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More and more foods bear a mishmash of warnings that they might accidentally contain ingredients that could seriously sicken people with food allergies. Yet there are signs that the labels are creating confusion among families that should heed them even as new testing shows there is a real, if probably small, chance that foods with even the most vaguely worded warnings truly pose a risk.
The disconnect is sparking calls for standards on what are now voluntary warning labels. The Food and Drug Administration plans to seek advice from consumers and food makers, perhaps by year's end, before considering whether to intervene.
Worried the labels may be losing credibility, the industry's Grocery Manufacturers/Food Products Association already is preparing to update its own guidelines on when foods should carry the warnings.
Consumers see the label "on so many products, they say, 'Oh heck, I'm going to ignore it,'" laments Dr. Steve Taylor, a food scientist at the University of Nebraska who co-authored a recent study about the confusion.
For the seriously allergic, "I've characterized it as akin to playing Russian roulette with a really big gun that has 100 chambers and only one bullet. Sooner or later if you eat these products, you're going to eat the wrong one," he said.
About 12 million Americans have some degree of food allergy. Severe food allergies trigger 30,000 emergency room visits a year, and 150 to 200 deaths a year. Food labels help the allergic avoid ingredients that could sicken them.
A law that took effect last year requires foods that intentionally contain highly allergenic ingredients such as peanuts, shellfish or eggs to disclose that in plain language.
The accidental-allergy warnings are different: They're aimed at foods that aren't supposed to contain a particular allergen but might become contaminated with it. They may be made in the same factory, or on the same machines as allergen-containing goods.
In a report to Congress last year, FDA said a quarter of recently inspected food factories had the potential for such a mix-up.
The warnings are voluntary, so different companies use different, sometimes vague, wording. Nor does anyone count how many foods bear them, although all sides agree more are. Enter the new research, in this month's Journal of Allergy and Clinical Immunology.
First, the Food Allergy & Anaphylaxis Network, an influential consumer group, surveyed more than 600 parents of food-allergic children. In 2006, 75 percent said they would never buy a food with an accidental-allergy warning down from 85 percent when the network posed the same question in 2003.
A warning's wording determined if some parents ignored it: "May contain peanuts" sounds scarier than "packaged in a facility that processes peanuts" and thus 88 percent said they heeded the first warning while just 64 percent heeded the latter.
That echoes an FDA experiment that found wording matters in persuading allergic consumers to believe the warning.
But are the warnings real? Nebraska's Taylor tested 179 products that bore a variety of accidental-peanut warnings, and found 7 percent did contain peanuts some of them traces, but some enough to seriously sicken.
That's a small proportion. But Taylor is quick to note he only tested samples from two batches of each product. Test more say the first batch of oatmeal cookies packaged after the machine was supposedly cleaned of peanut butter cookies and that number may grow.
Moreover, contrary to some parents' beliefs, peanuts were in some products with every version of the label, including two of 51 foods that bore a "may contain" warning and seven of 68 labeled "made in the same facility."
On the other hand, the allergy network is increasingly concerned that foods that never before carried warnings suddenly are getting them including puzzling ones, like canned vegetables with nut warnings a trend perhaps fueling confusion.
"We're seeing every week an increase in the number of these 'may contain' statements on products you wouldn't expect to see them on," says network founder Anne Munoz-Furlong, whose group is pushing FDA and industry for new labeling standards.
"Don't ignore it, because you don't know when it's true," she tells consumers.
The industry is "troubled by what appears to be an increased use of 'may contain' labeling," says Regina Hildwine, labeling policy chief for the grocery manufacturers. "This is not just something that you should put on a package without thinking."
Penny Ackerman of Bethlehem, Pa., is strict about label reading to protect her 3-year-old son, Gregory, who is severely allergic to peanuts and has a milder tree-nut allergy.
But, "we even have to watch labels we didn't used to," she says with frustration.
On a recent grocery trip, Ackerman didn't notice until she got home that the chocolate chips she had always bought with confidence now warned they were made in a factory that uses peanuts. She wonders if the change is because of a new factory, or just that the company hadn't gotten around to labeling until now.
"If you don't see it on the label, is it safe or is it not safe? Because you don't know."
Researchers have a new clue about why a widely used AIDS drug has certain side effects such as mysterious fat deposits, they reported on Monday.
Parallels between the side effects of protease inhibitors -- a critical component of HIV drug cocktails -- and genetic conditions that cause early aging may help explain the often debilitating fat deposits and other results, they said.
Protease inhibitors can cause metabolic problems such as an unhealthy buildup of cholesterol in the blood, high blood pressure, and increased risk of diabetes.
They also trigger a condition called lipodystrophy -- a strange redistribution of body fat that gives some patients wasted cheeks and limbs, and a so-called "buffalo hump" of fat on the back of the neck.
Doctors have long been mystified by how protease inhibitors and other HIV drugs cause such effects, which occur in tens of thousands of drug takers worldwide, said Dr. Charles Flexner at Johns Hopkins University School of Medicine, who was not involved in this study.
In an attempt to shed light on this, a group at the University of California Los Angeles and Purdue University in Indiana treated mouse and human cells with protease inhibitor, and found that they accumulated a particularly clumpy form of a protein called prelamin A.
The drug triggered this by blocking the action of another protein -- called ZMPSTE24 -- that converts prelamin A into its useful form, they reported in the Proceedings of the National Academy of Sciences.
Cells with lower levels of ZMPSTE24 to begin with were particularly affected by the protease inhibitor.
Purdue University's Christine Hrycyna, who worked on the study, said that blocking this protein might contribute to the metabolic side effects of protease inhibitors.
Patients with early aging syndromes, including Hutchinson-Gilford progeria, have symptoms that mimic the side effects, and the same protein is clumped in their cells, said Hrycyna. But how this might affect metabolism is not clear, she said.
"The side effects are probably due not to just one simple thing," Hrycyna said.
"I think this paper may provide new insights into possible mechanisms for some of the side effects of protease inhibitors," added Flexner.
The researchers also tested some of the other drugs that are commonly used in AIDS cocktails, known as highly active antiretroviral therapy or HAART.
But the other drugs did not cause the same protein accumulation, even though they can cause similar side effects in people, the researchers wrote.
"They are probably due to a combination of all these different drugs," Hrycyna added.
The researchers now want to see if their theory holds true in HIV patients, and if versions of protease inhibitors that do not block ZMPSTE24 as much might cause fewer side effects in these patients.
The various anti-inflammatory drugs (NSAIDs), such as ibuprofen and naproxen, which are used to treat arthritis and other painful conditions, differ in the risks of heart attacks and stroke, according to a report in the Annals of the Rheumatic Diseases. Much of the difference seems to depend on how the drug interacts with aspirin, which is commonly given to prevent heart attacks.
"Traditional NSAIDs, and ibuprofen in particular, do have the potential to interact with the effects of aspirin," Dr. Michael E. Farkouh from Mount Sinai School of Medicine, New York told Reuters Health. "For patients at high (risk of heart attack and stroke), this interaction is serious since these patients require aspirin to prevent" these cardiovascular problems.
Farkouh and associates investigated cardiovascular outcomes in high-risk patients with arthritis treated with ibuprofen, naproxen, or lumiracoxib. Their analyses were based on data for over 18,000 participants in the TARGET (Therapeutic Arthritis Research and Gastrointestinal Event Trial) study.
Among patients taking low-dose aspirin, the risk of death, heart attack, or stroke at 1 year was more common with ibuprofen than with lumiracoxib, the authors report, but did not differ significantly between naproxen and lumiracoxib.
Among patients not taking low-dose aspirin, there was no difference in outcomes between ibuprofen and lumiracoxib, the report indicates, but there were fewer cardiovascular events among those taking naproxen rather than lumiracoxib.
"For patients at high cardiovascular risk, naproxen is the drug of choice," Farkouh said. "It has the best overall safety record."
SOURCE: Annals of the Rheumatic Diseases, June 2007.
A protein in blood points to rising amounts of a particularly lethal form of body fat around organs, scientists say.
As levels of retinol-binding protein 4 (RBP4) rise, so do levels of "inter-abdominal fat" linked to an increased risk for heart disease and type 2 diabetes, the researchers say.
"Increased inter-abdominal fat is known to be associated with cardiovascular risk," said study co-author Dr. Barbara B. Kahn, chief of the Division of Endocrinology, Diabetes and Metabolism at Beth Israel Deaconess Medical Center, in Boston.
Reporting in the July issue of Cell Metabolism, her team noted that increased "deep belly" fat around organs has long been linked to an increased risk for insulin resistance and type 2 diabetes. "The regulation of this protein may tell us completely new information about what really causes type 2 diabetes," said Kahn, who is also a professor of medicine at Harvard Medical School.
In the study, the researchers found that the amount of RBP4 in the blood accurately reflected the amount of fat surrounding the abdominal organs. That means that "RBP4 might be able to be used as a marker to indicate cardiovascular risk," Kahn said.
She stressed that RBP4 is not a cause of obesity. However, increased levels appear be associated with this particular type of abdominal-fat obesity.
In the study, Kahn and colleagues looked at biopsy samples of abdominal fat from 196 people. They found that more RBP4 is made in visceral (deep belly) fat compared with the subcutaneous fat that lies just beneath the skin. In addition, blood levels of RBP4 are greater in people who are obese. These people have double or triple the amount of RBP4 compared with normal-weight people.
"The gene expression of RBP4 is increased more in visceral adipose [fat] tissue -- the adipose tissue surrounding the internal organs -- than it is in the subcutaneous adipose tissue," Kahn said. So, levels of RBP4 are higher in people who have a so-called "visceral pattern" of obesity compared with people that have a subcutaneous pattern of obesity, she said.
In earlier research, Kahn's team also found that the levels of RBP4 were elevated in people with insulin resistance, people who are obese, and people with type 2 diabetes. This was also the case in healthy people with a family history of diabetes.
According to Kahn, there's ongoing research into drugs that could lower RBP4 levels.
But there's another tried-and-true means of lowering RBP4, she added.
"Levels can also be regulated by physical exercise," Kahn said. In prior research, her team showed that "people who benefited from an exercise program lowered their levels of serum RBP4 when they got more insulin-sensitive," she said.
Kahn had also shown in earlier research that teens who went on a low-carbohydrate diet along with an exercise program lowered their RBP4 levels.
One expert thinks that lowering RBP4 levels might help treat heart disease and type 2 diabetes.
"This study suggests that RBP4 can be a good biomarker to quantify visceral adiposity, which is closely linked to metabolic syndrome," said Dr. Tae-Hwa Chun, from the Department of Internal Medicine, Metabolism, Endocrinology and Diabetes at the University of Michigan. "This article also supports the notion that all the fats are not equal in their functions."
In experiments with mice, RBP4 decreases insulin sensitivity of muscle and liver tissue, which is considered a precursor to diabetes, Chun said.
"It is still not clear whether RBP4 regulates insulin sensitivity by controlling retinoic acid metabolism or by directly acting on muscle or liver cells," Chun said. "The drug Fenretinide, which is shown to lower RBP4 levels, has been already used as a chemotherapeutic agent for cancer. The side effects of the drug, however, need to be carefully weighed against its possible benefit for metabolic diseases."
In another report published in the same issue of the journal, a research team led by Bruce Spiegelman of the Dana-Farber Cancer Institute in Boston identified a gene called PRDM16 that regulates the production of so-called "brown fat" in mice. Brown fat is a type of fat that actually generates heat and counters obesity caused by overeating.
"Brown fat is present in mice and in human infants, where it keeps them warm by dissipating food energy as heat, instead of storing it as 'white' fat," Spiegelman said in a prepared statement. "Human adults don't have much brown fat, but there is some, and from a therapeutic perspective, the question is whether that pathway can be reactivated."
The researchers hope their discovery will lead to new ways of treating obesity in humans.
Despite many hospitals' reluctance to make the investment, installing an electronic medical records system pays for itself in less than two years, a new study finds.
Such a system was put in place at the University of Rochester Medical Center, N.Y., and recouped its initial cost within 16 months, say the authors of a study in the July issue of the Journal of the American College of Surgeons.
That experience runs counter to the worries of many health care providers, who are often reluctant to invest in such tracking systems.
"Health care providers most frequently cite cost as a primary obstacle to adopting an electronic medical records system. And, until this point, evidence supporting a positive return on investment for electronic health records technologies has been largely anecdotal," study co-author Dr. David A. Krusch, of the department of surgery at the University of Rochester, said in a prepared statement.
He and his colleagues analyzed the return on investment of an electronic health records system used in five ambulatory offices representing 28 health care providers. The study compared the costs of a number of tasks -- such as pulling patient charts, creating new charts, filing time, support staff salary, and data transcription -- in the third quarter of 2005 (after the system was installed) to costs in the third quarter of 2003, when the tasks were still being done manually.
The new system reduced costs by almost $394,000 per year, the study found, and nearly two-thirds of those savings came from a drastic reduction in the amount of time required to manually pull patient charts. The electronic medical records system cost $484,577 to install and operate in the first year, which means the medical center recouped its investment within 16 months.
After the first year, it cost about $114,000 a year to operate the system. That means an annual savings of more than $279,500 for the medical center, which works out to close to $10,000 per health care provider using the system, the researchers said.