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Health Notes

Sure, he looks innocent, but is Orville Reddenbacher poisoning you?

Microwave popcorn made a splash in November 2001 when the Wall Street Journal reported on a rare disease that had appeared in workers at a popcorn plant in Missouri. Twenty-four workers at the plant had contracted bronchiolitis obliterans. This disease is rare, deadly, and hardly ever seen in clumps like this.

Even though it’s sort of “old news” these days, the disease outbreak doesn’t seem to have slowed production of microwave popcorn. In fact, today there are even more varieties lining grocery store shelves, all of them boasting massive amounts of “butter” flavor. This is what concerns me, especially since an investigation by the National Institute for Occupational Safety and Health (NIOSH) determined that the cause for this bizarre outbreak was the artificial butter flavoring added to the popcorn.

They isolated diacetyl, an FDA-approved chemical for food, as the offending agent in the phony butter. Diacetyl is also found in many wines, candies, cheese-flavored products, cookies, and beers. Granted, the popcorn plant workers are exposed to much more of it than you would consume, but don’t you think you should be eating real butter in place of all this ersatz stuff?

Action to take:

If you’re going to eat popcorn, make it in an air-popper and get your butter flavoring from real butter.

Reference:

“Butter Flavoring May Pose Risk to Food Workers,” Wall Street Journal, 10/3/01

From bad to worse: Prozac’s secret ingredient 

It’s bad enough that Prozac is an inherently dangerous drug, but now there’s another reason to steer clear of it: It comes with the additional baggage of supplying even more fluoride to your already over-fluoridated body. One of my favorite reference sources, Stratia Wire, has done some excellent investigative work on the drug, and it’s bad news for people taking Prozac. If they don’t kick the habit after reading this report, they deserve to be on it. And their psychiatrists need a reality check–or a good kick in the pants.

At any rate, Mr. Jon Rappoport, the editor of Stratia Wire, heard rumors that Prozac contains fluoride. So he asked a pharmacist at an organization called RxList for a statement about the possible fluoride content of Prozac.

The pharmacist gave him the disinterested data–and, boy, was it interesting. In fact, for those of us who could be considered veteran anti-fluoride guerrillas, it was the equivalent of being handed a ticking time bomb.

The kind of fluoride so many of us have been grumbling about for years is officially known as sodium fluoride. Each molecule of this kind of fluoride contains one fluoride atom. But the fluoride molecule in Prozac, called fluoxetime, contains three fluoride atoms.

Rappoport asked the pharmacist to clarify the physical chemistry involved, and the pharmacist explained that the molecular weight of the fluoride atom (chemical symbol F) is18.9984032. There are 3 Fs in each Prozac molecule, so 3 times 18.9984032 equals 57.

The overall molecular weight of the whole Prozac molecule is 345.79.

The proportion of fluoride in Prozac is 57 divided by 345.79, which equals .165–or 16.5 percent. Put simply, that means 16.5 percent of the entire weight of Prozac is fluoride.

A typical daily dose of Prozac is 20 milligrams. Sixteen and a half percent of that 20 mg is fluoride, which works out to a daily fluoride dose of 3.3 milligrams. That’s 3 1/2 times the maximum dosage considered safe for drinking water. If you take twice that much Prozac daily, which is not at all unusual, you are headed for fluoride-induced HELL, which might include problems like arteriosclerosis, osteoporosis, and Alzheimer’s disease.

Action to take:

Pure and simple–stay away from Prozac and any other form of fluoride.

Reference:

“Nailing down Prozac-fluorine connection,” Stratia Wire (www.stratiawire.com), 12/6/02

HGH sprays: Fitting an elephant through a pinhole 

Human growth hormone (HGH) is still a hot commodity for anti-aging, so everyone and their brother is trying to get in on the action, coming up with new ways to give the American public what it wants. The latest HGH product fad comes in the form of nasal and oral sprays claiming to have the same miraculous anti-aging effects as HGH injections. The public is being bombarded with all sorts of pseudo-scientific bunkum and surveys from gullible patients about improved libido, quality of life, strength, better complexion, deeper sleep, and anything else you might want to improve. But before you run out to buy yourself a bottle, consider this: If it were that easy, why would anyone have ever bothered with HGH injections in the first place?

The answer, as I’m sure you’ve already guessed, is that it ISN’T that easy. You see, HGH is a hormone, and hormones are large molecules that just won’t fit through the microscopic “openings” available to them in the mouth or nasal passages. You just can’t force an elephant through a pinhole.

The size of the molecules isn’t the only problem with this approach. HGH molecules are very fragile and complex. Once they are mixed with water, degradation sets in and the molecules will be completely inert in two weeks, under the best of conditions, i.e., refrigerated and not bounced around as though they were a bag of peanuts.

Action to take:

Be skeptical of all nasal sprays purporting to deliver hormones by passage through the mucous membranes of the nose or mouth. You are not going to absorb HGH from any orifice–nose, mouth, ear canal, eye socket, navel, urethra, vagina, or anus. Take it from a doctor by injection or forget it.

Reference:

Cranton, Elmer, M.D. “HGH oral or nasal spray? I doubt it!,” www.drcranton.com, 7/20/02

Alzheimer’s help in an all-natural amino acid

A few years ago, there were reports on a great breakthrough in relieving the suffering of Alzheimer’s patients and their families. According to a 1995 study published in the journal Neurobiology of Aging, Alzheimer’s disease appears to be significantly helped by the amino acid acetyl-l-carnitine (ALC). There hasn’t been much in the way of follow-up to these reports–most likely because the pharmaceutical industry hasn’t figured out a way to replicate ALC’s effects in a patentable (i.e. profitable) formula. But regardless of the lack of follow-up, the original study results are still significant enough to bear repeating.

Jay W. Pettegrew, M.D., of the University of Pittsburgh School of Medicine, and his associates gave 3 grams of ALC to seven Alzheimer’s patients every day for one year. Five other Alzheimer’s patients received a placebo.

Researchers tested all the patients at six and 12 months to assess their cognitive function. At the beginning of the study, both groups had virtually identical cognitive scores. But the ALC group ended the study with “significantly higher” scores. They had, according to the report, maintained their cognitive function, whereas the placebo group had deteriorated.

Pettegrew also monitored levels of phosphomonoesters and high-energy phosphates, which degrade in Alzheimer’s disease. This was the really significant part of the study since neurochemical measurements like these give studies more credibility than studies that measure “cognizance” by asking family members to observe progress or deterioration in the patient. These types of studies usually result in false positive reports based on a triumph of hope over cold reality.

But in this study, researchers noted that levels of actual chemical markers in the brain remained relatively high. This means that there is actual biochemical confirmation that the disease’s progression had been slowed among those patients taking ALC.

The question immediately arises: Should we start taking ALC while we’re still in full control of our faculties? I’m leaning toward an enthusiastic “yes.” Acetyl-l-carnitine is available in most natural food stores as well as through various on-line vitamin distributors. (To find a list of such sources, visit www.google.com and type “acetyl-l-carnitine” into the search field.)

Reference:

“Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease” Neurobiology of Aging 1995; 16(1): 1-4

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