No Proof Zinc Helps Prevent Diabetes

(HealthDay News) -- Despite claims by zinc supplement manufacturers that the pills can help prevent type 2 diabetes, there is no proof for that notion in randomized clinical trials, a new report concludes.

But even though there is no evidence from clinical studies, that doesn't mean that zinc has no role in diabetes prevention, say the authors of a research review article in the current issue of The Cochrane Library journal. Laboratory research suggests that zinc does help promote the production and action of insulin, the review authors point out.

The problem is a lack of good clinical trials on the issue, the review authors said
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They analyzed 192 clinical trials involving zinc, insulin and their use in type 2 diabetes.

However, just one of the studies met their content and quality criteria for inclusion in the review. That four-week study of 56 obese women found that zinc did not have an effect on factors associated with the development of diabetes.

"It is important to recognize that this systematic review was left with one trial that treated 56 people with either zinc or a placebo for four weeks and found no effect. This single trial is too small and too short to really tell us anything about the effectiveness of zinc," Dr. John Buse, an American Diabetes Association spokesman who was not involved in the review, said in a prepared statement.

"Basically, we know nothing that can definitively guide clinicians in providing advice regarding zinc supplementation in diabetes," Buse said.

More information
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases has more about preventing diabetes.

Research Seeks Clues to Sudden Cardiac Death in Athletes

(HealthDay News) -- Most endurance athletes with an irregular heartbeat called ventricular arrhythmia have dysfunction in their heart's right ventricle, European researchers report.

Ventricular arrhythmia is a condition in which the heart beats at an abnormal rate and rhythm, sometimes resulting in sudden death in otherwise healthy athletes. There are many underlying causes to the condition, which is often due to inherited problems, according to background information in the article.

Previous research has found that in endurance athletes with ventricular arrhythmias (such as runners and cyclists), the condition is often the result of a problem in the heart's right ventricle. Ventricles are those chambers of the heart that pump blood back out to the body.

In this study, Belgian researchers at the University of Leuven examined 22 endurance athletes with ventricular arrhythmia and compared them to 15 endurance athletes without the condition, as well as to a control group of non-athletes without ventricular arrhythmia.
The researchers concluded that the right ventricle was the definite or probable source of the defect in 82 percent of the athletes with the condition.

Endurance exercise itself may contribute to ventricular arrhythmia, the study authors suggested.

"The hypothesis that high-level endurance exercise is an underlying cause of the ventricular arrhythmia is supported by other studies," study team leader Hein Heidbuchel, professor of cardiology/electrophysiology, said in a prepared statement.

However, Heidbuchel added that ventricular arrhythmias aren't common, and endurance athletes don't need to worry about them too much.

"But they need to be vigilant and honest with themselves: If they have a family history of arrhythmogenic right ventricular cardiomyopathy (ARVC), arrhythmias, sudden death or other heart complaints, or if they have experienced exercise-induced light-headedness, palpitations or fainting, then they should see their doctor for an evaluation," Heidbuchel said.

More information
The American Academy of Family Physicians has more about arrhythmia.

Restarting Tumor-Suppressor Gene May Fight Cancer

(HealthDay News) -- Manipulation of a gene that normally protects against malignancy but is switched off in cancer cells could open up a promising new frontier in research, according to two new U.S. studies.

Whenever p53 was turned off, cancer cells in mice quickly went to work forming tumors, the studies found. But when researchers used high-tech tricks to switch the gene back on, "the tumor went away," said the leader of one of the studies, Scott Lowe, deputy director of the Cold Spring Harbor Cancer Center, in Cold Spring Harbor, N.Y.
"We would like to imagine that this would translate to human tumors," he said. "In such a system, you could have a very aggressive cancer that really depends on the continued inactivation of this gene to survive."

The study also uncovered surprising new insights into the power of the human immune system to "mop up" cancers weakened by reactivated p53.

Lowe's work and a related study were published online in the Jan. 25 issue of Nature.
"These studies indicate that this might be a fruitful path to explore from a cancer drug-development standpoint," said Dr. Ronald DePinho, a pioneer in this type of work and a professor of medicine at Harvard Medical School.

Although an actual drug for use in a clinical setting is still a long way off, "there are compounds that are now being directed toward the p53 kinase pathway that may enable re-establishment of p53 activity," said DePinho, who also authored a related commentary on the studies.
Almost all forms of cancer involve an inactivation of the p53 tumor-suppressor gene and its related biochemical pathway. So, the pathway has long been a favorite target of cancer research.
"What p53 does is help cells solve problems when they are stressed," Lowe explained. "So, if a cell is damaged in some way, it can make them stop growing, so they aren't dangerous and form a cancer. In fact, it can even kill cancer cells through a process called apoptosis," or programmed cell death.

Unfortunately, this cancer "safety net" is almost always switched off in tumor cells. Scientists have long known that shutting down p53 is key to triggering a cancer -- but what about maintaining its growth? Work by DePinho and others in the 1990s established that the genes that help start a cancer aren't always crucial to its continued survival.

Would that be the case with p53? To find out, Lowe's group used a highly advanced gene manipulation technique called RNA interference (RNAi) to first switch off p53 in cancer-prone mice and then switch it back on, watching to see what happened.

The results were heartening. Just like clockwork, the mouse tumors expanded in the absence of active p53, then shrank when the gene went back to work.

Lowe called the results "a nice proof-of-principle" that p53 inactivity is, indeed, crucial to tumor maintenance.

But there was a real surprise, too. Lowe said he had assumed that reactivated p53 would simply kill tumor cells directly by driving them into apoptosis.

"But when we looked carefully, that didn't seem to be the primary mechanism," he said. "In fact, we noticed something that was quite different -- p53 was inducing a process called 'cellular senescence.'"

In essence, reactivation of the p53 pathway caused the cell to become arrested in a particular stage in its life cycle, effectively putting it to sleep.
But that didn't explain why tumors continued to shrink under the influence of p53. "Where did the cells go?" Lowe said.

Further research yielded the answer. According to Lowe, restarting p53 "appears to up-regulate genes that are involved in recruiting the [mouse] immune system. It was the immune system that was gobbling up these tumor cells."

What's more, it wasn't the immune system's highly targeted killer cells (such a B- or T-cells) that were eating away at senescent tumor cells, but garden-variety macrophages and other immune cells that drive everyday inflammatory processes.

"That's really exciting and surprising," Lowe said. "We didn't anticipate it. It seems there's this interplay between events that happen within the tumor cell and then this recruitment of the immune system. We'd like to understand that in a better way to perhaps exploit it for treatment."

Another study in the journal, this time led by Tyler Jacks, of the Massachusetts Institute of Technology, also turned up interesting clues to p53. In its study, also conducted with mice, Jacks' team found that switching the gene back on led to speedy tumor regression.

But the researchers also found that the reasons behind that regression varied depending on the type of cancer targeted. For example, lymphoma cells died off due to p53-induced apoptosis, but in the case of sarcomas, p53 triggered tumor cell senescence and a concurrent suppression of cellular proliferation.

The experts stressed that p53 is one of a number of important genes affecting tumor survival.
DePinho's group, and others, have already done groundbreaking work in manipulating various "oncogenes" -- genes that, when they are turned on, actively promote cancer's spread.
"What these newer studies have done is look at the flip-side of that, to do work on the tumor-suppressor side," DePinho said.

Lowe said he also believes that "there are other members of the p53 pathway that can either turn the pathway on or execute the [relevant] biological response. All of them could have a similar biology, and we could imagine tinkering with them to do similar things."

But researchers have their work cut out for them, he said.

"It will still be a long time before we are finding small-molecule drugs that do exactly these things -- before they make their way to the clinic," Lowe said. "This isn't cancer being cured tomorrow. But it remains very exciting."

More information
Find out more about the genetics of cancer at the U.S. National Cancer Institute.

New Drug Fights Deadly Fungal Infections

(HealthDay News) -- Two studies have found that a new drug, Noxafil, prevents fungal infections better than existing medications among high-risk patients and also seems to have fewer side effects.

Invasive fungal infections are a leading cause of death among people undergoing chemotherapy for blood cancers, bone marrow transplants or organ transplants and who have low white blood cell counts as a result.

Data from both studies contributed to the recent U.S. Food and Drug Administration (FDA) approval of Noxafil (posaconazole) for preventing fungal infections. The studies, which appear in the Jan. 25 issue of the New England Journal of Medicine, were funded by the Schering-Plough Research Institute, which makes the drug.

"Noxafil seems to have a better side effect profile and less drug interaction problems than other antifungal agents," said Dr. Len Horovitz, a pulmonary specialist at Lenox Hill Hospital in New York City. "There certainly seems to be a place for this."

But expense will come into the equation, another expert said.

"The question is, how many people do you need to treat with drugs that are not cheap to prevent one infection?" said Dr. Jay Brooks, chairman of hematology/oncology at Ochsner Health System in Baton Rouge, La. "For most patients -- who you anticipate having low blood counts for a relatively short time -- this probably will not alter practice tremendously. But in patients who have prolonged episodes of low blood counts, this will give you an opportunity to change the way you plan to treat patients."

There's no doubt that fungal infections can be a big threat. "Fungal disease is very, very serious, and it kills people," Brooks said. "It's unusual, but it does occur."

A drug called Diflucan (fluconazole) is standard treatment but does not affect aspergillus species and other molds. Another drug, Sporanox (itraconazole), affects aspergillus, but is not well utilized by the body.

Noxafil is a newer agent that does affect aspergillus and other species.

The first trial compared Noxafil with Diflucan in preventing invasive fungal infections in 600 patients with graft-versus-host-disease (GVHD) who were receiving immunosuppressive therapy. GVHD can be a serious complication of bone marrow transplantation.

Noxafil was as effective as Diflucan in preventing all invasive fungal infections and was better in preventing invasive aspergillosis, the researchers report. Overall death rates were similar in the two groups, but the number of deaths from invasive fungal infections was lower in the Noxafil group. The proportion of patients experiencing side effects was similar in both groups.

"The study proved that targeted prophylaxis of a high-risk population prevents invasive fungal disease, especially invasive aspergillosis, and reduces the fungal disease-related mortality," said study author Dr. Andrew J. Ullmann, attending physician for hematology/oncology and infectious diseases at Klinikum Johannes Gutenberg University in Mainz, Germany. "Physicians should consider using the drug in these high-risk situations for prophylaxis. In Mainz, patients at high risk for invasive fungal disease receive posaconazole prophylaxis."

Researchers for the second study compared Noxafil with Diflucan or Sporanox for preventing invasive fungal infections in more than 600 patients undergoing chemotherapy for acute myelogenous leukemia (AML) or the myelodysplastic syndrome, which can be a precursor to AML.

Only 2 percent of patients in the Noxafil group developed invasive fungal infections vs. 8 percent in the Diflucan or Sporanox group. One percent of patients taking Noxafil had invasive aspergillosis compared with 7 percent in the competing group. Noxafil also improved survival.

"We introduced Noxafil for prophylaxis almost exactly a year ago and, during the year, it has really transformed what we are doing here," said study author Dr. Oliver A. Cornely, an assistant professor of internal medicine at University Hospital of Cologne in Germany. "Before posaconazole, we saw one case of aspergillosis every week and now we see one case in a year. It really changed things. It will become the standard."

More information

There's more on aspergillosis at the Mayo Clinic.
and: http://www.dreddyclinic.com/findinformation/ff/nailfungalinfection.htm

Telomere Length May Predict Heart Disease Risk

(HealthDay News) -- Size does matter: Men with short telomeres -- strips of DNA at the end of chromosomes -- may have a higher risk of developing coronary heart disease.

And those same men may benefit the most from treatment with cholesterol-lowering drugs known as statins, a new British study found.

Because telomeres get shorter every time a cell divides, they serve as a sort of biological clock. Older cells have shorter telomeres. While previous research had shown that people with coronary heart disease were more likely to have short telomeres, it had been unclear whether this was a result of heart disease or a predictive marker.

"The main implication of the findings is perhaps a better understanding of why some people develop heart disease early and some people, despite having similar risk factors, never develop or develop it later," said study author Dr. Nilesh J. Samani, British Heart Foundation chair of cardiology at the University of Leicester, in the United Kingdom.

For this paper, published in the Jan. 13 issue of The Lancet, the study authors compared telomere length of white blood cells in 484 men who later developed coronary heart disease, with telomere length in 1,058 control subjects who didn't develop coronary artery disease. All the participants were middle-aged men at high risk for heart disease.

The researchers also analyzed whether telomere length had any connection with benefits derived from treatment with statins.

Among men who were not treated with statins, the risk of coronary heart disease was almost double in those with short telomeres compared to long telomeres. But in patients who were taking statins, the risk of heart disease was considerably lower for those with short telomeres.

Shorter telomeres aren't a consequence of having coronary heart disease, the authors concluded. But the scientists still don't know if telomere length is just another marker indicating a higher risk for heart disease, or whether it actually plays a role in development of the disease.
But the fact that men with shorter telomeres who took statins had a benefit suggests that it might be the latter.

There are a number of potential explanations for the finding that people with shorter telomere length responded better to statin therapy, but one is especially intriguing.

"The simple explanation for this could be that statins are simply more effective in people at higher risk for any reason," Samani said. "But the more intriguing possibility is suggested by the fact that we see an interaction between telomere length and statins. We think we're seeing an interaction which suggests that statins may be working through mechanisms that related to retarding the accretion of the telomeres."

More information
To learn more about telomeres, visit Washington University.

Parents Doubt Their Discipline of Kids Works: Study

(HealthDay News) -- About a third of parents believe that their methods of disciplining their children are not all that effective, says a study that also found that many parents use the same discipline techniques as their own parents.

The study, published in the January issue of the journal Clinical Pediatrics, included parents from 32 states in the United States and from Puerto Rico and Canada. When it came to discipline methods, 45 percent of the parents said they used time-outs, 41.5 percent said they used removal of privileges, 13 percent said they yelled at their children, and 8.5 percent often or always used spanking.

About 31 percent of the parents said they "never" or "sometimes" perceived that their discipline methods were effective, the study found. It also found that 38 percent of parents said they used the same methods of discipline as their own parents -- an approach that was often considered ineffective.

"There was actually an inverse relationship between self-reports of yelling at children and perceived effectiveness of discipline," said study author Dr. Shari Barkin, chief of the division of general pediatrics at Monroe Carell Jr. Children's Hospital at Vanderbilt University Medical Center.

"But we strongly suspect that both yelling and spanking might be underreported, because we know when parents perceive their methods are not working, as a third reported, then emotion can quickly escalate," Barkin added in a prepared statement.

Parents with children ages 6 to 11 were about 25 percent less likely than parents with younger children to use time-outs and spanking. When children reached school age, parents were more likely to use yelling and removal of privileges as methods of discipline.

More information
The Nemours Foundation has more about disciplining children.

Health Tip: Don't Miss Breakfast

(HealthDay News) -- If you're in the habit of skipping breakfast, studies show you should rethink your morning routine.

Eating breakfast has health benefits and can help manage your weight, according to Rutland Regional Medical Center in Vermont.

Here's what the research indicates:

• Breakfast is linked to a lower body mass, compared to people who skip the meal.
• Breakfast is shown to reduce a person's risk of obesity and insulin resistance.
• Breakfast is one of the few proven strategies to maintaining long-term weight loss.
• Breakfast is shown to improve grades and behavior among school children.

more information: Obesity

People Make More Food Decisions Than They Think

(HealthDay News) -- While people estimate that they make about 15 food and beverage decisions each day, they actually make more than 200 such choices, Cornell University researchers say.

Their study, published in the January issue of Environment and Behavior, surveyed 139 Cornell staff and students to estimate how many decisions they make about food each day.

On average, the participants estimated they made about 15 food decisions per day.

But, when they answered specific questions about when, what, how much and where they ate, and who made decisions about meals, the participants actually made an average of 221 food-related decisions each day.

"So many food decisions are made on mindless autopilot," Brian Wansink, the John S. Dyson Professor of Marketing and of Applied Economics at Cornell, said in a prepared statement.

Wansink said that the problem with making more food decisions than we are aware of is that each decision can be influenced by the environment.

"It's really easier than we think to let small things around us -- plate size, package size, people around us, distractions -- influence these 200-plus decisions, because we are not aware of them in the first place," Wansink said.

Wansink added that, instead of trying to obsess over food decisions, people should change the environment so that it works for them. He offers the following tips to prevent overeating, from his recent book, Mindless Eating: Why We Eat More Than We Think" (Bantam Books):

Use smaller bowls.
Avoid eating directly from the package.
Bank your calories(e.g., skip the appetizer if you want to indulge in dessert).
Dine next to the slowest eater at the table.
Eat the foods you love but in smaller portions.
Pick two of the following: appetizer, drink or dessert.
Fill half your plate with vegetables, and the other half with protein and starch.
Keep tempting treats out of sight.
Sit at least an arm's length away from the buffet table or snack bowl.

More information
The American Academy of Family Physicians has more about healthful eating.