinson's.
Provided by VIB (the Flanders Institute for Biotechnology)

Editorial calls for comprehensive approach to cancer screening

May 9, 2012– An editorial by Marcus Plescia, MD, MPH, director of the Division of Cancer Prevention and Control at the Centers for Disease Control and Prevention (CDC), calls for a more organized and comprehensive approach to increase cancer screening participation among those who are insured or are likely to become insured through the Patient Protection and Affordable Care Act. The editorial, which appears in the American Cancer Society journal, CA: A Cancer Journal for Clinicians, says public health has a responsibility to lead a national approach to cancer control that is comprehensive, strategic, and organized, and that a system to improve cancer screening could act as a model for other clinical preventive services.

11 may 2012--Despite efforts to increase screening for breast and cervical cancers, rates have not improved in almost a decade. Meanwhile, screening rates for colorectal cancer are unacceptably low. Lack of insurance has traditionally been the main factor preventing adults from obtaining cancer screening. And while the Patient Protection and Affordable Care Act will help address this, access to health insurance and medical care are not the only factors that limit participation in cancer screening. Many people who currently have health insurance and regular access to medical care are not being screened.
Dr. Plescia says the infrastructure to promote and ensure cancer screening in the United States must be expanded to achieve desired screening goals. Efforts could include the development of centralized data systems for cancer screening, which could be used to develop more organized, systematic approaches.
While most patients are offered screening tests when they visit a medical provider for unrelated reasons, evidence-based interventions, including reminders to clients and providers to ensure that individuals are screened on time, have been shown to increase cancer screening rates. Screening registries have been found to improve the follow-up of patients with positive screening tests. But widespread implementation of these approaches has been challenging in a fragmented health care system. In a recent study of primary care physicians' practices, only 40% reported that they had a system in place to remind patients to come in for breast or cervical cancer screenings.
"In an era of health care reform, public health has opportunities to ensure that participation in cancer screening is widespread and equitable," concludes the editorial. "Given the magnitude of cancer morbidity and mortality… public health has a responsibility to lead a national approach to cancer control that is comprehensive, strategic, and organized."
More information: Plescia M., Richardson L.C., and Joseph D. New roles for public health in cancer screening [published online ahead of print May 9, 2012]. CA Cancer J Clin. 2012. doi: 10.3322/caac.21147
Provided by American Cancer Society

Researchers say genes and vascular risk modify effects of aging on brain and cognition

Efforts to understand how the aging process affects the brain and cognition have expanded beyond simply comparing younger and older adults.

10 may 2012--"Everybody ages differently. By looking at genetic variations and individual differences in markers of vascular health, we begin to understand that preventable factors may affect our chances for successful aging," said Wayne State University psychology doctoral student Andrew Bender, lead author of a study supported by the National Institute on Aging of the National Institutes of Health and now in press in the journal Neuropsychologia.
The report, "Age-related Differences in Memory and Executive Functions in Healthy APOE ε4 Carriers: The Contribution of Individual Differences in Prefrontal Volumes and Systolic Blood Pressure," focuses on carriers of the ε4 variant of the apolipoprotein (APOE) gene, present in roughly 25 percent of the population. Compared to those who possess other forms of the APOE gene, carriers of the ε4 allele are at significantly greater risk for Alzheimer's, dementia and cardiovascular disease.
Many studies also have shown that nondemented carriers of the APOE ε4 variant have smaller brain volumes and perform less well on cognitive tests than carriers of other gene variants. Those findings, however, are not consistent, and a possible explanation may come from examining interactions between the risky genes and other factors, such as markers of cardiovascular health. Prior research in typical samples of older adults has shown that indeed other vascular risk factors — such as elevated cholesterol, hypertension or diabetes — can exacerbate the impact of the APOE ε4 variant on brain and cognition, but it is unclear if such synergy of risks is present in healthy adults.
Thus, Wayne State researchers evaluated a group of volunteers from 19 to 77 years of age who self-reported as exceptionally healthy on a questionnaire that screened for a number of conditions, representing a "best case scenario" of healthy aging. The research project, led by Naftali Raz, Ph.D., professor of psychology and director of the Lifespan Cognitive Neuroscience Research Program at WSU's Institute of Gerontology, tested different cognitive abilities known for their sensitivity to aging and the effects of the APOE ε4 variant. Those abilities include speed of information processing, working memory (holding and manipulating information in one's mind) and episodic memory (memory for events).
Researchers also measured participants' blood pressure, performed genetic testing to determine which APOE variant participants carried, and measured the volumes of several critical brain regions using a high-resolution structural magnetic resonance imaging brain scan. Bender and Raz showed that for older APOE ε4 carriers, even minor increases in systolic blood pressure (the higher of the two numbers that are reported in blood pressure measures) were linked with smaller volumes of the prefrontal cortex and prefrontal white matter, slower speed of information processing, reduced working memory capacity and worse verbal memory. Notably, they said, that pattern was not evident in those who lacked the ε4 gene variant.
The study concludes that the APOE ε4 gene may make its carriers sensitive to negative effects of relatively subtle elevations in systolic blood pressure, and that the interplay between two risk factors, genetic and physiological, is detrimental to the key brain structures and associated cognitive functions.
"Although genes play a significant role in shaping the effects of age and vascular risk on the brain and cognition, the impact of single genetic variants is relatively small, and there are quite a few of them. Thus, one's aging should not be seen through the lens of one's genetic profile," cautioned the study's authors. They continued, "The negative impact of many genetic variations needs help from other risk factors, and while there isn't much one can do about genes, a lot can be done about vascular risk factors such as blood pressure or cholesterol."
"Everybody should try to keep those in check, although people with certain genetic variants more so than others." Raz said. "Practically speaking, even with the best deck of genetic cards dealt to you, it still makes sense to reduce risk through whatever works: exercise, diet or, if those fail, medication."
Because the study is part of a longitudinal project, he and Bender said the immediate future task now is to determine how the interaction between risky genes and vascular risk factors affect the trajectory of age-related changes — not differences, as in this cross-sectional study — in brain and cognition.
Provided by Wayne State University

Purpose in life may protect against harmful changes in the brain associated with Alzheimer's disease

Greater purpose in life may help stave off the harmful effects of plaques and tangles associated with Alzheimer's disease, according to a new study by researchers at Rush University Medical Center. The study, published in the May issue of the Archives of General Psychiatry, is available online.

09 may 2012--"Our study showed that people who reported greater purpose in life exhibited better cognition than those with less purpose in life even as plaques and tangles accumulated in their brains," said Patricia A. Boyle, PhD.
"These findings suggest that purpose in life protects against the harmful effects of plaques and tangles on memory and other thinking abilities. This is encouraging and suggests that engaging in meaningful and purposeful activities promotes cognitive health in old age."
Boyle and her colleagues from the Rush Alzheimer's Disease Center studied 246 participants from the Rush Memory and Aging Project who did not have dementia and who subsequently died and underwent brain autopsy. Participants received an annual clinical evaluation for up to approximately 10 years, which included detailed cognitive testing and neurological exams.
Participants also answered questions about purpose in life, the degree to which one derives meaning from life's experiences and is focused and intentional. Brain plaques and tangles were quantified after death. The authors then examined whether purpose in life slowed the rate of cognitive decline even as older persons accumulated plaques and tangles.
While plaques and tangles are very common among persons who develop Alzheimer's dementia (characterized by prominent memory loss and changes in other thinking abilities), recent data suggest that plaques and tangles accumulate in most older persons, even those without dementia. Plaques and tangles disrupt memory and other cognitive functions.
Boyle and colleagues note that much of the Alzheimer's research that is ongoing seeks to identify ways to prevent or limit the accumulation of plaques and tangles in the brain, a task that has proven quite difficult. Studies such as the current one are needed because, until effective preventive therapies are discovered, strategies that minimize the impact of plaques and tangles on cognition are urgently needed.
"These studies are challenging because many factors influence cognition and research studies often lack the brain specimen data needed to quantify Alzheimer's changes in the brain," Boyle said. "Identifying factors that promote cognitive health even as plaques and tangles accumulate will help combat the already large and rapidly increasing public health challenge posed by Alzheimer's disease."

More information: www.archgenpsychiatry.com
Provided by Rush University Medical Center

Eating fish, chicken, nuts may lower risk of Alzheimer's disease

A new study suggests that eating foods that contain omega-3 fatty acids, such as fish, chicken, salad dressing and nuts, may be associated with lower blood levels of a protein related to Alzheimer's disease and memory problems. The research is published in the May 2, 2012, online issue of Neurology, the medical journal of the American Academy of Neurology.

08 may 2012--"While it's not easy to measure the level of beta-amyloid deposits in the brain in this type of study, it is relatively easy to measure the levels of beta-amyloid in the blood, which, to a certain degree, relates to the level in the brain," said study author Nikolaos Scarmeas, MD, MS, with Columbia University Medical Center in New York and a member of the American Academy of Neurology.
For the study, 1,219 people older than age 65, free of dementia, provided information about their diet for an average of 1.2 years before their blood was tested for the beta-amyloid. Researchers looked specifically at 10 nutrients, including saturated fatty acids, omega-3 and omega-6 polyunsaturated fatty acids, mono-unsaturated fatty acid, vitamin E, vitamin C, beta-carotene, vitamin B12, folate and vitamin D.
The study found that the more omega-3 fatty acids a person took in, the lower their blood beta-amyloid levels. Consuming one gram of omega-3 per day (equal to approximately half a fillet of salmon per week) more than the average omega-3 consumed by people in the study is associated with 20 to 30 percent lower blood beta-amyloid levels.
Other nutrients were not associated with plasma beta-amyloid levels. The results stayed the same after adjusting for age, education, gender, ethnicity, amount of calories consumed and whether a participant had the APOE gene, a risk factor for Alzheimer's disease.
"Determining through further research whether omega-3 fatty acids or other nutrients relate to spinal fluid or brain beta-amyloid levels or levels of other Alzheimer's disease related proteins can strengthen our confidence on beneficial effects of parts of our diet in preventing dementia," said Scarmeas.

Provided by American Academy of Neurology

Freezing Parkinson's in its tracks

Parkinson's disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It's characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age.

07 may 2012--The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University's Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine- producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.
Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.
Guarding dopamine levels
As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson's patient or aging normally, says Dr. Lev.
The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. "We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain," explains Dr. Lev.
In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson's disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.
Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.
Filling an urgent need
According to Dr. Lev, this peptide could fill a gap in the treatment of Parkinson's disease. "Current treatments are lacking because they can only address symptoms — there is nothing that can change or halt the disease," she says. "Until now, we have lacked tools for neuroprotection."
The researchers also note the potential for the peptides to be used preventatively. In some cases, Parkinson's can be diagnosed before motor symptoms begin with the help of brain scans, explains Dr. Lev, and patients who have a genetic link to the disease might opt for early testing. A preventative therapy could help many potential Parkinson's patients live a normal life.
Provided by Tel Aviv University

Researchers determine vitamin D blood level for reducing major medical risks in older adults

Vitamin D blood levels are lower during the dark days of winter.

In testing older patients' blood vitamin D levels, there's uncertainty about where the dividing line falls between enough and not enough. The threshold amount has become controversial as several scientific societies set different targets.

06 may 2012--To help resolve this debate, University of Washington researchers conducted an observational study. They wanted to learn how much vitamin D must be circulating in the blood to lower the risk of a major medical event. This category included heart attack, hip fracture, diagnosis of cancer, or death.
Their findings are reported today, May 1, in the Annals of Internal Medicine. Dr. Ian de Boer, assistant professor of medicine in the Division of Nephrology and a member of the Kidney Research Institute, led the project. He also holds an appointment in the Department of Epidemiology, UW School of Public Health.
Vitamin D is measured in the blood as 25-hydroxy-vitamin D, abbreviated 25(OH)D.
The researchers tested 25(OH)D concentrations from a biorepository of blood samples of 1,621 Caucasian adults. These adults had enrolled in the early 1990s in the Cardiovascular Health Study, originally designed to look at risk factors and progression of heart disease in people age 65 and over. The participants lived in one of four areas in the United States: Forsyth County, North Carolina; Sacramento, County, California; Washington County, Maryland; and Philadelphia, Pennsylvania.
Over about an 11-year follow-up, researchers looked at the association between each individual's 25(OH)D test results and the time that a first defining medical event occurred. Among the participants, 1,018 had such an event. There were 137 hip fractures, 186 heart attacks (myocardial infarctions), 335 incidences of cancer, and 360 deaths.
Through their statistical analysis, the researchers concluded that the risk of these disease events rose when the concentration of 25(OH)D fell below 20 ng/milliliter or 50 nmol/liter.
"Our results," de Boer said, "lend support to the threshold level recently recommended by the Institute of Medicine, a national, independent government advisory group."
He added, "This target level for adults is considerably lower than that set by other expert panels.'
His research team also found that the association of low 25(OH)D blood concentrations with risk of major disease events varied with the season. Because people soak up most of their Vitamin D from the sun, their levels run highest in the summer and lowest in the winter. Levels in autumn are generally above those in spring.
"In evaluating health risk," the researchers concluded, "Season-specific targets for 25(OH)D blood concentration may be more appropriate than a static target when evaluating patients health risk."
Future research in this area, de Boer said, will require clinical trials. Researcher will look, for example, at the health effects of attempts to raise 25(OH)D in patients whose levels fall below the target. Interventions might include supplements, dietary changes and increasing outdoor activity.
"Sun exposure is tricky," de Boer said, "because people have to protect themselves from skin cancer and other sun damage." Sunscreen blocks the UVB waves responsible for producing Vitamin D. Food sources for Vitamin D are milk, fortified juice and cereal and oily fish like salmon, mackerel, cod and herring.
Vitamin D provides many different beneficial effects on health because it is actually not a vitamin, but a prohormone. It can suppress the hormonal systems that cause fluid to be retained and blood pressure to go up, modulate the function of immune cells, and stop abnormal cells from overgrowing.
Provided by University of Washington

Researchers find potential 'dark side' to diets high in beta-carotene

New research suggests that there could be health hazards associated with consuming excessive amounts of beta-carotene.

05 may 2012--This antioxidant is a naturally occurring pigment that gives color to foods such as carrots, sweet potatoes and certain greens. It also converts to vitamin A, and foods and supplements are the only sources for this essential nutrient.
But scientists at Ohio State University have found that certain molecules that derive from beta-carotene have an opposite effect in the body: They actually block some actions of vitamin A, which is critical to human vision, bone and skin health, metabolism and immune function.
Because these molecules derive from beta-carotene, researchers predict that a large amount of this antioxidant is accompanied by a larger amount of these anti-vitamin-A molecules, as well.
Vitamin A provides its health benefits by activating hundreds of genes. This means that if compounds contained in a typical source of the vitamin are actually lowering its activity instead of promoting its benefits, too much beta-carotene could paradoxically result in too little vitamin A.
The findings also might explain why, in a decades-old clinical trial, more people who were heavily supplemented with beta-carotene ended up with lung cancer than did research participants who took no beta-carotene at all. The trial was ended early because of that unexpected outcome.
The scientists aren't recommending against eating foods high in beta-carotene, and they are continuing their studies to determine what environmental and biological conditions are most likely to lead to these molecules' production.
"We determined that these compounds are in foods, they're present under normal circumstances, and they're pretty routinely found in blood in humans, and therefore they may represent a dark side of beta-carotene," said Earl Harrison, Dean's Distinguished Professor of Human Nutrition at Ohio State and lead author of the study. "These materials definitely have anti-vitamin-A properties, and they could basically disrupt or at least affect the whole body metabolism and action of vitamin A. But we have to study them further to know for sure."
The study is scheduled for publication in the May 4, 2012, issue of the Journal of Biological Chemistry.
Previous research has already established that when beta-carotene is metabolized, it is broken in half by an enzyme, which produces two vitamin A molecules.
In this new study, the Ohio State researchers showed that some of these molecules are produced when beta-carotene is broken in a different place by processes that are not yet fully understood and act to antagonize vitamin A.
Harrison is an expert in the study of antioxidants called carotenoids, which give certain fruits and vegetables their distinctive colors. Carotenoids' antioxidant properties are associated with protecting cells and regulating cell growth and death, all of which play a role in multiple disease processes.
For this work, he joined forces with co-authors Robert Curley, professor of medicinal chemistry and pharmacognosy, and Steven Schwartz, professor of food science and technology, both at Ohio State. Curley specializes in producing synthetic molecules in the pursuit of drug development, and Schwartz is an expert at carotenoid analysis.
Curley manufactured a series of beta-carotene-derived molecules in the lab that match those that exist in nature. The researchers then exposed these molecules to conditions mimicking their metabolism and action in the body.
Of the 11 synthetic molecules produced, five appeared to function as inhibitors of vitamin A action based on how they interacted with receptors that would normally launch the function of vitamin A molecules.
"The original idea was that maybe these compounds work the way vitamin A works, by activating what are called retinoic acid receptors. What we found was they don't activate those receptors. Instead, they inhibit activation of the receptor by retinoic acid," Curley said. "From a drug point of view, vitamin A would be called an agonist that activates a particular pathway, and these are antagonists. They compete for the site where the agonist binds, but they don't activate the site. They inhibit the activation that would normally be expected to occur."
Once that role was defined, the researchers sought to determine how prevalent these molecular components might be in the human body. Analyzing blood samples obtained from six healthy human volunteers, the scientists in the Schwartz lab found that some of these anti-vitamin-A molecules were present in every sample studied, suggesting that they are a common product of beta-carotene metabolism.
The compounds also have been found previously in cantaloupe and other orange-fleshed melons, suggesting humans might even absorb these molecules directly from their diet.
Harrison noted that the findings might explain the outcome of a well-known clinical trial that has left scientists puzzled for years. In that trial, people at high risk for lung cancer - smokers and asbestos workers - were given massive doses of beta-carotene over a long period of time in an attempt to lower that risk. The trial ended early because more supplemented participants developed cancer than did those who received no beta-carotene. This outcome was reinforced by results of a follow-up animal study.
"Those trials are still sending shockwaves 20 years later to the scientific community," said Harrison, also an investigator in Ohio State's Comprehensive Cancer Center. "What we found provides a plausible explanation of why larger amounts of beta-carotene might have led to unexpected effects in these trials."
The research also has implications for efforts to bio-engineer staple crops in developing countries so they contain excess beta-carotene, which is considered a sustainable way to provide these populations with pro-vitamin A. Existing projects include production of golden rice in Asia, golden maize in South America and cassava in Africa.
"A concern is that if you engineer these crops to have unusually high levels of beta-carotene, they might also have high levels of these compounds," Harrison said.
The researchers are continuing to study these compounds, including whether food processing or specific biological processes affect their prevalence. Previous studies have suggested that oxidative stress, which can result from smoking and air pollution exposure, can lead to higher production of these anti-vitamin-A molecules, Harrison noted.

Provided by The Ohio State University

Expert advises against high doses of supplements

05 may 2012-- That vitamin D and calcium you're taking could be causing more harm than good, a new article in the Journal of the National Cancer Institute says.

The paper, co-authored by a professor at the University of Arizona's Mel and Enid Zuckerman College of Public Health, cites evidence that high doses of some supplements increase cancer risk.
"You may not need to take supplements if you have a healthy diet," said article co-author Elizabeth Jacobs, a UA associate professor of epidemiology and a researcher at the Arizona Cancer Center. She cited an old phrase: "The dose makes the poison."
"If you are deficient in nutrients, taking a supplement is probably not going to cause any harm, but if you are already adequate in nutrients, then taking a supplement at a minimum has no benefit and in some cases has been shown to cause harm," Jacobs said.
Jacobs said the authors are not trying to say people who take supplements will get cancer. But she cautions about taking megadoses like 10,000 I.U.s of vitamin D per day, for example.
"A lot of literature has shown that often the people who take dietary supplements need them the least, so they already eat a good diet, they have a lot of nutrients in their diet, they exercise, they don't necessarily need extra nutrients," Jacobs said. "And those are the people who tend to take supplements - they are very health conscious, and that's where the danger is because you are already getting enough of these vitamins or minerals in your diet, and then you are adding more."
The article, titled "Dietary Supplements and Cancer Prevention: Balancing Potential Benefits Against Proven Harms," appeared in the April 25 issue of the Journal of the National Cancer Institute. Its lead author is María Elena Martinez of the University of California-San Diego, who is a former UA College of Public Health epidemiology professor.
"Undoubtedly, use is driven by a common belief that supplements can improve health and protect against disease, and that at worst, they are harmless," the scientists write. "However, the assumption that any dietary supplement is safe under all circumstances and in all quantities is no longer empirically reasonable."
In an email, Martinez stressed that the article is not a study but rather an invited commentary that she hopes will "continue to increase awareness among the scientific community, policymakers and relevant government agencies about the scientific evidence on the topic, especially as it relates to harm related to these products."
Nutritional supplements are an estimated $30 billion-per-year industry.
"If you have too much of anything, that is not a good thing," said Cara Welch, vice president of scientific and regulatory affairs for the Washington, D.C.-based Natural Products Association, a nonprofit group representing natural-products retailers and suppliers. "The article was looking at very high doses in particular populations. It is against the law to market your supplement to treat or prevent cancer - at that point it turns into a drug. There's no way around it. You can't imply you prevent cancer."
Both Martinez and Jacobs say there are certainly people who need supplements, such as women of childbearing age who are considering getting pregnant, people who have been diagnosed with a specific nutrient deficiency like anemia and people with food allergies or intolerances, like lactose intolerance.
Folic acid is recommended for women considering pregnancy, but it is an example of a supplement that could be harmful for people who don't need it, Jacobs said.
"When you are older, folic acid is shaking out to be one of the more worrisome supplements," Jacobs said. "It's not natural. It's completely synthetic folic acid, and so your body is getting this new compound and we're just not as efficient at metabolizing folic acid as folate. So that is some cause for concern."
Jacobs said her personal hope is that the article will inspire better regulation and oversight of the supplement industry.
For most claims made in the labeling of dietary supplements, the law does not require the manufacturer or seller to prove to the government's "satisfaction" that the claim is accurate or truthful before it appears on the product, Food and Drug Administration literature says.
Welch said her organization has a research and education arm that works with companies to ensure "truth in advertising."
And the industry is not regulated in the same way as pharmaceuticals for a reason, she said.
"We're not regulated as drugs because we're not drugs," she said.
Welch said a majority of Americans take supplements like multivitamins and Omega-3 to maintain health. "Unfortunately, the standard U.S. diet doesn't give us all the nutrients we need," she said.
None of the article's five scientist authors takes any supplements, not even the much-heralded vitamin D, Jacobs said.
"Eat a variety of food, exercise, don't smoke - that is superior to taking a supplement," Jacobs said. "You aren't supposed to get the recommended dietary allowance (of nutrients) every day. It rarely happens. You are supposed to just average over time. You just do the best you can. But in the U.S. our problem isn't really under-nutrition, it's over-nutrition."
"You aren't supposed to get the recommended dietary allowance (of nutrients) every day. It rarely happens. You are supposed to just average over time. You just do the best you can. But in the U.S., our problem isn't really under-nutrition, it's over-nutrition."
Read more: http://azstarnet.com/news/science/health-med-fit/ua-expert-advises-against-high-doses-of-supplements/article_c3c3c91d-9939-5387-adea-15bea5184f58.html#ixzz1tsvDO4ej
Provided by University of Arizona

American Geriatrics Society Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults

04 may 2012--Potentially inappropriate medications (PIMs) continue to be prescribed and used as  first-line treatment for the most vulnerable of older adults, despite evidence of poor outcomes from the use of PIMs in older adults. PIMs now form an integral part of policy and practice and are incorporated into several quality measures.

The specific aim of this project was to update the previous Beers Criteria using a comprehensive, systematic review and grading of the evidence on drug-related problems and adverse drug events (ADEs) in older adults. This was accomplished through the support of The American Geriatrics Society (AGS) and the work of an interdisciplinary panel of 11 experts in geriatric care and pharmacotherapy who applied a modi- fied Delphi method to the systematic review and grading to reach consensus on the updated 2012 AGS Beers Criteria.

Fifty-three medications or medication classes encompass the final updated Criteria, which are divided into three categories: potentially inappropriate medications and classes to avoid in older adults, potentially inappropriate medications and classes to avoid in older adults with certain diseases and syndromes that the drugs listed can exacerbate, and finally medications to be used with caution in older adults.

This update has much strength, including the use of an evidence-based approach using the Institute of Medicine standards and the development of a partnership to regularly update the Criteria. Thoughtful application of the Criteria will allow for (a) closer monitoring of drug use, (b) application of real-time e-prescribing and interventions to decrease ADEs in older adults, and (c) better patient outcomes.