A recent report on www.sciencedaily.com piqued my interest, and I did some investigation.
The report was: "Free-radical Busting Antioxidants Might Not Promote Healthy Hearts," which some might interpret as, "free radicals/oxidative stress are not the cause of heart disease," but the opposite actually is the case, as my investigation of this researcher's work revealed. The report was based upon a study by Roland Stocker's group, and can be found in the Journal of Experimental Medicine. I examined Stocker's work and was impressed, but I was also disappointed to see that he, like so many others, does not seem to realize the dietary implications of his findings.
Let's take a look at the report first:
"Antioxidants, such as beta-carotene and Vitamin E, have been touted for their ability to protect against heart disease. This protective effect is attributed to their ability to prevent the oxidation of bad cholesterol by free radicals -- a process thought to contribute to the build-up of disease-causing fatty deposits on artery walls. But a new study, published online on April 10 in The Journal of Experimental Medicine, suggests that the heart-healthy effect of one antioxidant has little to do with cholesterol oxidation.
A group of researchers at the University of New South Wales in Australia, led by Roland Stocker, studied a cholesterol-lowering drug called Probucol (Lorelco) in laboratory rodents with vascular disease. Probucol reduces the risk of heart disease in humans, but is no longer prescribed in the US and Australia because of adverse side effects: a tendency to lower good cholesterol along with the bad and the potential to induce an irregular heartbeat. Probucol is still available in Canada and Europe.
In their new study, Stocker and his colleagues show that the protective effect of probucol has nothing to do with its ability to scavenge oxygen free radicals, as the free radical-busting part of the drug alone was ineffective in protecting animals against heart disease. Instead, a different part of the probucol molecule was doing the beneficial work.
In fact, contrary to widely accepted opinion, the group found no relationship between the levels of oxidized cholesterol in blood vessels and the severity of heart disease. This might help explain the disappointing results of clinical trials with other free radical-scavenging antioxidants, such as Vitamin E, which have shown no protective effect against heart disease in humans.
The protective effect of these compounds depended on the induction of a cellular enzyme called heme oxygenase-1 (HO-1). HO-1 is known to protect against atherosclerosis in animal models, although the mechanism is not completely clear. Not surprisingly, HO-1 was not induced by Vitamin E.
Drugs closely related to probucol that contain the protective part of the drug were just as protective as the original drug. If these probucol relatives -- one of which is now being tested in humans -- are free of side effects, they may provide a more effective alternative to current therapies."
So they don't know the mechanism. Should they? Have they read the literature of which they purport to be experts? I did a quite internet search and found the following:
Hum. Genet. 2002 Jul;111(1):1-8. Epub 2002 Jun 19.
Microsatellite polymorphism in promoter of heme oxygenase-1 gene is associated with susceptibility to coronary artery disease in type 2 diabetic patients.
In this study, the researchers say: "Induction of heme oxygenase-1 is implicated in the antioxidant defense mechanism" and then explain how. Why doesn't the Stocker group know this? In any case, the measurement of serum oxidized cholesterol may not be a good "marker," because it's the oxidized cholesterol that gets taken up by macrophages and becomes part of the plaque that form that one needs to worry about, and so what's in the blood may not be a good marker for this.
In a different study done by the Stocker group, it was stated that: "It has recently been shown that alpha-tocopherol (alpha-TOH) can act either as an antioxidant or prooxidant for isolated low density lipoprotein (LDL). In the absence of an effective co-antioxidant, alpha-TOH is a prooxidant and this activity is evidently due to reaction of the alpha-tocopheroxyl radical (alpha-TO.) with the LDL's polyunsaturated lipids..."
Source: J Biol Chem. 1995 Mar 17;270(11):5756-63.
Prevention of tocopherol-mediated peroxidation in ubiquinol-10-free human low density lipoprotein.
It turns out that the reduced form of what is sold in stores as "CoQ10" (the reduced form), but what they discovered is that it's the PUFAs that are the problem. If there were very few PUFAs in the LDL, there may very well be hardly any heart disease, and if one looks at the historical and demographic evidence, this indeed seems to be the case.
In another study by the Stocker group, as similar point is made:
"These and other unusual findings about LDL peroxidation in the presence of -TOH (17, 19, 20, 21) have led us to conclude that -TOH in LDL can have prooxidant activity arising from a reaction between the -tocopheroxyl radical ( -TO ) and the active bisallylic methylene groups of polyunsaturated fatty acids (LH) of the LDL."
Source: J Biol Chem. 1995 Mar 17;270(11):5756-63.
Prevention of tocopherol-mediated peroxidation in ubiquinol-10-free human low density lipoprotein.
Thus, one is compelled to ask, "why are these researchers not considering that the problem could be solved if people ate much less PUFAs?" Why are they "trying to reinvent the wheel" and experimenting with on rats with a drug that has been banned in the USA and Australia (at least) due to toxic effects? This all seems ridiculous, if one understands the evidence as a whole, and sadly, researchers seem to simply accept the textbook dogma and seek to find a research direction that is "marketable." Now I understand that they "need to feed their families," but I'm can't have sympathy for this notion if it comes at the expense of my health! |
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