When used properly, many herbal supplements may be safe and possibly beneficial to health. However, a few natural supplements can cause life-threatening problems or dangerous interactions with medications.

Natural doesn’t always mean safe when it comes to herbal supplements, according to the Mayo Clinic Health Newsletter. The newsletter covers some of the known interactions between herbal supplements and medications:

Garlic, ginseng, ginger and feverfew:
Patients who take anti-clotting medications such as aspirin, warfarin (Coumadin) and clopidogrel (Plavix) should avoid these natural supplements. They may increase the risk of bleeding. Supplements chondroitin and glucosamine also may interfere with warfarin.

Ginkgo:
Ginkgo may increase the risk of bleeding in patients taking anti-clotting medications. Ginkgo can counteract the blood pressure-lowering benefits of thiazide diuretic drugs. It also can interfere with anti-seizure medications.

Kava:
Kava is a sedative herb and is associated with serious liver problems, even when taken for a short time. Many medications, such as cholesterol-lowering drugs, pose a risk of liver damage. Taking kava supplements may increase the risk of liver problems even more.

St. John’s wort:
This supplement can greatly increase or decrease the potency of many medications and cause serious side effects. Patients who take antidepressants, anti-blood-clotting drugs, certain asthma drugs, immune-suppressing medications or steroids should probably avoid St. John’s wort.

S-adenosylmethionine (SAM-e):
This can cause serious side effects when taken with antidepressant medications that affect serotonin.

It’s always best to keep health care providers informed about natural herbal supplement you use, especially when starting a new medication or preparing for a medical procedure. Some herbal supplements need to be discontinued two to three weeks before certain surgical procedures, because they affect blood clotting, response to sedation and blood pressure control.

Study Shows Aspirin Use Boosts Survival Rate of People With Colon Cancer

Certain patients with colorectal cancer who begin regular aspirin use after the disease develops may greatly improve their odds of survival, researchers in Boston report.

Aspirin is often praised for its anticancer effects. Numerous studies have suggested that regular aspirin use may help lower the risk of colon polyps and colorectal cancer. Now, a study published in this week’s issue of the Journal of the American Medical Association is among the first to link aspirin use and colon cancer survival.

For the study, researchers from Massachusetts General Hospital, Dana-Farber Cancer Institute, and Brigham and Women’s Hospital looked at the link between aspirin use and survival among 1,279 adults with stage I, II, or III nonmetastatic colorectal cancer, or cancer that had not spread to distant areas.

The patients had enrolled in two large studies in the 1980s prior to their cancer diagnosis and agreed to answer questions about their health over the years. Researchers followed them through June 2008.

In general, study participants who reported aspirin use after being diagnosed with colorectal cancer had a 29% lower risk of colorectal cancer death and a 21% lower risk of overall death, compared to non-aspirin users. The researchers note that the main reasons reported for aspirin use included headache, arthritis, musculoskeletal pain, and treatment and prevention of cardiovascular disease.

Taking aspirin for the first time after a diagnosis improved a patient’s odds even more.

The study showed that starting regular aspirin use for the first time after a colorectal cancer diagnosis greatly reduced the risk of colorectal cancer-related death, but taking aspirin before colorectal cancer developed and continuing to do so after diagnosis did not significantly influence survival rates. In other words, former regular aspirin users do not reap as much benefit as those who are new to regular aspirin use.

That might raise an eyebrow or two, particularly since aspirin use has been linked to reduced risk of colorectal cancer.

U.S. researchers have discovered a compound that can kill breast cancer stem cells, a kind of master cancer cell that resists conventional treatment and may explain why many cancers grow back, they reported on Thursday.

The discovery came using a new method of screening for drugs that specifically target and kill cancer stem cells, and it could be used to find drugs targeting other cancer stem cells as well, they said.

Many teams have been looking for ways to destroy these master cancer cells in hopes of making cancer easier to cure.

“There is a lot of evidence to suggest now that these cells are responsible for many of the recurrences that are observed after treatment has stopped,” Piyush Gupta of the Massachusetts Institute of Technology and the Broad Institute, whose study appears in the journal Cell, said in a telephone interview on Thursday.

The problem is that cancer stem cells are rare and difficult to study in the lab because they quickly change into other types of cells. And they are hard to kill.

“It wasn’t clear it would be possible to find compounds that selectively kill cancer stem cells,” Gupta said in a statement. “That’s what we did.”

To study the cells, Gupta’s team first devised a method for stabilizing cancer stem cells in the lab and getting them to multiply. They then tested them against 16,000 natural and commercial chemical compounds to see which ones were able to kill the cancer stem cells specifically.

That turned up 32 contenders.

They narrowed down this list to a handful of chemicals, and tested these in the lab and in mice.

A chemical called salinomycin hit the target. It was 100 times more potent at killing breast cancer stem cells than Bristol-Myers Squibb Co’s cancer drug Taxol, or paclitaxel.

Cancer stem cells treated with salinomycin were far less able to start breast cancers when injected into mice than cancer stem cells treated by paclitaxel. And the treatment also appeared to slow the growth of tumors in the mice.

Gupta said it is not clear if salinomycin will emerge as the best drug compound for killing breast cancer stem cells — or that it will be safe to use in people with cancer.

But the study offers a new roadmap for drug companies to isolate and test compounds capable of killing the cells.

“We now have an approach that can be used very systematically to find such compounds,” he said.

Researchers are still trying to understand the role cancer stem cells play in promoting different types of cancer, but many teams think they may explain why so many cancers come back even after treatment with powerful chemotherapy and radiation.

“The theory is these cells are self-renewing, which means they can make identical copies of themselves,” Robert Weinberg of MIT, who worked on the study, said in a telephone interview.

“They have the power to generate a new tumor, and they are resistant to existing anti-cancer therapeutics. That suggests the need to develop therapies for cancer stem cells,” he said.

Weinberg said it will take several years before therapies targeting cancer stem cells can be used in people. But the finding does hold promise for a new way of looking for cancer treatments.

“Ideally, if one hit the cancer stem cell, sooner or later the bulk of the cells of the tumor, which lack a self-renewal capability, would gradually poop out and the tumor would eventually die just by attrition,” Weinberg said.

Cancer is the No. 2 killer of Americans, with about 560,000 deaths annually, topped only by heart disease, according to the American Cancer Society.

source: Reuters

A growing number of Americans now have a positive opinion on psychiatric medications, a new study contends. About five out of six people surveyed felt psychiatric medications could help people control psychiatric symptoms, but many also expected the medications could help people deal with day-to-day stresses, help them feel better about themselves and make things easier with family and friends.

“People’s attitudes regarding psychiatric medications became more favorable between 1998 and 2006,” said study author Dr. Ramin Mojtabai, an associate professor in the department of mental health at Johns Hopkins Bloomberg School of Public Health in Baltimore.

Mojtabai wanted to assess American’s opinions of psychiatric medications for a number of reasons. One is that the use of such medications has soared in recent years. Between 1990 and 2000, he said, the use of antidepressants increased fivefold. Another reason is that the government has allowed direct-to-consumer advertising for the drugs. And finally, he said that he wanted to learn if the recent FDA black box warnings on some antidepressants and antipsychotics had any effect on people’s opinions of these drugs.

Using data from the U.S. General Social Surveys from 1998 and 2006, Mojtabai compared the two periods to examine people’s attitudes toward psychiatric medications.

In 1998, 84 percent of people agreed with the statement, “These medications help people control their symptoms.” In 2006, that number had edged up slightly, to 86 percent.

By 2006, more people believed that psychiatric medications could help people feel better about themselves (68 percent vs. 60 percent), help people deal with stress (83 percent compared to 78 percent), and make things easier with family and friends (76 percent compared to 68 percent).

People were somewhat more willing to take these medications themselves: 29 percent in 2006 vs. 23 percent in 1998. Opinions about the drugs’ potential adverse effects didn’t change over time, according to the study.

Mojtabai said that advertising may have helped increased people’s positive perceptions of these drugs. But, he added, there is also an increasing awareness that many psychiatric disorders have a biological or organic cause that medications may be able to help correct.

A young mother who lived on a diet of soup and water starved herself to death, an inquest has heard.

Helen Anderson, 26, was found dead in bed by her mother at her home in UK last month. For several months before her death, the talented musician, who played violin, piano and guitar, and once auditioned for the Northern Sinfonia, existed on a diet of just water and soup. She lost almost six stones in weight, despite her parents, Michael and Hazel Anderson, pleading with her to eat more.

Her body was so starved of sugar it began to eat into its own reserve of fat. This caused a metabolic chemical reaction called ketoacidosis, which killed her.

Recording a verdict of accidental death, the coroner said: “This phenomenon – this poison if you like – which developed within her body was made by her body itself. It arises as a result of the body reacting to a lack of sugar within itself and that was in part a consequence of the intensive diet with which Helen was attempting to balance her weight. The sad truth of the matter is there has been a development within her body, a natural phenomena, which has set up this poisoning of her body’s system and has led to her death.”

Miss Anderson, who had a five-year-old daughter, by a previous marriage had been dieting to lose weight she put on as a side effect to medication.

Forensic pathologist Dr Stuart Hamilton said she had also been taking slimming tablets to speed up her weight loss, but these did not contribute to her death. At 5ft 9in, the mother-of-one weighed 9st 2lb when she died, having been 15st, and was at the lower end of the Body Mass Index (BMI) scale.

She was due to become engaged to a Swedish man she met through the internet and the couple were planning a big engagement party in Sweden, before tragedy struck.

Scientists may be closer to solving a medical mystery with huge implications for personal and public health: Why obese people are prone to developing type 2 diabetes.

A series of studies appearing online July 26 in Nature Medicine suggest that inflammation within the fat tissues of heavy individuals could trigger the blood sugar disease.

What’s more, each of the four completely independent studies, from two continents and three countries, showed that interfering with these immune-cell processes actually reversed diabetes in mice.

The long-term implications of the findings are enticing: perhaps one day a cure for type 2 diabetes, a condition that now plagues more than 23 million people in the United States alone.

“This group of papers suggests that cellular immunity may regulate inflammation in fat,” said Dr. Vivian Fonseca, professor of medicine at Texas A&M Health Science Center College of Medicine and director of the Diabetes Institute at Scott & White. “The authors do suggest that if you change the inflammatory response by changing the way the body cells respond to a trigger for inflammation, you might be able to get at the real heart of diabetes and that suggests you could cure it.”

But Fonseca warned, all these studies were conducted in mice and have yet to be proven in humans

In type 2 diabetes, the body often becomes resistant to insulin and doesn’t use it effectively. In the last decade or so, researchers have presented evidence that suppressing inflammation in animals could improve insulin resistance and other processes involved with diabetes. Inflammation is now widely believed to be involved in many metabolic diseases afflicting obese individuals. Inflammation in fat tissue, in particular, seems to be a culprit, by changing fat tissue function, thereby contributing to insulin resistance.

But the exact mechanisms of the phenomenon have been unclear.

Three papers, one from Japan, one from Canada and one from the United States, showed that immune system cells known as T cells were deficient in obese mice, pushing the immune system to somehow initiate insulin resistance.

Restoring T cells to more normal levels actually reversed weight gain and improved insulin resistance, even when the mice continued on a high-fat diet.

The fourth study looked at another class of immune cells called mast cells, which are more commonly linked to allergies.

An over-abundance of mast cells contributed to obesity and diabetes in mice, but when mast cells were removed from the system the problem was corrected, explained study senior author Guo-Ping Shi, a biochemist with Brigham and Women’s Hospital in Boston.

“We gave mice a high-fat diet for three months and they developed obesity and diabetes,” he said. But mice that had been stripped of mast cells did not. “These mice are protected from the disease if they are without these cells,” Shi said.

Shi’s team also gave wild-type (“normal”) mice allergy medicines, which work to “stabilize” mast cells. This also led to improvements in the mice.

“We can use the drugs to manipulate cell activity or prevent disease in this case,” Shi said.

Shi said he has signed a contract with a local company to develop a version of the drugs to combat diabetes in humans.

Multiple sclerosis (MS) patients who smoke have a speedier progression of the disease, a new study in the Archives of Neurology suggests.

Dr. Alberto Ascherio of the Harvard School of Public Health in Boston and his colleagues also found that smokers with MS were more likely to have the progressive form of the disease, in which symptoms steadily get worse, rather than the relapsing-remitting form, in which a person has MS symptoms intermittently.

“Most of the adverse effects were seen for current smokers, which in some way is good news because it suggests that stopping smoking can help,” Ascherio told Reuters Health.

People who smoke are known to be at increased MS risk, but research on whether smoking affects the course of the illness has had conflicting results, he and his colleagues note. They followed 1,465 MS patients, 17.5% of whom were current smokers, for an average of just over three years to investigate.

Of the 891 patients the team followed for that period to determine the rate of progression from one form of disease to the other, 72 saw their MS progress to the worse relapsing-remitting form: 20 of 154 smokers, 20 of 237 ex-smokers, and 32 of 500 never-smokers.

That meant that the smokers were 2.4 times as likely as non-smokers to have primary progressive MS, and those who had relapsing-remitting disease were 2.5 times more likely than never-smokers to develop secondary progressive MS during the follow-up period.

At the study’s outset, the smokers had more disability, more severe disease, and more atrophy in their brains. Over time, they also showed a faster increase in the total amount of injured brain tissue and their degree of brain atrophy.

The mechanism through which cigarette smoking could worsen MS isn’t clear, Ascherio said. Smoking has been linked to some other autoimmune conditions, such as rheumatoid arthritis, he noted, but not others, so the habit’s effects on the immune system could be a factor; another possibility would be that cigarette smoke is toxic to the nervous system.

There are currently no proven risk factors for progression of MS that a patient can do anything about, Ascherio noted.

“Although causality remains to be proved,” he and his colleagues write, “these findings suggest that patients with MS who quit smoking may not only reduce their risk of smoking-related diseases but also delay the progression of MS.”

A drug used to help prevent recurring breast cancer appears to hold promise as a treatment for deadly fungal infections, new research has found.

University of Rochester Medical Center researchers found that tamoxifen kills yeast in mice with Candida infections, which can be fatal to people with compromised immune systems, including people with cancer or HIV and those taking immunosuppressants for chronic conditions.

At extremely high levels, tamoxifen slashed yeast levels by 150-fold, causing most fungus cells to break up and die while halting surviving cells from progressing into a disease-causing state, their study found.

“It’s still early, but if tamoxifen, or molecules like it, turns out to be an effective treatment against serious fungal infections, it’ll be a welcome addition to our arsenal,” Dr. Damian Krysan, an assistant professor of pediatrics at the university and an author of the study, said in a university news release.

The results are published in the August issue of Antimicrobial Agents and Chemotherapy.

Available antifungal medications pose some issues for people who need them the most, according to background information in the news release. The only new class of antifungals approved for use in the past two decades is generally effective, but they can only be taken intravenously, which poses logistic and other problems for some patients. And the most common oral antifungal medication only slows fungus cell growth, making it difficult for immune-compromised patients to completely shake their infections.

“We don’t have vaccines against fungal infections, and the few drugs we do have aren’t always effective,” Krysan said. “We’ve got a lot more work to do to figure out whether tamoxifen could be used in high doses or whether it could be used in combination with other treatments, but we’re excited about the possibility of giving doctors another way to help these critically ill patients.”

The American Academy of Environmental Medicine states,”Genetically Modified foods have not been properly tested and pose a serious health risk. There is more than a casual association between GM foods and adverse health effects. There is causation.”

Last May the American Academy of Environmental Medicine (AAEM) called on “Physicians to educate their patients, the medical community, and the public to avoid GM (genetically modified) foods when possible and provide educational materials concerning GM foods and health risks.” They called for a moratorium on GM foods, long-term independent studies, and labeling.

AAEM’s position paper stated, “Several animal studies indicate serious health risks associated with GM food,” including infertility, immune problems, accelerated aging, insulin regulation, and changes in major organs and the gastrointestinal system. They conclude, “There is more than a casual association between GM foods and adverse health effects. There is causation,” as defined by recognized scientific criteria. “The strength of association and consistency between GM foods and disease is confirmed in several animal studies.”

More and more doctors are already prescribing GM-free diets. Dr. Amy Dean, a Michigan internal medicine specialist, and board member of AAEM says, “I strongly recommend patients eat strictly non-genetically modified foods.” Ohio allergist Dr. John Boyles says “I used to test for soy allergies all the time, but now that soy is genetically engineered, it is so dangerous that I tell people never to eat it.”

Dr. Jennifer Armstrong, President of AAEM, says, “Physicians are probably seeing the effects in their patients, but need to know how to ask the right questions.” World renowned biologist Pushpa M. Bhargava goes one step further. After reviewing more than 600 scientific journals, he concludes that genetically modified organisms (GMOs) are a major contributor to the sharply deteriorating health of Americans.

Among the population, biologist David Schubert of the Salk Institute warns that “children are the most likely to be adversely effected by toxins and other dietary problems” related to GM foods. He says without adequate studies, the children become “the experimental animals.”

Selenium is a trace element crucial to life – too little or too much of it is fatal. In the July 17 issue of the journal Science, researchers at Yale University and University of Illinois at Chicago detail the molecular mechanisms that govern its metabolism in the human body.

“It must require an intricately regulated uptake system,” said Dieter Söll, co-senior author of the paper, Sterling Professor of Molecular Biophysics and Biochemistry at Yale. “There are 25 human selenoproteins, and most of them are probably essential for life.”

Selenium is thought to offer protection from diverse human ailments including adverse mood states, cardiovascular disease, viral infections and cancer.

Selenocysteine is the most active metabolite of selenium in humans. It is unique among amino acids because it is the only one synthesized directly on a transfer RNA (tRNA) molecule, which shuttles the amino acids to the protein-making machinery within cells. Proteins that contain selenocysteine are responsible for recycling protective antioxidants such as vitamin C and coenzyme Q10.

Söll’s team for the first time captured images of how selenocysteine is created on a super-sized tRNA molecule, which seems to have a highly specialized role in nature. The 20 other amino acids and their associated tRNAs use the same protein vehicle, called an elongation factor, for transport to the ribosome. However, nature has provided this large tRNA molecule with a specialized elongation factor that chauffeurs only selenocysteine to the ribosome.

“This structure reveals most aspects of the mechanism for the formation of selenocysteine and provides an answer to 20 years of biochemical work in the field,” said Sotiria Palioura, lead author of the study and an M.D./Ph.D. candidate at Yale.

The findings may lead to greater understanding of autoimmune liver disease. The tRNA complex described in the Science paper is the target of antibodies in patients with Type 1 autoimmune hepatitis. “The region that the antibody is supposed to recognize is at the business end of this molecule, where we see the reaction happening,” Palioura said.

“Selenocysteine has been found to be a critical component of enzymes involved in a number of normal and disease processes,” said Michael Bender of the National Institutes of Health’s National Institute of General Medical Sciences. “This basic study, which has shed light on selenocysteine’s unique biosynthetic pathway, could ultimately have an impact on many aspects of human health, including the immune response, neurodegeneration, cardiovascular disease, and cancer.”

Other Yale authors on the paper were R. Lynn Sherrer and Thomas A. Steitz. Senior co-author on the paper was Miljan Simonovic of the University of Illinois at Chicago.

Funding for the research was provided by the National Institute for General Medical Sciences, the Department of Energy, and the Howard Hughes Medical Institute at Yale University.