Friday, June 22, 2007

Fatty Goose Liver: Not What the Doctor Ordered

A couple weeks ago, I wrote a column for Science News about the apparent link between fast-food diets and fatty liver disease, a serious and potentially lethal condition in people. In this week's column for that magazine, I cover what might be considered its counterpoise—how eating fatty-liver products can induce a serious and potentially lethal condition, at least in the mice being tested. Presumably, humans could face a similar risk.

The fatty-liver comestible at issue: foie gras.

One somewhat reassuring aspect, at least in the United States, people don't tend to consume much foie gras. It's the excessively fatty liver of ducks or geese—often served pureed into a mousse or pâté and then doctored with any of various spices. I say doctored because I'm not a liver aficianado by any means and it would take a lot of doctoring to make it go down.

I used to take 2 hours to eat about 4 ounces of liver as a child, and I only bothered to try because in our household, the only alternative to finishing it was to leave the dinner table and go straight to bed—at 4:30 p.m. Those episodes left a bad taste in my mouth for anything linked to liver.

As I matured, I lost much of the genetically ingrained taste for fatty foods. So, as you might imagine, fatty liver is one of the last foods that would appeal to me.
However, it appeals to plenty of others, especially many who consider themselves gourmands.

A new study by researchers in the United States and Sweden now finds that the process of overfeeding waterfowl to make their livers especially fatty really stresses those livers. And that stress can lead to the development of protein abnormalities—a misfolding of the proteins into hair-like shapes known as amyloids.

In the June 26 Proceedings of the National Academy of Sciences, those researchers now show that when amyloid-rich foie gras is fed to mice, it can seed tissues in the rodents to begin making even more amyloid. The researchers describe this as the fatty-liver-based food "infecting" the animals with a propensity for amyloidosis: life-threatening disease where the affected tissues—which can be liver, heart, or gastrointestinal tract—don't work properly because their proteins' shape is all wrong.

There are plenty of caveats associated with the findings. And I would direct you to read the longer article in Science News to learn more about them. They explain why there is probably little immediate cause for panic, even among most foie gras lovers.

Among the biggest of these: Affected animals were all at high risk for amyloidosis to start with. Among human populations that would match that condition—individuals with tuberculosis and leprosy. When you think about it, the people in the United States most likely to suffer from either of those diseases are indigents. Such individuals are hardly likely to eat, much less overindulge, in foie gras, which typically goes for $6 or more per ounce.

Monday, June 18, 2007

EPA Compresses Press Access

One nice thing about being a reporter is that we usually get rather open access to a range of ordinarily closed venues—from the White House and various Cabinet level agencies, to behind-the-scenes settings at museums, university labs, industrial centers, control rooms in nuclear power plants, even the command center on ice breakers in the Arctic Ocean (yes, I was there, ferried to the deck on a Coast Guard chopper from Barrow, AK).

We also get an opportunity to ask questions—and usually are rewarded with answers—from newsmakers, like the Environmental Protection Agency Administrator, last Thursday. These events are called press conferences even though increasingly, the reporters who take part don't publish in materials that actually run through presses.

June 14th's press conference was a virtual one in every sense of the word. First, EPA Administrator Stephen L. Johnson wasn't in town, but on a farm in New England, and patched into reporters by phone. The reporters, similarly, didn't go to the event. We just dialed into a conference call to listen to a host of disembodied voices.

What was particularly weird about this one—on the launching of a study to sample air emissions from confined-animal-feeding operations, or CAFOs—was that it started on the dot at 12:15 p.m. EDT and ended 15 minutes later. Johnson was joined by three other individuals, including the Purdue scientist who was leading the study. All said a little to reporters.

Then, they opened the event to questions. But not many.

Each news organization, we learned, would be allowed one question. But not every news organization would get to ask one because after about five, time was up and they ended the press conference.

Mind you, they told us so little during the introduction, that most of the details had to be elicited, bit by bit, during our one-question-per-reporter access. And with time for few questions, little information was exchanged.

I've NEVER attended a news conference that was so brief and conveyed so little data.

Yes, I'm annoyed at the new limits on access to newsmakers. But the big loser is the public. We get to serve as its voice, asking the questions our readers or listeners would like to if they were here.

Of course, we were directed to check the agency's website for more info. But as one might expect, that information was limited and certainly didn't answer my questions. Less than a minute after the press conference ended, I was on the phone to EPA's news office to ask a public-information officer for more details. I was put into his voicemail, and got a call back long after I needed the information.

This isn't an isolated instance. I'd heard of this happening before from colleagues, but has thought they must be exaggerating the brevity of access. Even my husband, a reporter and bureau chief for a major energy publication, has encountered this phenomenon—the excessive truncation of news conferences.

Remember, it's the public that is really losing access here, and in this case to the people that are supposed to be their servants.

I think the real message is that public servants are short-changing we, the people, on service.

Friday, June 15, 2007

Chinese Toothpaste Scare Hits Colgate

Remember the Chinese toothpaste scare that broke 2 weeks ago? At the time, the Food & Drug Administration noted that only off-brand products might carry the toxic tainting with diethylene glycol (DEG). Well, now comes word that products carrying the Colgate name might also be affected.

FDA announced that it had confirmed it had identified "counterfeit" toothpaste, imported from South Africa, carrying the Colgate name. It wasn't made by Colgate, but had been fraudulently labeled as such, according to spokespersons for the company. Colgate doesn't have manufacturing plants in South Africa or import toothpaste from there.

Yesterday, Colgate-Palmolive reported that the misbranded product "has been found in several dollar-type discount stores in four states: New York, New Jersey, Pennsylvania, and Maryland. There are indications that this product does not contain fluoride and may contain Diethylene Glycol." Clues that will help recognize these fakes: they're labeled as coming from South Africa and contain misspellings, such as South Afrlca and South African Dental Assoxiation.

DEG, as you may recall, is a solvent commonly used as an anti-freeze. It's poisonous and doesn't belong in anything that makes contact with the mouth. In some developing countries, low-cost DEG is substituted for the more costly glycerin, a popular sweetener used in liquid over-the-counter and prescription-drug products—and now, apparently, in toothpastes as well.

Just a month before the DEG-toothpaste link made news, FDA warned drug manufacturers and health professionals that unscrupulous foreign firms had occasionally been swapping the toxic DEG for glycerin. In one episode last September, in Panama, DEG tainted medicines resulted in 40 deaths.

"Colgate is working closely with the US FDA to help to identify those responsible for the counterfeit product," a company press release announced yesterday. It recommended that consumers who suspect they may have purchased such a fake to call Colgate's toll-free number at (800)-468-6502.

Monday, June 11, 2007

Why Alcohol Might Be Good for Diabetics

Several studies over the years have found that diabetics who regularly drink a little—and we do mean alcohol—tend to live longer and keep their glucose under better control. For instance, I reported in 1999 that "diabetes sufferers who enjoy an occasional libation, compared with those who eschew alcohol, have just half the risk of dying from coronary artery disease. Those
who down a drink a day face only 20 percent of the teetotalers’ heart-disease mortality."

It's perplexed physicians as to why. And posed a dilemma. After all, doctors don't usually want to prescribe alcohol since it's basically empty calories, can addle thinking, and can contribute to the development of alcoholism in some individuals. So, particularly where a mechanism to explain the association remained murky, doctors generally ignored the link.

It may become a little harder to do so, now.

A study published in this month's American Journal of Clinical Nutrition finds that when people were served alcohol with a meal, their bodies more slowly converted the carbohydrates in the meal into blood sugar. And that's a good thing.

Australian researchers at the University of Sydney's Human Nutrition Unit fed a group of 10 men and women "meals"—usually amounting to no more than white bread with margarine or mashed potatoes. Why these carbs? Because ordinarily the body breaks them down into gluocse—blood sugar—so quickly that eating them is not much better than directly downing a teaspoon of table sugar.

However, when alcohol was consumed with the food—or even up to an hour beforehand—the body digested the food into glucose far more slowly. It parsed out the glucose into blood at a nice, steady pace, which is exactly what the doctor wants to see happen. Why? Because spikes in blood sugar can confuse the body's insulin-making machinery, leading to a spike in insulin, which is NOT good for the blood vessels.

Jennie C. Brand-Miller and her colleagues conclude that "under realistic conditions," moderate quantities of beer, wine, or gin—all three of which were tested in amounts equivalent to two predinner drinks—can lower blood-sugar values following a meal by up to 37 percent,. This, of course, is all relative to dining alcoholfree.

"These effects may provide a hitherto unreconized benefit of moderate alcohol consumption for cardiovascular health," the scientists say.

There is a caveat—isn't there always: The test subjects were all lean and healthy, i.e. not diabetic. However, there is the expectation that this may be one way for people who are at least prediabetic to stay that way.

Here's another caveat: In the new study, the scientists administered white wine in one round of the tests. In fact, red wines might have provided an even more robust advantage, based on data I reported 3 years ago. In that story, experiments—admittedly conducted in diabetic rats—showed that even without its alcohol, red wine's constituents could control their blood sugar after a meal as well as nondiabetic animals.

Wednesday, June 6, 2007

Boys Just Start Out Bigger

Everyone knows why girls generally don't play on boys' football or basketball teams—they're too small to match the competition. But I always thought that any size advantage in males was due to genetic programming that caused them to grow faster and bigger, starting in toddlerhood.

Wrong. Boys start out bigger in the womb and just keep building on that size advantage after birth.

The revelation comes from a paper by Radek Bukowski of the University of Texas Medical Branch and his colleagues at 10 other U.S. medical institutions, not to mention the University of Cambridge, England and Royal College of Surgeons in Dublin, Ireland.

This august group studied fetal growth in nearly 29,000 babies. Even at just 8 to 12 weeks following conception, boys were bigger than girls. The difference was small, which was why it took so many babies to statistically confirm it was something other than a fluke finding.

Boys retained their subtle size advantage through birth, when they weighed in at some 120 grams more, on average, than girls. That's among boys that were conceived the old fashioned way. However, even among those conceived in a test-tube—and these accounted for 3.5 percent of the babies—boys weighed an average of 90 grams more at birth than girls.

Accounting for mom's height, weight, smoking status, or race didn't alter the trend, the researchers report in the May 15 American Journal of Epidemiology.

Tuesday, June 5, 2007

Antifreeze Doesn't Belong in Toothpastes

Few people would knowingly reach for a tube of Chinese toothpaste—at least in a U.S. supermarket, pharmacy, or big-box store. However, a number of bargain brands are, in fact, Chinese imports. And even that wouldn't necessarily be a problem, except that our Food & Drug Administration inspectors have identified several shipments of these Chinese toothpastes tainted with a poison: diethylene glycol (DEG), also known as diglycol.

On June 1, FDA issued an "import alert" about these products" and announced that: "Out of an abundance of caution," it recommends that consumers pitch out away toothpaste labeled as originating in China.

DEG is an antifreeze and solvent used in many commercial resins, dyes, oils and organic chemicals. It's also a "humectant"—an additive that keeps products moist—for tobacco, cork and glues. Although toxic to animals, including humans, China permits the use of DEG in toothpastes. The United States does not. In some of the imported products tested by FDA, DEG constituted 3 to 4% by weight of the toothpastes. Not all of the products were even labeled as containing DEG.

FDA identified about a dozen different brands of tainted toothpastes—none major name brands. Interestingly, none of the contaminated brands had received an American Dental Association Seal of Acceptance either. This is a designation that ADA deems the labeled product safe and effective.

According to FDA, DEG is commonly used in some developing countries as a cheap substitute for glycerin and propylene glycol. Where it has been used in products such as over-the-counter cough syrups and pain relievers, deaths have resulted.

Bottom line: Sometimes it pays to ante up for a name brand, or at least one with a medical group's seal of approval.

Hot Flash Newsflash III

Women of a certain age, as we like to say, find themselves prone to hot flashes—a sudden flush and drenching sweat. Not only are these episodes uncomfortable and potentially embarrassing, but they can also become a major distraction from any events at hand. Which is why they're not usually welcomed. However, a new study suggests that perhaps they should be in certain breast-cancer survivors—those taking the drug tamoxifen to ward off a cancer recurrence.

Joanne Mortimer of the Moores Cancer Center at the University of California, San Francisco School of Medicine led a study that followed 1,551 women. All had survived early-stage breast cancer and were taking part in a Women's Healthy Eating and Living study, which began in 1995. The study was designed to evaluate whether l0w-fat diets that were high in fiber, fruits, and vegetables might help limit the cancer's return. Slightly more than half of the recruits had been prescribed tamoxifen, and more than 75 percent of these women—674, to be exact—experienced hot flashes.

That's not surprising, since hot flashes are a common side effect of breast-cancer treatment, notes Mortimer. However, among tamoxifen users, hot flashes proved a strong predictor that a woman's cancer would not come back, Mortimer's team reported at the American Society of Clinical Oncology meeting, yesterday. Breast cancer returned in roughly 13 percent of the patients who'd experienced hot flashes, but in 21 percent of those who didn't.

These findings held for women at any age, and proved a better predictor of whether cancer would return than how advanced her cancer had been at diagnosis or whether the cancer was estrogen-receptor negative—the type most resistant to therapy with a synthetic hormone, such as tamoxifen.