Personal Health




Friday, April 16, 2010


Diet High in B Vitamins Lowers Heart Risks in Japanese Study



Friday, April 16, 2010


ScienceDaily (Apr. 15, 2010) — Eating more foods containing the B-vitamins folate and B-6 lowers the risk of death from stroke and heart disease for women and may reduce the risk of heart failure in men, according to Japanese research reported in Stroke: Journal of the American Heart Association.


"Japanese people need more dietary intake of folate and vitamin B-6, which may lead to the prevention of heart disease," said Hiroyasu Iso, M.D., professor of public health at Osaka University.


The findings on the value of B vitamins were consistent with studies in Europe and North America, although the dietary consumption of vitamin B-6 is generally lower in Japan than in the United States.


Researchers analyzed data from 23,119 men and 35,611 women (ages 40-79) who completed food frequency questionnaires as part of the large Japan Collaborative Cohort (JACC) Study. During a median 14 years of follow-up, 986 died from stroke, 424 from heart disease and 2,087 from all diseases related to the cardiovascular system.


Investigators divided participants into five groups based on their intake of folate, vitamin B-6 and vitamin B-12. Comparing those with the diets lowest and highest for each nutrient, they found that higher consumption of folate and vitamin B-6 was associated with significantly fewer deaths from heart failure in men, and significantly fewer deaths from stroke, heart disease and total cardiovascular diseases in women. Vitamin B-12 intake was not associated with reduced mortality risk.


The protective effects of folate and vitamin B-6 didn't change when researchers adjusted for the presence of cardiovascular risk factors, nor when they eliminated supplement users from the analysis. Folate and vitamin B-6 may help guard against cardiovascular disease by lowering homocysteine levels, the investigators said. Homocysteine is an amino acid in the blood that's affected by diet and heredity. Folic acid and other B vitamins help break down homocysteine in the body.


A direct causal link hasn't been established, but evidence has shown that too much homocysteine may damage the inner lining of arteries and promote the formation of blood clots.


Sources of folate include vegetables and fruits, whole or enriched grains, fortified cereals, beans and legumes. Sources of vitamin B-6 include vegetables, fish, liver, meats, whole grains and fortified cereals.


Co-authors include: Renzhe Cui, M.D.; Chigusa Date, M.D.; Shogo Kikuchi, M.D.; Akiko Tamakoshi, M.D.; and the JACC study group. Author disclosures and funding sources are on the manuscript.

Journal Reference:

Renzhe Cui, Hiroyasu Iso, Chigusa Date, Shogo Kikuchi, Akiko Tamakoshi for the Japan Collaborative Cohort Study Group. Dietary Folate and Vitamin B6 and B12 Intake in Relation to Mortality From Cardiovascular Diseases. Japan Collaborative Cohort Study. Stroke, 2010; DOI: 10.1161/STROKEAHA.110.578906

Abnormal Heart Rhythm Linked to Alzheimer's


By Amanda Gardner
HealthDay Reporter
HealthDay News

Friday, April 16, 2010

FRIDAY, April 16 (HealthDay News) -- People with atrial fibrillation, a form of abnormal heart rhythm, are more likely than others to develop dementia, including Alzheimer's disease, a new study finds.

The presence of atrial fibrillation also predicted higher death rates in dementia patients, especially among younger patients in the group studied, meaning under the age of 70.

"This leaves us with the finding that atrial fibrillation, independent of everything else, is a risk factor [for dementia]," said Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City. "This is adding one more brick in the road toward understanding that cardiovascular disease is a major risk factor for dementia."

"Alzheimer's disease, in particular, is one where we don't quite understand the risk factors and what causes it, so studies [like this] that try to investigate the causative effect will help us understand that and ultimately design therapies and approaches to prevent or minimize disease," added Dr. Jared Bunch, lead author of a study appearing in the April edition of the HeartRhythm Journal and a cardiologist/ electrophysiologist with Intermountain Medical Center in Murray, Utah.

This study, however, was not specifically set up to establish a direct cause-and-effect relationship.

The authors looked at 37,025 patients without atrial fibrillation or dementia, aged 60 to 90, over a five-year period.

Individuals who developed atrial fibrillation had a higher risk of all types of dementia, even when other risk factors were taken into account. Alzheimer's disease is by far the most common form of dementia.

More surprising was that those in the younger group -- under age 70 -- who had atrial fibrillation had the highest risk of developing dementia, even though dementia is normally associated with aging. People in this group were also at a 38 percent higher risk of dying.

Among the 764 patients who developed both conditions, diagnosis of atrial fibrillation usually happened first, followed by a diagnosis of dementia. Sometimes the diagnoses occurred simultaneously, the researchers noted.

The authors hypothesized that both atrial fibrillation and dementia may arise from the same risk factors, such as hypertension. Another possibility is that atrial fibrillation increases inflammation, and dementia has been shown to be higher in people with signs of systemic inflammation. Investigating whether treatment of hypertension and/or inflammation in AF patients might help curb the risk of dementia is an area of future study, the researchers added.

"From a public health perspective, the best thing we can do to decrease the coming epidemic of Alzheimer's disease is to do a much better, more aggressive job of helping people with heart disease," Kennedy said. "That means diet and exercise, of course -- everyone knows that. We need to look at obstacles that people encounter beyond their own behavior, obstacles we put up environmentally in the workplace, in the school, that keep people from having better diet and exercise. A heart-healthy diet and lifestyle are really the best means we have available to prevent dementia."

About 2.2 million Americans have atrial fibrillation, while an estimated 5.5 million suffer from Alzheimer's.

More information

The American Heart Association has more on atrial fibrillation.

Stress may be a trigger of bowel disease symptoms


By Amy Norton

Reuters Health

Friday, April 16, 2010

NEW YORK (Reuters Health) – People with inflammatory bowel disease commonly believe that stress can trigger their symptoms, and a new study suggests they may be right.

Canadian researchers found that among 552 bowel-disease patients they followed for a year, the risk of a symptom flare-up increased when patients were feeling particularly stressed.

The findings, reported in the American Journal of Gastroenterology, lend support to what many people with inflammatory bowel disease (IBD) have believed to be true.

IBD refers to a group of conditions marked by chronic inflammation in the intestines, leading to symptoms like abdominal pain and diarrhea. The major forms are Crohn's disease and ulcerative colitis.

The precise cause of the conditions is unclear, but they are thought to involve an immune system overreaction that injures the body's own intestinal tissue. While stress does not cause IBD, it is one of the environmental factors suspected of triggering symptom flare-ups in some people.

Studies show that many people with IBD feel that stress worsens their symptoms, but there has been relatively little scientific evidence of that.

"This is among the first evidence to show that the perception of stress had a direct association with disease course," Dr. Charles N. Bernstein, the lead researcher on the new study, told Reuters Health in an email.

"We are proposing that, based on this study and other emerging data, that clinicians make more of an effort to identify and manage psychological problems and stress that patients may have," said Bernstein, who directs the IBD Clinical and Research Center at the University of Manitoba in Winnipeg.

The findings are based on 552 men and women with Crohn's disease or colitis who completed surveys every three months for one year. The surveys asked about, among other things, symptom flare-ups, stressful events and perceived stress -- that is, how well patients felt they could deal with their daily stresses.

Overall, 174 patients reported a symptom flare-up during the study period, meaning they had a three-month period of symptoms after having been symptom-free the previous three months.

The researchers found that patients' risk of a symptom flare-up increased by more than two-fold when they had reported high levels of perceived stress in the preceding three-month period.

Of patients who reported a flare-up, 52 percent had had high perceived stress levels in the preceding three months, compared with 29 percent of those who remained symptom-free.

On the other hand, certain other factors suspected of triggering IBD symptoms showed no relationship to flare-ups. Those factors included use of antibiotics or non-steroidal anti-inflammatory painkillers -- such as aspirin and ibuprofen -- and infections such as colds, pneumonia and urinary tract infections.

There are biological reasons to believe that a person's response to stress would trigger or worsen IBD symptoms, Bernstein and his colleagues note.

The sympathetic nervous system, which jumps into action during times of stress, acts on the lining of the colon, and might exacerbate existing inflammation. There is also evidence that stress hormones may help harmful bacteria take up residence in the intestines, which might, in turn, affect symptoms.

If stress does trigger IBD symptoms in some people, then it's possible that learning better ways of managing stress would help stave off flare-ups. Bernstein suggested that people who feel that stress is a trigger of their symptoms talk with their doctors about it.

"Patients with IBD should feel willing to discuss stress with their physicians," he said, adding that doctors are increasingly recognizing the effect stress may have on the disease.

Source: American Journal of Gastroenterology, online April 6, 2010.


Thursday, April 15, 2010


Deadly breast cancer had 50 mutations, study finds



Thursday, April 15, 2010

WASHINGTON (Reuters) – Breast tumors that killed an American woman with so-called "triple negative" cancer had 50 separate mutations, including 20 that helped them spread, researchers reported on Wednesday.

New techniques for sequencing the entire genetic map of cells helped the team figure out the changes needed for cancer to spread and kill.

The findings may lead to new tests and new treatments for cancer, they reported in the journal Nature.

Rick Wilson of Washington University in St. Louis and colleagues have been at the forefront of efforts to sequence first the entire human genome and now various types of diseased cells.

They looked at the DNA in four samples from a 44-year-old woman who died when her "triple negative" cancer spread to her brain. This type of cancer disproportionately affects blacks and younger women.

"We've learned some significant lessons about cancer from sequencing the genomes of individual patients and their tumors, but it's clearly just the tip of the iceberg," Wilson said in a statement.

"Moving forward, we'll be comparing tumor genomes from many patients with the same type of cancer to find common genetic alterations. This comprehensive understanding of cancer can aid in the development of new approaches to cancer diagnosis and treatment."

The samples showed that cancer is just as complex as experts had predicted it would be and show that designing drugs to target one or two mutations is unlikely to be useful.

The patient, the first African-American woman to have her entire genome sequenced, had undergone chemotherapy and radiation, but the tumors spread anyway and she died within a year of being diagnosed.

They found 20 mutations that were not common in the early, primary tumors but very common in tumors that popped up outside the breast.

"This indicates that a small subset of cells with a lethal mutation repertoire break free from the primary tumor, circulate in the body, set up residence in other organs and grow aggressively," Dr. Matthew Ellis, another researcher from Washington University who worked on the study, said in a statement. (Reporting by Maggie Fox; Editing by Julie Steenhuysen)

Low Vitamin D Levels Associated With More Asthma Symptoms and Medication Use 



Thursday, April 15, 2010


ScienceDaily (Apr. 15, 2010) — Low levels of vitamin D are associated with lower lung function and greater medication use in children with asthma, according to researchers at National Jewish Health. In a paper published online this week in the Journal of Allergy & Clinical Immunology, Daniel Searing, MD, and his colleagues also reported that vitamin D enhances the activity of corticosteroids, the most effective controller medication for asthma "Asthmatic children in our study who had low levels of vitamin D were more allergic, had poorer lung function and used more medications," said Dr. Searing. "Conversely, our findings suggest that vitamin D supplementation may help reverse steroid resistance in asthmatic children and reduce the effective dose of steroids needed for our patients."


The researchers examined electronic medical records of 100 pediatric asthma patients referred to National Jewish Health. Overall, 47 percent of them had vitamin D levels considered insufficient, below 30 nanograms per milliliter of blood (ng/mL). Seventeen percent of the patients had levels below 20 ng/mL, which is considered deficient. These levels were similar to vitamin D levels found in the general population.


Patients low in vitamin D generally had higher levels of IgE, a marker of allergy, and responded positively to more allergens in a skin prick test. Allergies to the specific indoor allergens, dog and house dust mite, were higher in patients with low vitamin D levels. Low vitamin D also correlated with low FEV1, the amount of air a person can exhale in one second, and lower FEV1/FVC, another measure of lung function. Use of inhaled steroids, oral steroids and long-acting beta agonists were all higher in patients low in vitamin D.


"Our findings suggest two possible explanations," said senior author Donald Leung, MD, PhD. "It could be that lower vitamin D levels contribute to increasing asthma severity, which requires more corticosteroid therapy. Or, it may be that vitamin D directly affects steroid activity, and that low levels of vitamin D make the steroids less effective, thus requiring more medication for the same effect."


The researchers performed a series of laboratory experiments that indicated vitamin D enhances the action of corticosteroids. They cultured some immune cells with the corticosteroid dexamethasone alone and others with vitamin D first, then dexamethasone. The vitamin D significantly increased the effectiveness of dexamethasone. In one experiment vitamin D and dexamethasone together were more effective than 10 times as much dexamethasone alone.


The researchers also incubated immune-system cells for 72 hours with a staphylococcal toxin to induce corticosteroid resistance. Vitamin D restored the activity of dexamethasone.


"Our work suggests that vitamin D enhances the anti-inflammatory function of corticosteroids,' said Dr. Leung. "If future studies confirm these findings vitamin D may help asthma patients achieve better control of their respiratory symptoms with less medication."


This study comes on the heels of another paper by National Jewish Health faculty, which showed that low levels of vitamin D in adult asthma patients are associated with lower lung function and reduced responsiveness to corticosteroids.

Journal Reference:

Searing et al. Decreased serum vitamin D levels in children with asthma are associated with increased corticosteroid use. The Journal of Allergy and Clinical Immunology, 2010; DOI: 10.1016/j.jaci.2010.03.008

B-vitamins Help Protect Against Stroke, Heart Disease


HealthDay News

Thursday, April 15, 2010

THURSDAY, April 15 (HealthDay News) -- People who eat a diet high in B-vitamins are less likely to die from cardiovascular disease, say Japanese researchers.

They analyzed dietary questionnaires completed by more than 23,000 men and almost 36,000 women who were part of the Japan Collaborative Cohort Study. During a median 14 years of follow-up, 986 of the people died from stroke, 424 from heart disease, and 2,087 from all diseases related to the cardiovascular system.

The study found that women who ate more foods with the B-vitamins folate and B-6 were less likely to die from stroke and heart disease, while men who ate a diet high in these B-vitamins were less likely to die of heart failure.

Vitamin B-12 intake was not associated with reduced risk of death from cardiovascular disease.

The researchers believe that folate and vitamin B-6 may help protect against cardiovascular disease by lowering levels of homocysteine, an amino acid in the blood that's affected by diet and heredity. Previous research suggests that too much homocysteine may damage the inner lining of arteries and promote the formation of blood clots.

Fish, liver, meats, whole grains and fortified cereals are sources of vitamin B-6, while vegetables and fruits, whole or enriched grains, fortified cereals, beans and legumes are sources of folate.

The study appears online April 15 in the journal Stroke.

More information

The Office of Dietary Supplement, U.S. National Institutes of Health has more about vitamin B-6.

Wednesday, April 14, 2010


Prostate Cancer Patients at Higher Risk of Blood Clots


By Amanda Gardner
HealthDay Reporter
HealthDay News

Wednesday, April 14, 2010

WEDNESDAY, April 14 (HealthDay News) -- Men with prostate cancer are at greater risk for developing blood clots, especially if they're undergoing hormone therapy, new research shows.

"Our findings indicate that it is important to consider thromboembolic [blood-clotting] side effects when treating patients with prostate cancer, especially those who require endocrine treatment," said Mieke van Hemelrijck, lead author of a study in the April 13 online issue of The Lancet Oncology.

Still, the findings shouldn't change the way men with this type of tumor are treated, just perhaps the way they are monitored, van Hemelrijck added.

"Endocrine treatment is currently the cornerstone of therapy for men with locally advanced or metastatic disease. It is thus not possible to change the treatment, but doctors can be more aware of the risk of thromboembolic diseases and check for certain symptoms when following up their patients," said van Hemelrijck, who is a doctoral candidate at Kings College London.

And the findings do give an extra round of reassurance that this is indeed a risk, another expert noted.

"We have known for decades that cancer patients have a greater risk of blood clots, [but] it hasn't been as well-defined in the prostate cancer population," said Dr. Steven Clinton, director of prostate and genitourinary oncology at The Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove Research Institute in Columbus. "For the first time, this puts some numbers on the risk in that population. It's an enormous study, and it does give us some numbers to work with."

According to background information in the study, cancer patients in general have about a fourfold greater risk of developing blood clots than people who are cancer-free.

Advancing age and other treatments for cancer, including prostatectomy or removal of the prostate gland, might further elevate that clotting risk.

These authors analyzed data from Sweden's National Prostate Cancer Register, which includes 96 percent of all prostate cancer cases in that country. Men were divided into three groups: those receiving endocrine or hormone therapy to reduce levels of male hormones (including testosterone), those receiving surgery and/or radiation and those who were simply being watched.

Men taking hormone therapy had a 2.48 increased risk of developing a blood clot and almost double the chance of a pulmonary embolism (when the clot travels to the lung), compared to men without prostate cancer.

Those in the prostatectomy group had a 73 percent increased risk of blood clots and double the risk of a pulmonary embolism. Those in the "watch-and-wait group had a 27 percent increased risk of blood clots and a 57 percent increased risk of that clot moving to the lung.

None of the groups saw an increased risk of arterial embolism, when clots block an artery.

Those under the age of 65 and those with more advanced disease had even more risk. Given that men in the no-treatment-yet group also had more blood clots, much of the risk was likely from the cancer itself.

"This is probably telling us that something about the cancer and its biology may be impacting coagulation," Clinton said.

However, the type of treatment obviously also plays a role.

Still, the absolute number of blood clots seen in the study was relatively low -- about four per 1,000 person-years, up from 2.

"One should be aware of [the increased risk] and make sure that that the patient is being monitoring for symptoms of blood clots but you're not going to go so far as to recommend that we give [blood thinners] to everybody to prevent it," Clinton said.

More information

The National Cancer Institute has more on prostate cancer.

Is Cleanliness to Blame for Increasing Allergies?



Wednesday, April 14, 2010


ScienceDaily (Apr. 14, 2010) — Allergies have become a widespread in developed countries: hay fever, eczema, hives and asthma are all increasingly prevalent. The reason? Excessive cleanliness is to blame according to Dr. Guy Delespesse, a professor at the Université de Montréal Faculty of Medicine.


Allergies can be caused by family history, air pollution, processed foods, stress, tobacco use, etc. Yet our limited exposure to bacteria concerns Dr. Delespesse, who is also director of the Laboratory for Allergy Research at the Centre hospitalier de l'Université de Montréal.


"There is an inverse relationship between the level of hygiene and the incidence of allergies and autoimmune diseases," says Dr. Delespesse. "The more sterile the environment a child lives in, the higher the risk he or she will develop allergies or an immune problem in their lifetime."


In 1980, 10 percent of the Western population suffered from allergies. Today, it is 30 percent. In 2010, one out of 10 children is said to be asthmatic and the mortality rate resulting from this affliction increased 28 percent between 1980 and 1994.


"It's not just the prevalence but the gravity of the cases," says Dr. Delespesse. "Regions in which the sanitary conditions have remained stable have also maintained a constant level of allergies and inflammatory diseases."


"Allergies and other autoimmune diseases such as Type 1 diabetes and multiple sclerosis are the result of our immune system turning against us," says Dr. Delespesse.


Why does this happen? "The bacteria in our digestive system are essential to digestion and also serve to educate our immune system. They teach it how to react to strange substances. This remains a key in the development of a child's immune system."


Although hygiene does reduce our exposure to harmful bacteria it also limits our exposure to beneficial microorganisms. As a result, the bacterial flora of our digestive system isn't as rich and diversified as it used to be.


Dr. Delespesse recommends probiotics to enrich our intestinal flora. Probiotics are intestinal bacteria that have a beneficial impact on health. They've been used for decades to make yogurt. Probiotics have a proven effect on treating diarrhea, and studies are increasingly concluding similar benefits for the immune system and allergies.


"Consuming probiotics during pregnancy could help reduce allergies in the child," says Dr. Delespesse. "They are not a miracle remedy, yet they are one of many elements that improve our diet and our health."


Artificial pancreas works in 11 patients: study


By Julie Steenhuysen


Wednesday, April 14, 2010

CHICAGO (Reuters) – A test run of an "artificial pancreas" that monitors blood sugar and delivers both insulin and regulatory hormone called glucagon helped patients achieve near-normal blood sugar levels for more than 24 hours, U.S. researchers said on Wednesday.

The system -- made up of a glucose monitor, two pumps and a laptop -- is designed to better mimic the body's natural mechanism of controlling both high and low blood sugar.

In previous tests of artificial pancreas systems that deliver only insulin, some patients have developed dangerously low blood sugar, known as hypoglycemia.

Adding small doses of glucagon, a hormone released by the pancreas to raise blood sugar levels, helped overcome this, according to the study published in the journal Science Translational Medicine.

After some adjustments to a sophisticated computer program that acts as the brain of the system, all 11 adults in the study had good blood sugar control without experiencing hypoglycemia, even after eating three high-carbohydrate meals.

"This is the first artificial pancreas device that has used both insulin and glucagon," said Dr. Steven Russell of Massachusetts General Hospital in Boston, who helped lead the study.

The finding is the latest in what has become a race to develop a fully functioning artificial pancreas that can give patients with type 1 diabetes an automated way to control their blood sugar.

Type 1 diabetes is an autoimmune disease in which the body destroys its own ability to make insulin, rendering sufferers unable to properly break down sugar. People with the condition must frequently monitor and take insulin to regulate blood sugar and prevent diabetic complications such as eye damage, kidney failure and heart disease.

Devices like continuous glucose monitors, such as those made by Medtronic or Abbott Laboratories, that constantly track blood sugar and pumps that inject insulin help, but patients still risk hypoglycemia.

That is where glucagon comes in, Russell said. In people with type 1 diabetes, glucagon does not work properly. Building this into the system helps balance out both the highs and the lows of blood sugar control.

Surprise Findings

The system was developed in the lab of Edward Damiano, a biomedical engineer at Boston University whose son David developed type 1 diabetes when he was a year old.

Damiano's team developed the brains of the device, the computer program that constantly analyzes blood sugar and calculates when diabetics need a dose of insulin or glucagon.

Initial tests of the system revealed a surprise. While the computer program was based on recommended doses of the fast-acting insulin Humalog, made by Eli Lilly and Co, they discovered that many diabetics in their study process insulin much more slowly than expected.

Tweaks to the computer program fixed the problem but the issue demonstrates the complexities of treating diabetes.

In February, British researchers tested a similar system on 17 children and found it kept their blood sugar levels within the normal range for 60 percent of the time.

The Juvenile Diabetes Research Foundation has teamed up with Johnson & Johnson's unit Animas, which makes insulin pumps, and DexCom Inc, which makes continuous glucose monitoring devices, to develop and test an artificial pancreas system.

(Editing by Maggie Fox and Doina Chiacu)

Lack of Omega-6 Fatty Acid Linked to Severe Dermatitis



Wednesday, April 14, 2010


ScienceDaily (Apr. 14, 2010)University of Illinois scientists have learned that a specific omega-6 fatty acid may be critical to maintaining skin health.


"In experiments with mice, we knocked out a gene responsible for an enzyme that helps the body to make arachidonic acid. Without arachidonic acid, the mice developed severe ulcerative dermatitis. The animals were very itchy, they scratched themselves continuously, and they developed a lot of bleeding sores," said Manabu Nakamura, a U of I associate professor of food science and human nutrition.


When arachidonic acid was added to the animals' diet, the itching went away, he said.


Nakamura's team has been focusing on understanding the function of omega-3 and -6 fatty acids, and doctoral student Chad Stroud developed a mouse model to help them understand the physiological roles of these fats. By knocking out genes, they can create deficiencies of certain fats and learn about their functions.


"Knocking out a gene that enables the body to make the delta-6-desaturase enzyme has led to some surprising discoveries. In this instance, we learned that arachidonic acid is essential for healthy skin function. This new understanding may have implications for treating the flaky, itchy skin that sometimes develops without an attributable cause in infants," he said.


Nakamura explained that our bodies make arachidonic acid from linoleic acid, an essential fatty acid that we must obtain through our diets. It is found mainly in vegetable oils.


Scientists have long attributed healthy skin function to linoleic acid, which is important because it provides the lipids that coat the outer layer of the skin, keeping the body from losing water and energy, which would retard growth, the scientist said.


But skin function seems to be more complicated than that. These itchy mice had plenty of linoleic acid. They just couldn't convert it to arachidonic acid because the gene to make the necessary enzyme had been knocked out, he noted.


Arachidonic acid is also essential to the production of prostaglandins, compounds that can lead to inflammatory reactions and are important to immune function. Common painkillers like aspirin and ibuprofen work by inhibiting the conversion of arachidonic acid to prostaglandins.


"We usually think of inflammation as a bad thing, but in this case, prostaglandins prevented dermatitis, which is an inflammatory reaction. We measured prostaglandin levels in the animals' skin, and when we fed arachidonic acid to the knockout mice, they resumed making these important chemical compounds," he said.


Nakamura cautioned that there are still things they don't understand about the function of this omega-6 fatty acid. "This new knowledge is a starting point in understanding the mechanisms that are involved, and we need to do more research at the cellular level."


The study was published in a recent issue of the Journal of Lipid Research. Co-authors are Chad K. Stroud, Takayuki Y. Nara, Manuel Roqueta-Rivera, Emily C. Radlowski, Byung H. Cho, Mariangela Segre, Rex A. Hess, and Wanda M. Haschek, all of the U of I, and Peter Lawrence, Ying Zhang, and J. Thomas Brenna of Cornell University. Funding was provided in part by a USDA National Needs Fellowship Award and a grant from the National Institutes of Health.

Journal Reference:

Stroud et al. Disruption of FADS2 gene in mice impairs male reproduction and causes dermal and intestinal ulceration. The Journal of Lipid Research, 2009; 50 (9): 1870 DOI: 10.1194/jlr.M900039-JLR200

Despite concerns, soy probably safe for thyroid


By Amy Norton

Reuters Health

Wednesday, April 14, 2010

NEW YORK (Reuters Health) – Despite some concerns to the contrary, the soy-based dietary supplement genistein may not harm postmenopausal women's thyroid function, a new study finds.

Genistein is a type of soy isoflavone, a plant chemical that is structurally similar to estrogen and may have certain estrogen-like effects in the human body. In a 2007 clinical trial, Italian researchers found that genistein supplements, along with calcium and vitamin D, appeared to help boost bone mass in postmenopausal women with thinning bones.

In this latest study, the researchers evaluated data from the same clinical trial -- this time looking at whether the genistein supplements had any effects on the women's thyroid function.

The question stems from lab research showing that genistein and other isoflavones may decrease thyroid-hormone production. Thyroid hormones help govern metabolism, and an underactive thyroid gland, called hypothyroidism, can lead to problems like fatigue, weight gain and intolerance to cold.

The earlier research suggested that isoflavones can affect thyroid hormones by interfering with iodine, which is needed for thyroid- hormone production, explained Dr. Francesco Squadrito of the University of Messina, the senior researcher on the study.

However, he told Reuters Health by email, those studies used genistein doses that were 10 to 250 times higher than the doses used in his team's clinical trial -- 54 milligrams (mg) per day.

Squadrito and his colleagues found that among 77 study participants they followed for three years, those who used the genistein supplement during that time showed no overall differences in thyroid function compared with women who were given a placebo.

The findings are published in the Journal of Clinical Endocrinology and Metabolism.

According to Squadrito, it is not surprising that studies would find thyroid effects of very high doses of genistein. However, he said, women are unlikely to consume such levels from soy-protein products, or from soy foods like tofu.

As far as thyroid function is concerned, Squadrito said, "it is possible to conclude that genistein therapy is safe in postmenopausal women -- at least at the dose of 54 mg a day."

However, soy contains several types of isoflavones, and more studies are needed to establish the safety of those compounds, according to Squadrito and his colleagues.

Source: Journal of Clinical Endocrinology and Metabolism, online March 31, 2010.


Childhood Obesity Linked to Stiff Arteries



Wednesday, April 14, 2010


ScienceDaily (Apr. 14, 2010) — Children with more body fat and less endurance than their fitter, leaner counterparts have stiffer arteries at a young age, Medical College of Georgia researchers said.


Stiff arteries are a hallmark of atherosclerosis, a typically adult condition in which blood vessels become clogged.


"When children at such a young age start getting diseases only adults used to get, it's like the sky is falling," said Dr. Catherine L. Davis, clinical health psychologist in MCG's Georgia Prevention Institute and principal investigator on the study. The findings were presented during the 31st Annual Society of Behavioral Medicine Meeting.


Using a non-invasive measure of pulse wave velocity, Davis discovered that children with a greater body mass index, more body fat and less endurance had stiffer central arteries compared to leaner and fitter children. Identifying these children early could hasten preventive measures, she noted.


Her most recent National Heart, Lung and Blood Institute-funded study involves overweight or obese 8-11-year-old children, half of whom participate in aerobic exercises such as jumping rope and shooting hoops weekdays after school while the other half participate in sedentary activities, including board games and crafts.

Among a similar cohort of children, Davis also found that regular exercise decreases metabolic risks linked to cardiovascular disease and diabetes. The new study will examine the effects of exercise on nonalcoholic fatty liver disease and atherosclerosis.


Nonalcoholic fatty liver disease, which affects about 40 percent of obese children, initially is often symptomless. But its long-term risk of inflammation and scarring, which can cause liver damage and failure, also is related to hardening of the arteries.


"It's essentially another aspect of the metabolic imbalance these children are experiencing when they're overweight and inactive and is a signal they're at very high risk for diabetes," Davis said.


She already found that exercise reduces inflammation, visceral fat (a type of fat situated between the organs), body mass index and insulin levels. Children who exercised showed improvement on virtually all of those measures after just 20 to 40 minutes of daily aerobic exercise for 12 weeks. She presented the findings at the American Heart Association's Nutrition, Physical Activity and Metabolism Conference in March.


Davis is working with Dr. Sudipta Misra, MCG pediatric hepatologist, to use novel ultrasound technology instead of the traditional biopsies to gauge liver fibrosis.


"A gentle pulse will pass through the liver, and the echo will determine if the liver is stiff (indicating disease) or nice and soft," Davis said.


Davis hopes her research will encourage programs to keep children active and hold lifestyle-related diseases at bay.


U.S. team discovers new Alzheimer's risk gene


By Julie Steenhuysen


Wednesday, April 14, 2010

CHICAGO (Reuters) – People with a common variation in a gene linked with coronary artery disease have nearly double the risk of developing Alzheimer's disease compared with others, U.S. researchers said on Wednesday.

The gene MTHFD1L helps control production of the amino acid homocysteine in the blood. Different variations of the gene have been linked with a higher risk of coronary artery disease.

Because blood vessel function may also play a role in Alzheimer's, the finding may help explain the role of homocysteine in both conditions.

"Identifying this gene is important because the gene is known to be involved in influencing the body's levels of homocysteine," Margaret Pericak-Vance of the University of Miami, who led the research presented on Wednesday at the American Academy of Neurology meeting in Toronto.

The finding adds to a growing understanding of the genetic basis for Alzheimer's disease, a mind-wasting condition for which there are few treatments and no cure and which affects 26 million people globally.

"We are hopeful our identification of MTHFD1L as a risk gene for Alzheimer's disease will help us to better understand how this disease develops and potentially serve as a marker for people who may be at increased risk," Adam Naj of the University of Miami, who worked on the study, said in a statement.

Pericak-Vance and colleagues looked at slight differences in the genetic code of 2,269 people with late-onset Alzheimer's disease and 3,107 people without the disease.

Despite decades of research, doctors still have few treatments for Alzheimer's disease, which is expected to affect 100 million people by 2050.

Identifying people who are at risk may help them take steps to prevent or delay the disease, such as exercising and eating a diet low in saturated fat.

Late pregnancy multivitamins linked to prematurity


By Lynne Peeples

Reuters Health

Wednesday, April 14, 2010

NEW YORK (Reuters Health) – For a woman eating a healthy diet, multivitamin supplements during late pregnancy could do more harm than good, a new study suggests.

British researchers found that a woman's risk of delivering prematurely tripled if she continued taking the prenatal pills into her third trimester.

"These supplements are available over-the-counter in the United Kingdom and frequently promoted as being beneficial for mums-to-be," Dr. Nigel Simpson of the University of Leeds in the U.K., and one of the authors of the study, told Reuters Health by email.

However, some weaknesses in the study may stand in the way of translating the finding into practice, Dr. James Mills, of the U.S. National Institute of Child Health and Human Development told Reuters Health.

While some studies in developing countries have found prenatal supplements to be beneficial, whether or not it also is in developed countries-where most women are presumably already well-nourished-has not been thoroughly studied.

To fill this void, Simpson and his colleagues assessed the diets and supplement use of nearly 1,300 pregnant women recruited at Leeds Teaching Hospitals between 2003 and 2006.

Overall, slightly more than 4 percent of babies were born weighing less than 2500 grams and categorized as low birthweight. About the same number of babies were born prematurely, defined as before 37 weeks of pregnancy.

The team saw no differences in the risks of having a low birthweight baby for the more than 80 percent of women who took supplements at any point during pregnancy compared with those who took none.

However, the approximately 30 percent of women taking supplements during their third trimester were three times as likely to have a premature delivery, after taking smoking, alcohol consumption and other relevant factors into account.

Why this would be true is unclear. One possibility, according to the authors, is that interactions between different vitamins and minerals led to a reduction in the nutrients available for the growing fetus.

And women in the study were already getting enough of most vitamins and minerals contained in prenatal supplements from their diets, with the exceptions of vitamin D, iron, folate, selenium and iodine, note the authors in the British Journal of Obstetrics and Gynecology.

The U.S. National Institute of Child Health and Human Development's Mills said that a few weaknesses of the study make its significance less clear. Since the U.K. stops short of officially recommending prenatal multivitamins, British women who chose to take the supplements may have been those who were already at a greater risk for pregnancy problems.

Mills is also concerned that the relationship with premature delivery could have simply appeared by chance, given the large number of comparisons the researchers made between various birth outcomes and supplement use.

The study team acknowledges that larger, more rigorous studies are necessary to confirm their results. For now, Simpson says pregnant women probably don't need multivitamins past their first three months, after which time they might actually do harm.

"Eating a healthy diet," he said, "is likely to be sufficient for expectant mums."

Source: British Journal of Obstetrics and Gynecology, March 29, 2010.

Tuesday, April 13, 2010

Walking may ease some burdens of menopause


By Rachael Myers Lowe

Reuters Health

Tuesday, April 13, 2010

NEW YORK (Reuters Health) – Walking for 45 minutes a few times a week may help women in the "battle of the bulge" that often accompanies menopause, and at the same time improve overall well being, hints new research from Canada.

Pointing out that the 45 minutes can be broken up into shorter jaunts, researcher Dr. Pascale Mauriège, of Quebec's Laval University, told Reuters Health in an email it's a program that could be "easily incorporated" into a woman's daily life.

The researchers wanted to know if a 16-week walking program would help older overweight inactive women lose some weight, increase their lean body mass and experience a better health-related quality of life.

They enrolled 35 moderately obese and sedentary white women who were either nearing menopause or newly post-menopausal. Thirty women finished the program - 16 premenopausal and 14 postmenopausal.

The women, guided by trainers, walked for 45 minutes on an indoor track every other day for 16 weeks. The intensity of the walking was not unlike the intensity of walking a dog, Mauriège said. While moderately obese, all participants were healthy.

Of the five participants who dropped out of the study early, three bristled at the program's restrictions and wanted to walk more than three days a week.

At the beginning of the study, post and premenopausal women tended to have similar health-related quality of life ratings on such things as body pain, health, vitality, physical and social functioning and emotional and mental health.

At the end of the program, both groups of women appeared to benefit physically and mentally although in different ways, the researchers report in the journal Menopause.

Greater weight loss was achieved by the premenopausal women who lost an average of about 4.4 pounds compared to 1.5 pounds for the postmenopausal women. They also tended to lose more fat mass. Postmenopausal women, however, tended to benefit with a larger drop in their waist size and from gains in lean body mass.

The program also appeared to have a "non-negligible impact" on both groups' sense of physical and mental well being, the researchers report.

Postmenopausal women had the larger gains in health-related quality of life scores in bodily pain, daily physical functioning, general health, emotional and mental health while premenopausal women had the greater gains in all physical activities of life, vitality and social functioning.

Mauriège said, to her knowledge, this is the first study to test the impact of a walking program on the various mental functioning scores in pre- and postmenopausal women.

But the study's small size and lack of a control group (a group of women similar to participants who did not take part in the study's exercise regimen) limits the validity of the findings.

Still, the findings do suggest that "moderate-intensity and moderate-frequency exercise" easily integrated in life habits seems to be enough to improve health-related quality of life in both premenopausal and early postmenopausal women, the researchers conclude.

Source: Menopause, April 2010.


Hormones Tied to Diabetes Might Also Influence Fertility


HealthDay News

Tuesday, April 13, 2010

TUESDAY, April 13 (HealthDay News) -- A new study in mice suggests that the hormones leptin and insulin work together in the brain to control blood sugar levels and, in a surprise to researchers, female fertility.

The findings also appear to suggest that diabetes and obesity aren't always necessarily connected.

"Many people, and even many physicians, think you develop diabetes that is solely secondary to obesity," study senior author Dr. Joel Elmquist, professor of internal medicine and pharmacology at University of Texas Southwestern Medical Center, said in a news release. "Our findings indicate that is not necessarily the case, at least in mice. We can make the animals very diabetic without obesity, suggesting that there may be a circuit or path of resistance to these signals in the brain that helps explain the powerful anti-diabetic actions of leptin."

Also, Elmquist said, the research suggests that people don't need to be obese in order to develop type 2 diabetes.

Elmquist said the findings provide new insight into how brain cells regulate glucose and insulin. Scientists think certain brain cells play a major role in prompting weight loss by suppressing appetite.

In addition to their findings about metabolism, the researchers found that female mice with the most brain cells that couldn't process the hormones had trouble breeding and produced smaller litters.

The study findings were released online April 7 in the journal Cell Metabolism.

More information

The National Institutes of Health has more on type 2 diabetes.

Study shows wild birds could spread avian flu



Tuesday, April 13, 2010

WASHINGTON (Reuters) – Wild ducks that are immune to the effects of H5N1 avian influenza could be spreading the virus far and wide, U.S. government researchers said on Monday.

Satellite tracking of migrating northern pintail ducks showed they flew from a bird flu-infected marsh in Japan to nesting areas in Russia, said the scientists from the U.S. Geological Survey and the University of Tokyo said.

The study does not prove the pintails carried the virus, but the species can be infected with H5N1 with no ill effects.

H5N1 bird flu has been circulating in Asia and the Middle East, with occasional outbreaks in Europe, since 2003. It rarely infects people but when it does it is deadly: the World Health Organization has documented 493 cases and 292 deaths.

It wipes out chickens, who have no immunity, and some other bird species and can seriously damage poultry farms. Experts fear it has the potential to cause a human flu pandemic that would be much worse than the H1N1 swine flu pandemic.

Experts have argued about whether wild birds, spread the virus, or the poultry trade, or both.

Writing in the journal Ibis, the researchers described how they attached satellite transmitters to 92 northern pintail ducks several months before the H5N1 virus was discovered in dead and dying whooper swans in a wetlands in Japan.

Twelve percent of marked pintails used the same wetlands as infected swans. Then some of them migrated more than 2,000 miles to nesting areas in eastern Russia.

Birds can spread flu viruses orally and in their droppings.

"Consequently, infected wild birds that do not become ill, or birds that shed the virus before they become ill, may contribute to the spread of H5N1," said Jerry Hupp of the


USGS scientists have been testing birds in Alaska, considered a potential place where H5N1 could enter the Americas from Asia. So far, no case of highly pathogenic H5N1 has been found in either birds or people in the Americas.

(Reporting by Maggie Fox)

Blacks Hit Hardest by Lung Cancer

By Amanda Gardner
HealthDay Reporter
HealthDay News

Tuesday, April 13, 2010

TUESDAY, April 13 (HealthDay News) -- Blacks are hit the hardest when it comes to both developing and dying from lung cancer.

A new report from the American Lung Association paints a grim picture of how environmental factors, biological factors, cultural attitudes and biases in the health-care system conspire to make this deadly disease even deadlier among members of this minority group.

"Despite lower smoking rates, African-Americans are more likely to develop and die from lung cancer than whites. African-Americans are more likely to be diagnosed later when the cancer is more advanced. Also, African-Americans are more likely to wait longer after the diagnosis to receive treatment or perhaps to refuse treatment and to die in the hospital after surgery," Dr. William J. Hicks, professor of clinical medicine at The Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute in Columbus, said during a Monday news conference.

Black men bear an even more disproportionate share of the burden, being 37 percent more likely to be diagnosed with lung cancer and 22 percent more likely to die of the disease than white men.

Only 12 percent of blacks will be alive five years after their lung cancer diagnosis, compared with 16 percent of whites, the ALA report notes.

The report points to a number of factors that could explain the disparity, including differences in socioeconomic status, big business behavior and environmental exposure.

For instance, thanks to concerted marketing efforts by the tobacco industry, blacks have higher rates of smoking menthol cigarettes than other groups. Smokers of menthol cigarettes tend to have higher blood levels of cotinine, an indicator of how much nicotine a person is absorbing. The U.S. Food and Drug Administration is expected to issue a report on the public health impact of menthol cigarettes in March of 2011.

Education and income levels also play a role. Not only do these factors impact lifestyle choices and access to health care, including health insurance, but they largely determine where blacks are likely to work and live.

According to one study, predominantly black neighborhoods have noticeably higher levels of air pollution than other communities.

And a greater proportion of blacks work in the transportation industry, where they are exposed to diesel fumes, known to contribute to lung cancer risk.

Meanwhile, blacks are less likely to have a gene variant that is targeted by a widely used cancer drug.

The good news is that if individuals, regardless of race, receive equal treatment for lung cancer, their outcomes are likely to be similar.

However, as Hicks pointed out, "the sad truth is that not all patients receive equal treatment and for those who do not, their health outcomes are poorer."

Blacks are also less likely to be seen by experienced or credentialed doctors and hospitals, less likely to have their disease staged, less likely to have surgery and less likely to undergo chemotherapy.

These problems have to do with both patient and provider attitudes.

"We're looking not just at system failures but also at issues that are deeply rooted in the history, culture and beliefs of African-Americans," Hicks said. "This is not post-racial America. For people of color in the United States, race and discrimination are facts of everyday life, and clearly take a toll both mentally and with regard to one's physical health."

There is, first of all, the legacy of the Tuskegee (syphilis) and other medical experiments of the past, in which blacks were exploited by the U.S. health-care establishment. That's made trust in the medical establishment an ongoing issue, the experts said.

And while doctors appear less likely to funnel black patients to the right kind of specialists, blacks are more likely to refuse gold-standard treatment even when it is offered and available, they added.

"This is not an issue that can be solved overnight," said Chuck D. Connor, president and CEO of the American Lung Association. "We've made progress in reducing smoking rates and exposure to secondhand smoke, but there is still much work that needs to be done."

Hicks said he hoped experts and community members could arrive at a new approach that will "hopefully render this very preventable form of cancer to its state of 125 years ago, when it was a very rarely encountered medical issue, primarily before the advent of widespread cigarette smoking."

More information

The American Lung Association has the full report.

New Pathway Involved in Rheumatoid Arthritis Identified



Tuesday, April 13, 2010


ScienceDaily (Apr. 13, 2010) — Investigators from Hospital for Special Surgery have identified a pathway involved in turning off inflammation that does not work properly in people with inflammatory arthritis. The finding, reported in the April 23 issue of the journal Immunity, could lead to the development of new therapeutic approaches to treating arthritis in the future.


"This is the first study to link this pathway to rheumatoid arthritis. In the twenty years or so that I have been studying regulation of inflammation, this seems to be the most potent inhibitory mechanism that we have seen," said Lionel Ivashkiv, M.D., associate chief scientific officer at Hospital for Special Surgery in New York City and lead author of the study that has appeared online ahead of print.


For several years, Dr. Ivashkiv's lab has been studying what regulates the production of cytokines in inflammatory diseases. Cytokines are small proteins that regulate inflammation; some cytokines spark inflammation and some cytokines are anti-inflammatory. By identifying pathways involved in cytokine production, the researchers hope to open up new therapeutic avenues for diseases such as arthritis in which cytokine production does not work properly.


Prior to this study, researchers knew that so-called immunoreceptor tyrosine-based activation motif (ITAM)-coupled receptors were involved in regulating inflammation, but they did not know how the ITAM pathways actually turned off inflammatory signaling. Previous studies had shown that the ITAM pathway signaling components directly suppressed so-called Toll-like receptor signaling molecules involved in inflammation, but there was a hint that an alternative pathway may also be involved. The researchers thought that maybe the ITAM pathway might be involved in triggering another pathway that then inhibits inflammation.


In studies using white blood cells similar to those that cause disease, the researchers set out to investigate what signaling pathways might be induced by the activation of ITAM-associated receptors. They used fibrin(ogen) and immune complexes, proteins that are highly expressed at inflammatory sites, to activate the ITAM-associated receptors and then watched what happened. The researchers found that activation of the ITAM receptor set off a pathway known as DAP12-Syk-Pyk2-p38-MSK that was dependent on calcium signaling and discouraged pro-inflammatory cytokine production.


They also found that ITAM receptors induce IL-10, an anti-inflammatory cytokine, and proteins SOCS3, ABIN-3, A20, and Hes1 that have been implicated in the suppression of cytokines. In other studies, they showed that this ITAM inhibitory pathway does not work properly in people with inflammatory arthritis.


"When we looked at macrophages from patients with arthritis, we found that the whole inhibitory pathway would not work," Dr. Ivashkiv said. "What this study suggests is that one of the things that contributes to inflammation in arthritis is crippling of beneficial pathways that usually serve to turn inflammation off." He said clinicians in the future may be able to focus on therapies that will augment or reinstitute these beneficial or homeostatic pathways as a way of turning off inflammation in chronic arthritis.


"Before this study we knew that ITAM-coupled receptors had the potential to inhibit inflammatory cytokine production, but there was very limited knowledge about how that worked," Dr. Ivashkiv said. "What we accomplished with the study is that we have increased our understanding of an indirect inhibitory mechanism that we think can serve as the basis for designing new approaches to therapy. This work implicates for the first time a negative role for calcium signaling downstream of these ITAM-coupled receptors and explains how that works."He added that investigators believe that there is extensive crosstalk among the various pathways and they think that the ITAM receptors play a very important role in deciding how all the signaling gets integrated. "In terms of the homeostatic pathways that control inflammation, we think that this pathway that we have described is one of the strongest ones. It completely turns things off," Dr. Ivashkiv said. "What you usually see are these partial inhibitions or attenuations in terms of inflammatory cytokine production. What we saw was a complete inhibition of the response."


Dr. Ivashkiv said future work would focus on further elucidating molecular details of the pathway and further testing of its importance in arthritis and animal models of disease.


The work was funded by grants from the National Institutes of Health. Other authors of the study include Lu Wang, Ph.D., Rachael Gordon, Linda Huynh, Xiaodi Su, Kyung-Hyun Park Min, M.D., and George D. Kalliolias, M.D., from Hospital for Special Surgery; Jiahuai Han, Ph.D., from the Scripps Research Institute in La Jolla, Calif.; and J. Simon Arthur, M.D., from the MRC Protein Phosphorylation Unit, University of Dundee in Dundee, Scotland.

Journal Reference:

Lu Wang, Rachael A. Gordon, Linda Huynh, Xiaodi Su, Kyung-Hyun Park Min, Jiahuai Han, J. Simon Arthur, George D. Kalliolias, Lionel B. Ivashkiv. Indirect Inhibition of Toll-like Receptor and Type I Interferon Responses by ITAM-Coupled Receptors and Integrins. Immunity, 2010; DOI: 10.1016/j.immuni.2010.03.014

Subbing 'bad' carbs for 'bad' fats ups heart risk


By Anne Harding

Reuters Health

Tuesday, April 13, 2010

NEW YORK (Reuters Health) – People who cut out saturated fatty acids while upping their intake of white bread, pasta and other refined carbohydrates that can cause blood sugar to spike aren't doing their heart any favors, new research from Denmark shows.

But reducing saturated fatty acid intake while eating more whole grain bread, vegetables (aside from potatoes), and other carbohydrates with a less dramatic effect on blood sugar may improve heart health, Dr. Marianne U. Jakobsen of Aarhus University Hospital and her colleagues found. "The type of carbohydrate matters," Jakobsen told Reuters Health.

A recent analysis of 21 studies including 350,000 people found "no significant evidence" that saturated fat in and of itself increased heart disease risk, but the authors of that analysis suggested that what people replaced those saturated fat calories with might be more important. A subsequent study found that this was indeed the case; people who upped their polyunsaturated fatty acid intake while cutting saturated fat showed improved heart health.

In the current study, Jakobsen and her team looked at the carbohydrate side of the equation. Specifically, they accounted for the "glycemic index" of different types of carbohydrates.

Glycemic index is a measure of how quickly blood sugar jumps after eating a particular type of carbohydrate. Low glycemic index foods tend to be high in fiber and less refined, such as foods made from whole grains; high glycemic foods are often lower in fiber and more highly refined, and include white bread, pasta made from white flour, and bananas.

To investigate how increasing carb intake while reducing saturated fatty acid intake affected the heart, the researchers looked at 53,644 men and women who had never suffered heart attacks. During follow-up, which averaged about 12 years, nearly 2,000 heart attacks were documented.

Jakobsen and her team divided the study participants into three groups based on the average glycemic index of the carbohydrates in their diet, and then calculated heart attack risk based on the composition of their diet.

They found that heart attack risk fell by 12 percent for every additional 5 percent of a person's total calorie intake that came from carbohydrates -- if a person's average dietary glycemic index was low. However, this reduction wasn't statistically significant, meaning it could have been due to chance.

But among the people with the highest average dietary glycemic index, every 5 percent increase in carbohydrate calories upped heart attack risk by 33 percent. For people whose average glycemic index fell in the middle, an increase in carb intake along with a reduction in saturated fatty acid intake had no effect on heart risk.

"We cannot say that saturated fatty acids are not associated with increased risk of coronary heart disease because it depends on what you compare," Jakobsen told Reuters Health.

Unfortunately, she added, figuring out the glycemic index of a particular food is not straightforward. "It's a scientific way of classifying foods, so it's not really public-health-friendly," she said.

Nevertheless, the researcher added, people can likely decrease their glycemic index by eating "less refined foods."

Source: American Journal of Clinical Nutrition, April 7, 2010.

Anti-Aging Hormones: Little or No Benefit and the Risks Are High, According to Experts



Tuesday, April 13, 2010


ScienceDaily (Apr. 13, 2010) — In the wake of the American Medical Association's (AMA) Council on Science and Public Health's recently released report "The use of hormones for "anti-aging": a review of efficacy and safety," a leading medical authority has criticized the use of anti-aging hormones. Dr. Thomas T. Perls, an associate professor of medicine at Boston University School of Medicine has long spoken out against the promotion and distribution of growth hormones for non-medical uses such as anti-aging and sports.


In an editorial appearing in the Future Medicine journal Aging Health, Dr. Perls applauds the courage and example displayed by the AMA in its recently published assessment of the risks and benefits of growth hormone, testosterone, estrogen and DHEA for anti-aging. 


There have always been nostrums and potions peddled for eternal youth. Most recently these have been what some entrepreneurs call "bio-identical" or "all-natural" hormones. What they mean by these terms varies from substances made from vegetables -- such as soy or yams, which some claim have estrogen-like effects to, more commonly, drugs that are exactly the same as hormones prescribed by endocrinologists for specific diseases. Dr. Perls remarked: "The terms bio-identical or all-natural, particularly in the case of the drugs prescribed by endocrinologists, misleadingly convey a sense of safety to the gullible customer. Arsenic is all-natural to, and it even has some medical uses, but it is anything but safe."


"The AMA's review of the risks and benefits of these hormones in the setting of anti-aging and athletic enhancement is very important given its inclusion of the consensus and position statements of the key professional medical societies as well as the federal agencies that guard public health." states Dr. Perls in the editorial.


The editorial summarizes the AMA's assessment for each of the purported anti-aging hormones and essentially the bottom line of his argument is that in terms of anti-aging, the risks of these hormones out-weigh the little or no benefit. Dr. Perls denounces the marketing of these hormones, particularly growth hormone and anabolic steroids (anabolic steroids are variations of testosterone), for anti-aging. He also provides guidelines for spotting "red flags of quackery" and basic advice that physicians can lend to their patients in their pursuit of healthy aging.

Journal Reference:

Thomas T Perls. Anti-aging medicine: what should we tell our patients? April 2010, Vol. 6, No. 2, Pages 149-154, Aging Health DOI: 10.2217/ahe.10.11


Smoking May Erase Heart Benefits of Light Drinking


By Alan Mozes
HealthDay Reporter
HealthDay News

Tuesday, April 13, 2010

TUESDAY, April 13 (HealthDay News) - If you indulge in moderate drinking, you've probably heard that it might reduce your risk for heart trouble, including stroke.

A new British study supports that notion, but it also finds that light drinking's benefit in lowering stroke risk does not apply to smokers.

"Any potential beneficial effect of drinking moderate amounts of alcohol on stroke may be counteracted by cigarette smoking," said lead researcher Yangmei Li, a doctoral candidate in the Institute of Public Health at the University of Cambridge.

Li presented her findings Monday at a press conference held by the American Academy of Neurology during its annual meeting in Toronto.

The authors note that prior studies exploring the potential protective relationship between stroke risk and light-to-moderate drinking have found conflicting results. The fact that many people both drink and smoke might be a factor.

Smoking is a significant risk factor for stroke, Li noted, with current smokers having a 64 percent higher risk for stroke than those who have never smoked.

To help tease out these relationships, the authors tracked the drinking and smoking histories of more than 22,500 British residents (approximately 10,000 men and 12,000 women) for an average of 12 years.

The study began as early as 1993 and ended by 2008. All the study subjects were between the ages of 39 and 79, and none had a history of heart attack, cancer, or stroke prior to the study launch. By the end of the study, 864 strokes had occurred.

The researchers found that heavy drinkers gained no protection from stroke relative to non-drinkers. In fact, excessive alcohol use was linked to a potential rise in stroke risk.

On the other hand, light-to-moderate drinking did appear to lower the odds for stroke compared to no alcohol consumption. That's in keeping with other studies on moderate drinking and cardiovascular health.

However, the apparent protective effect of moderate tippling did not hold true for smokers.

The lowest stroke risk was observed among nonsmokers who consumed between three to 14 "units" of alcohol per week, each unit being equal to about a glass of wine.

This level of consumption -- below what the authors defined as the upper "moderate consumption" limit of 21 glasses per week -- afforded participants a 37 percent reduction in stroke risk.

However, smokers who drank a similar amount of alcohol had no such decline in their odds for stroke.

Li and her colleagues conclude that "smoking may modify [the] relationship between alcohol and stroke risk."

For his part, Dr. Ralph Sacco, chairman of the department of neurology at the University of Miami, said the finding confirms that "smoking is a powerful risk factor for stroke".

"In my own research, the protective affect of moderate alcohol consumption was seen among both smokers and nonsmokers," he noted. "However, it is possible that we'll ultimately find that smoking wipes out the benefit, because it certainly does increase stroke risk in general."

"And so while it's hard for us to advocate that people should start drinking a little alcohol if they don't do so already, we do need to get the message out that if you're currently drinking heavy amounts of alcohol you need to reduce down to small amounts," Sacco said. "And we need to make sure that people don't smoke."

More information

Find out more about stroke risk factors at the National Stroke Association .

Individuals With Alzheimer's Disease May Lose Muscle Mass



Tuesday, April 13, 2010


ScienceDaily (Apr. 13, 2010) — Lean mass -- the weight of an individual's bones, muscles and organs without body fat -- appears to decline among patients with Alzheimer's disease, according to a report in the April issue of Archives of Neurology, one of the JAMA/Archives journals. These decreases may be associated with declines in brain volume and function.


Unintended weight loss often occurs among individuals with Alzheimer's disease and frequently begins prior to memory loss or other cognitive symptoms, according to background information in the article. This weight loss is associated with the severity of dementia and with faster progression of Alzheimer's disease. "Although obesity in midlife is a risk factor for developing dementia, overweight and obesity in late life are associated with lower dementia risk," the authors write.


Jeffrey M. Burns, M.D., M.S., of the University of Kansas School of Medicine, Kansas City, and colleagues used dual-energy x-ray absorptiometry (DEXA) to assess body composition in 70 individuals age 60 and older without dementia and 70 with early-stage Alzheimer's disease. Participants were also evaluated with brain magnetic resonance imaging (MRI) and neuropsychological testing.


After controlling for sex, lean mass was reduced among patients with Alzheimer's disease compared with healthy controls. Decreases in the volume of the whole brain and of white matter only, along with declines in cognitive performance, were associated with loss of lean mass. However, total body fat and body fat percentage were not different between individuals with and without dementia and were not associated with cognitive ability or brain volume.


The findings suggest that lean mass, as opposed to body mass index or other measures of overall weight or fat levels, may be a more sensitive measure of the changes in body composition associated with dementia. "We observed a direct correlation between whole-brain volume (an estimate of brain atrophy) and lean mass, suggesting that brain atrophy and loss of muscle mass may co-occur," the authors write. "Brain atrophy is considered a neuroimaging measure reflective of Alzheimer's disease pathology. Thus, our data are consistent with other studies suggesting that brain pathology may contribute to decline in body composition, perhaps by disrupting central nervous system regulation of energy metabolism and food intake."


Sarcopenia -- the loss of muscle mass typically associated with aging -- is most strongly associated with reductions in physical activity, the authors note. Individuals in the study with Alzheimer's disease had lower levels of physical activity; therefore, behavioral changes associated with dementia may contribute to the loss of lean mass, the authors note. Alternatively, Alzheimer's disease and sarcopenia may share an underlying mechanism, such as inflammation or changes in the process of building tissue.

Journal Reference:

Jeffrey M. Burns; David K. Johnson; Amber Watts; Russell H. Swerdlow; William M. Brooks. Reduced Lean Mass in Early Alzheimer Disease and Its Association With Brain Atrophy. Arch Neurol, 2010; 67 (4): 428-433 [link]


Monday, April 12, 2010


Diet can sharply cut Alzheimer's risk: study


By Julie Steenhuysen


Monday, April 12, 2010

CHICAGO (Reuters) – A diet rich in olive oil, nuts, fish, poultry and certain fruits and vegetables may have a powerful effect at staving off Alzheimer's disease, researchers reported on Monday.

People who ate nutrients specifically selected for brain health had a 40 percent lower risk of developing Alzheimer's disease compared with others, Yian Gu, an Alzheimer's disease researcher at Columbia University in New York and colleagues found.

"Diet is probably the easiest way to modify disease risk," said Gu, whose study appears in Archives of Neurology.

She said because there are no cures for Alzheimer's, prevention is key, especially as the population ages.

"If we follow this diet, that means the risk of getting the disease will be lowered for the population," Gu said in a telephone interview.

While other studies have looked at individual nutrients, Gu's team studied groups of foods high in nutrients that have been shown to be associated with Alzheimer's disease risk.

Some, such as saturated fatty acids in red meat and butter, need to be avoided. Others, such as omega-3 fatty acids, omega-6 fatty acids, vitamin E, vitamin B12 and folate, benefit the brain.

To study this, the team collected information on the diets of 2,148 healthy people over 65 for an average of 4 years. They were checked for Alzheimer's disease every 18 months.

Of these, 253 developed Alzheimer's, which has no cure.

Those least likely to develop the disease ate more olive oil-based salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables such as broccoli, fruits, and dark and green leafy vegetables and ate less red meat, organ meat or high-fat dairy products.

"People who adhered mostly to this dietary pattern compared to others have about a 40 percent reduction in the risk of developing Alzheimer's disease," Gu said.

She said the diet likely works in two ways. Because it is rich in heart-healthy foods, it may be protecting the brain from strokes that could make it more vulnerable to Alzheimer's disease.

But it also may be that the nutrients -- such as omega-3 fatty acids, antioxidants and folate -- directly protect the brain.

Current treatments helps with some symptoms, but cannot reverse the course of Alzheimer's, a mind-robbing form of dementia that affects more than 26 million people globally.

(Editing by Cynthia Osterman)

Teen drinking tied to breast disease

By Frederik Joelving

Reuters Health

Monday, April 12, 2010

NEW YORK (Reuters Health) – Young women who drink alcohol may put themselves at higher risk of developing breast disease that is a known risk factor for cancer, a new study suggests.

In a group of nearly 6,900 women aged 16 to 23, researchers found that those who drank six or seven days a week had more than five times the odds of developing so-called benign breast disease years later.

Women with benign breast disease have hard lumps in their breasts, which may in some instances turn cancerous. The broad group of conditions includes irregular cysts, breast discomfort, sensitive nipples, and itching, according to the National Cancer Institute.

Earlier reports have linked adolescent drinking to benign breast disease based on women's recollections many years later, but the new study is the first to survey alcohol drinking directly during adolescence and follow the girls into adulthood.

It's not clear why alcohol would have an effect on the condition, but researchers speculate that alcohol's effect on estrogen could promote breast tissue growth.

"Our study results give older girls and adolescents another reason to avoid alcohol," Catherine Berkey of Harvard Medical School, who led the research, told Reuters Health in an e-mail.

When the women were interviewed later at age 18 to 27, 67 -- or about 1 percent -- said they had been diagnosed with benign breast disease and had the diagnosis confirmed with a biopsy. Those who drank more were also more likely to suffer from the condition, with each average daily drink adding to the risk.

"We saw health effects with alcohol amounts that are not intoxicating, so teen girls would be wise to totally avoid alcohol at least until they are of legal drinking age," Berkey said.

Source: Pediatrics, online April 12, 2010.

High glycemic diet may raise female heart risk: study


By Kate Kelland


Monday, April 12, 2010

LONDON (Reuters) – Women who eat lots of high glycemic index (GI) carbohydrates like white bread and ice-cream may be at greater risk of heart disease, but men do not seem to be affected, Italian scientists said on Monday.

In a study of almost 48,000 adults, the scientists found that the 25 percent of women who ate the most carbohydrates overall had around double the risk of heart disease of the 25 percent who ate the least.

When these carbohydrates were separated into high and low glycemic index categories, the researchers found that eating more high GI foods was strongly linked to greater risk of coronary heart disease, whereas low GI foods were not.

"A high consumption of carbohydrates from high glycemic index foods, rather than the overall quantity of carbohydrates consumed, appears to influence the risk of developing coronary heart disease," the scientists wrote in a study in the Archives of Internal Medicine journal.

Heart disease is the leading killer of men and women in Europe, the United States and many other rich nations. Together with diabetes, cardiovascular diseases accounted for almost one third of all deaths around the world in 2005, according to the Geneva-based World Health Organization.

High-carbohydrate diets are known to increase the levels of blood glucose and of harmful blood fats known as triglycerides while reducing levels of protective HDL or "good" cholesterol, increasing heart disease risk.

But not all carbohydrates have the same effect on blood glucose levels, and the glycemic index is a measure of how much a food raises blood glucose levels compared with the same amount of glucose or white bread.

Low GI foods include beans, lentils and nuts, whereas foods like white bread, doughnuts and ice-cream have a high GI rating.

When they analyzed the data for men -- who accounted for 15,171 of the 47,749 Italian adults in the study -- the researchers led by Sabina Sieri of the Fondazione IRCCS Istituto Nazionale dei Tumori in Milan found no link between overall carbohydrate intake, glycemic index or glycemic load and heart disease risk.

Among women, the 25 percent of women whose diet had the highest glycemic load had 2.24 times the risk of heart disease compared with the 25 percent with the lowest glycemic load.

This could be because the adverse changes linked to carbohydrate intake, including triglyceride levels, are stronger risk factors for heart disease in women than in men, they wrote.

The adverse effects of a high glycemic diet in women might be due to differences in the way women and men break down and absorb sugars and fats, they added.

(Editing by Myra MacDonald)

Many Hispanics Lack Access to Colon Cancer Screening


HealthDay News

Monday, April 12, 2010

MONDAY, April 12 (HealthDay News) -- Colorectal cancer screening tests, such as colonoscopies, are harder to find in areas of the United States with large Hispanic populations, new research suggests.

The finding could help explain why Hispanics are less likely to get screened than non-Hispanic whites, the study authors said.

A group led by Dr. Jennifer Haas of Brigham and Women's Hospital and Harvard Medical School in Boston examined statistics on colorectal screening taken from a national health survey, Medicare data and a cancer monitoring program.

The researchers found that Hispanics typically lived in counties with less access to the screening tests. Residents were more likely to be screened if the tests were more available in their regions.

The findings suggest "that interventions designed to reduce disparities in the use of colorectal cancer screening or stage at diagnosis should consider not only improving local capacity for screening but also address other characteristics of the areas that may limit the dissemination of information about the importance of colorectal cancer screening," the study authors wrote.

The report is published online April 12 in the journal Cancer.

An estimated one in 19 people will develop colorectal cancer in their lives.

More information

There's more on colon cancer screening at the American Cancer Society.

Cheap antifungal drug may fight cancer: study



Monday, April 12, 2010

WASHINGTON (Reuters) – A common antifungal drug can slow tumors growing in mice and should be investigated as a potentially cheap and easy way to fight cancer in people, researchers reported on Monday.

Although it did not completely wipe out the tumors, the drug called itraconazole may boost the effects of other drugs, the researchers reported in the journal Cancer Cell.

Itraconazole is marketed under the brand name Sporanox by Johnson & Johnson subsidiary Janssen Pharmaceutica, mostly for treating a fungal infection called aspergillus.

The drug affects a so-called cascade of effects through a molecular pathway called Hedgehog, the researchers reported.

The researchers at Stanford University in California were looking for potential cancer drugs. They know that the Hedgehog pathway is involved in the development of cancer, so they looked for drugs that interfere with it.

"There is a fairly broad range of tumors in which this molecular cascade, called the Hedgehog pathway, plays an important role," Stanford's Philip Beachy, who worked on the study, said in a statement.

"The virtue of screening existing drugs is that you already have all the information about dosage and toxicity, and you can move into clinical trials fairly readily."

The researchers looked at 2,400 different drugs in a so-called library of drugs that had either been tested in people or already approved by the Food and Drug Administration, looking at the mechanism of action. The least toxic one they found was itraconazole.

"Itraconazole has been studied for nearly 25 years, and we therefore have a good understanding of its safety and potential side effects," the researchers wrote.

They tested mice and found an oral solution of itraconazole significantly slowed the growth of tumors injected under the skin. Untreated mice grew giant tumors during the same time and were euthanized.

Testing mice this way is far different from the natural development of cancer in people, but the drug should be tested in cancer patients, the researchers said.

"It might be possible with two compounds to achieve a more potent block at even lower drug concentrations," said Beachy. "If so, it's possible that there is a population of patients that can be treated relatively soon."

(Editing by Vicki Allen)

Kids' Suicide Risk Same for All Antidepressants 


By Steven Reinberg
HealthDay Reporter
HealthDay News

Monday, April 12, 2010

MONDAY, April 12 (HealthDay News) -- There appears to be no difference among antidepressants in raising a kid's risk of suicidal thoughts, a new long-term study shows.

The research supports the U.S. Food and Drug Administration's decision in 2004 to mandate a "black box" warning on all antidepressants for an increased suicidality risk in children and adolescents who go on the medications. And it answers an oft-raised question about which medications carry the most risk.

"Across the most frequently prescribed antidepressant agents, there was no difference in risk of suicide attempts and completed suicides," said lead researcher Dr. Sebastian Schneeweiss, an associate professor of epidemiology at the Harvard School of Public Health.

The FDA showed a doubling in the risk of suicidal ideation among children taking antidepressants, compared with placebo, Schneeweiss noted.

But, Schneeweiss added, the FDA analysis did not specify which medications were used. so there was no way to tell whether there were differences in risk.

"Physicians need to know if there is an agent where the risk is reduced or particularly elevated," he said. "That is important for clinical practice."

The report is published in the April 12 online edition of Pediatrics.

For the study, Schneeweiss's team collected data on 20,906 children aged 10 to 18 who had been diagnosed with depression in British Columbia. They were followed for nine years.

The children and adolescents in the study were on a variety of commonly prescribed antidepressants called selective serotonin reuptake inhibitors (SSRIs), including citalopram (Celexa), fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), and sertraline (Zoloft).

In the first year after starting treatment with antidepressants, there were 266 suicide attempts and three completed suicides. However, no significant difference in suicide attempts or completed suicides was noted based on which antidepressant the adolescent was taking, the researchers found.

Given these findings, doctors can focus their attention on which of the several SSRIs is most effective for an individual patient and not be concerned about increasing the potential risk of suicide, Schneeweiss said.

Different SSRIs act differently in individual patients, so now the doctor can find the most effective one and, because the risk is the same with all, "take safety out of the equation," he added.

"Nevertheless, you will still have to monitor the patient very carefully, because the elevated risk is still there," Schneeweiss said.

Much debate followed the FDA's decision to place a black box warning on antidepressants. One of the continuing arguments is that by imposing such a warning, clinicians will shy away from prescribing antidepressants to children and adolescents who really need them. This could in turn make their depression worse, which could lead to suicide.

Dr. David Fassler, a clinical professor of psychiatry at the University of Vermont College of Medicine, said that "the results of this study are consistent with previous reports and with general clinical experience."

The article represents a contribution to the growing literature on this complex issue, Fassler said.

"However, it does not shed much light on the larger question of whether or not the decision to impose a black box warning on these medications was correct and justified in the first place. Nor does the current analysis contribute to our understanding of the public health consequences of the FDA's action. Hopefully, subsequent large-scale, longitudinal studies will be designed, which will help us more fully address these critical, and as-yet unanswered, questions," he said.

Another expert, Dr. David A. Brent, a professor of psychiatry at the University of Pittsburgh, said that he was "not sure how they draw the conclusion that these findings support the black box warning."

The fact that those who use the drugs have similar rates of suicide does not justify the black box warning; it just indicates that whatever the warning should be, it should be similar across drugs, Brent said.

"The authors themselves say that the fivefold increased rate of suicide is probably a function of comorbidity and depression rather than drug. In fact, most psychological autopsy studies estimate the risk for suicide with depression to be 10 to 30 times higher, and most of those kids were untreated," he said. "So there may actually be a protective effect, but certainly the rate is not any higher than in depressed folks without exposure to antidepressants."

"The conclusions from the paper supporting the black box warning don't logically follow from the data that they provide," Brent added. "At a minimum, you would have to show that the incidence of suicidal acts and completions is higher in those who were treated vs. those not treated, and that was not done."

More information

For more information on adolescent depression, visit the U.S. National Library of Medicine.

Targeting the Blood-Brain Barrier May Delay Progression of Alzheimer's Disease



Monday, April 12, 2010


ScienceDaily (Apr. 12, 2010) — Researchers may be one step closer to slowing the onset and progression of Alzheimer's disease. An animal study supported by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health, shows that by targeting the blood-brain barrier, researchers are able to slow the accumulation of a protein associated with the progression of the illness.


The blood-brain barrier separates the brain from circulating blood, and it protects the brain by removing toxic metabolites and proteins formed in the brain and preventing entry of toxic chemicals from the blood.

"This study may provide the experimental basis for new strategies that can be used to treat Alzheimer's patients," said David S. Miller, Ph.D., chief of the Laboratory of Toxicology and Pharmacology at NIEHS and an author on the paper that appears in the May issue of Molecular Pharmacology.


Alzheimer's is an irreversible, progressive brain disease that slowly destroys memory and thinking skills, and eventually disrupts function of major organs. Estimates vary, but experts suggest that as many as 2.6 million to 5.1 million Americans may have Alzheimer's. One hallmark of Alzheimer's is the deposition of beta-amyloid protein in the brain. This protein clumps to form plaques that destroy neurons and lead to cognitive impairment and memory loss in Alzheimer patients.


"What we've shown in our mouse models is that we can reduce the accumulation of beta-amyloid protein in the brain by targeting a certain receptor in the brain known as the pregnane X receptor, or PXR," said Miller.

The researchers from NIEHS and the University of Minnesota Duluth demonstrated that when 12-week-old genetically modified mice expressing human beta-amyloid protein are treated with a steroid-like chemical that activates PXR, the amount of beta-amyloid protein in the brain is reduced. The activation of the PXR was found to increase the expression of a blood-brain barrier protein known as P-glycoprotein. This protein transports beta-amyloid out of the brain.


"Our results show several new findings. We now know that P-glycoprotein plays a pivotal role in clearing beta-amyloid from the brain. Secondly, we know P-glycoprotein levels are reduced in the blood-brain barrier, and that the Alzheimer's mice treated with the chemical to activate PXR were able to reduce their beta-amyloid levels to that of mice without Alzheimer's," said Bjorn Bauer, Ph.D., assistant professor at the University of Minnesota and senior author on the paper.


Anika Hartz, Ph.D., lead author on the study, added that it is also likely that reduced P-glycoprotein expression at the blood-brain barrier may be an early indicator of Alzheimer's disease, even before the cognitive symptoms appear. One of the challenges confronting the diagnosis and treatment of Alzheimer's is being able to clearly diagnose the disease process when brain damage is minimal, before any symptoms occur.

"More research is needed before this animal model discovery can be tested in humans, but the paper suggests some new targets for treatment that offer hope to patients and families dealing with this devastating disease," said NIEHS Director Linda Birnbaum, Ph.D.


The researchers plan to conduct a study where the Alzheimer's mice are fed a PXR-activating compound in their diet for 12-18 months. The cognitive skills of the animals will be monitored regularly, along with their P-glycoprotein levels, to determine whether the feeding regimen delays the onset of cognitive impairment.

Journal Reference:

A. M. S. Hartz, D. S. Miller, B. Bauer. Restoring Blood-Brain Barrier P-glycoprotein Reduces Brain A  in a Mouse Model of Alzheimer's Disease. Molecular Pharmacology, 2010; DOI: 10.1124/mol.109.061754

Many With Serious Eating Disorders Could Go Undiagnosed


HealthDay News

Monday, April 12, 2010

MONDAY, April 12 (HealthDay News) -- The standard criteria psychiatrists use to diagnose anorexia nervosa and bulimia may be too rigid and exclude many patients who urgently require treatment for eating disorders, a new study suggests.

These patients are typically categorized as "Eating Disorder Not Otherwise Specified" (EDNOS), which has become a "mosh pit" that lumps dissimilar patients into a single category that's poorly recognized by doctors and health insurers, according to primary author Dr. Rebecka Peebles, an adolescent medicine specialist with the Comprehensive Eating Disorders Program at Lucile Packard Children's Hospital in California.

The EDNOS label is "a bit misleading to patients -- it can make them feel like they don't have a real eating disorder," Peebles said in a hospital news release.

She and her colleagues investigated whether adolescents with EDNOS are less ill than those who meet the full diagnostic criteria for anorexia or bulimia. The researchers examined the medical records of more than 1,300 female patients treated for eating disorders at Packard Children's, and created categories of "partial anorexia nervosa" and "partial bulimia nervosa" for patients who didn't quite meet the full criteria for these diseases.

Among the findings:

  • Nearly two-thirds of the patients had been categorized as EDNOS.
  • Patients with partial anorexia were more similar to patients with full-blown anorexia than to other EDNOS patients with partial bulimia.
  • About 60 percent of the EDNOS patients met medical criteria for hospitalization and, on average, were sicker than patients diagnosed with full-blown bulimia.

The sickest EDNOS patients were those who had lost more than 25 percent of their body weight before diagnosis and had severe malnutrition. These girls had been overweight and lost weight too fast and dangerously in order to achieve what's considered a normal weight. In some ways, these girls were worse off than underweight patients diagnosed with anorexia.

"People were initially just patting them on the back for their weight loss. It often took months or years for others to realize that what they were doing didn't seem healthy," Peebles said in the news release.

She believes that the findings, published online April 12 in the journal Pediatrics, suggest the need for re-evaluation of the medical criteria for eating disorders.

More information

The U.S. National Women's Health Information Center has more about eating disorders.

Keeping the Weight Off After a Very-Low-Energy Diet



Monday, April 12, 2010


ScienceDaily (Apr. 12, 2010) — Simple advice can reduce the risk of weight regain after a very-low-energy diet: the secret to keeping the weight off is to switch back to normal food gradually, reveals a dissertation from the Sahlgrenska Academy, at the University of Gothenburg, Sweden, which also contains new research results for patients who have undergone obesity surgery


For 12 weeks a group of just over 260 patients swapped their normal food for a very-low-energy diet in the form of soups and milkshakes. 169 of the patients lost a lot of weight, averaging 16 per cent of their body weight. They were then divided into two groups so that they could switch back at different rates from the very-low-energy diet to energy reduced portions of normal food. One group completed the refeeding in a week, while the other took six weeks.


"After ten months the patients with the six-week refeeding period had gained 4 per cent in weight from their minimum weight, while the patients with the one-week refeeding period had gained eight per cent," says Lena Gripeteg, researcher at the Sahlgrenska Academy.


Very-low-energy diets have been used for many years in the health service to achieve rapid and safe weight loss in obese patients. While this treatment method is well-studied, there is a risk that patients will gain weight when they start to eat normal food again.


"We therefore want to look at the importance of different treatment advice on the transition from the very-low-energy diet back to normal food, and assess what actually works," says Gripeteg. "A simple tip that seems to work for patients is to revert slowly to normal food after losing weight on a very-low-energy diet."


Her dissertation also includes research results from the current national SOS (Swedish Obese Subjects) study, which has followed 2,010 patients who have undergone surgical treatment for obesity and 2,037 matched control patients for up to 20 years. It shows that men who have undergone obesity surgery are less likely to need a disability pension, while obese women are just as likely to need a disability pension whether they lose weight or not.


"On the basis of this study, we can't explain why there is a difference in the sexes," says Gripeteg. "It may well be that the underlying health problems differ between women and men, which could explain why there is a significant improvement in the ability to work in men, but no effect in women after surgical obesity treatment."