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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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And here is a citation that makes it clear why diet is so important in this context:
"Oxidizability of antioxidant-depleted LDL was largely determined by LDL PUFA content."
Source: Free Radic Res. 1996 Feb;24(2):135-47. |
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And this report is right on point:
QUOTE: Researchers from the Jean Mayer USDA Human Nutrition Research Center (USDA HNRCA) at Tufts University and colleagues have found another link among genes, heart disease and diet. The study, published in Circulation, examined apolipoprotein A5 (APOA5), a gene that codes for a protein, which in turn plays a role in the metabolism of fats in the blood. The results show that people who carry a particular variant of APOA5 may have elevated risk factors that are associated with heart disease, but only if they also consumed high amounts of omega-6 fatty acids in their diets. UNQUOTE.
Source: http://www.sciencedaily.com/releases/2006/10/061007111419.htm |
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Here's a recent study on this subject: Free Radic Biol Med. 2006 Dec 1;41(11):1678-1683. Epub 2006 Sep 8. TITLE: Systemic elevations of free radical oxidation products of arachidonic acid are associated with angiographic evidence of coronary artery disease. QUOTE: Oxidant stress is widely believed to participate in cardiovascular disease pathogenesis.... Of the markers monitored, only 9-HETE and F(2)-isoprostanes, both products of free radical-mediated arachidonic acid oxidation, were significantly elevated in patients with angiographically defined CAD ...Systemic levels of 9-HETE and F(2)-isoprostanes are independently associated with angiographic evidence of CAD and appear superior to other specific oxidation products of arachidonic and linoleic acids as predictors of the presence of angiographically evident coronary artery disease. UNQUOTE. The only problem with this abstract, as far as I can tell, is that they say this mechanism is widely believed to participate in the "disease," and yet I almost always hear "experts" talk about "saturated fat" causing heart disease. The reality, of course, is that saturated fatty acids cannot be made into these molecules (the "markers" that the researchers refer to). |
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And here is a passage from an abstract of a study - more of the same: QUOTE: Macrophages play a central role in the development and progression of atherosclerotic lesions. It is well known that oxidized low density lipoprotein (ox-LDL) promotes the recruitment of monocytes (which differentiate to macrophages) into the intima... These results indicate that ox-LDL prevents apoptosis in M-CSF-deprived macrophages at least in part by inhibiting acid sphingomyelinase. This in turn prevents ceramide-induced down-regulation of PKB, the activity of which is required to maintain production of Bcl-XL. UNQUOTE. TITLE: Oxidized low density lipoprotein inhibits macrophage apoptosis by blocking ceramide generation, thereby maintaining protein kinase B activation and Bcl-XL levels. |
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Here's a good abstract that is consistent with my views: Levick, SP, et al. Arachidonic Acid metabolism as a potential mediator of cardiac fibrosis associated with inflammation. An increase in left ventricular collagen (cardiac fibrosis) is a detrimental process that adversely affects heart function. Strong evidence implicates the infiltration of inflammatory cells as a critical part of the process resulting in cardiac fibrosis. Inflammatory cells are capable of releasing arachidonic acid, which may be further metabolized by cyclooxygenase, lipoxygenase, and cytochrome P450 monooxygenase enzymes to biologically active products, including PGs, leukotrienes, epoxyeicosatrienoic acids, and hydroxyeicosatetraenoic acids. Some of these products have profibrotic properties and may represent a pathway by which inflammatory cells initiate and mediate the development of cardiac fibrosis. In this study, we critically review the current literature on the potential link between this pathway and cardiac fibrosis. |
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Here is a passage from an essay written by fatty acid researcher Mary Enig, which provides some historical information that people often ask me about:
QUOTE: In the years that followed, a number of population studies demonstrated that the animal model—especially one derived from vegetarian animals—was not a valid approach for the problem of heart disease in human omnivores. A much publicized 1955 report on artery plaques in soldiers killed during the Korean War showed high levels of atherosclerosis, but another report—one that did not make it to the front pages—found that Japanese natives had almost as much pathogenic plaque�?5% versus 75%—even though the Japanese diet at the time was lower in animal products and fat.4 A 1957 study of the largely vegetarian Bantu found that they had as much atheroma—occlusions or plaque buildup in the arteries—as other races from South Africa who ate more meat.5 A 1958 report noted that Jamaican Blacks showed a degree of atherosclerosis comparable to that found in the United States, although they suffered from lower rates of heart disease.6 A 1960 report noted that the severity of atherosclerotic lesions in Japan approached that of the United States.7 The 1968 International Atherosclerosis Project, in which over 22,000 corpses in 14 nations were cut open and examined for plaques in the arteries, showed the same degree of atheroma in all parts of the world—in populations that consumed large amounts of fatty animal products and those that were largely vegetarian, and in populations that suffered from a great deal of heart disease and in populations that had very little or none at all.8 All of these studies pointed to the fact that the thickening of the arterial walls is a natural, unavoidable process. The lipid hypothesis did not hold up to these population studies, nor did it explain the tendency to fatal clots that caused myocardial infarction.
In 1956, an American Heart Association (AHA) fund-raiser aired on all three major networks. The MC interviewed, among others, Irving Page and Jeremiah Stamler of the AHA, and researcher Ancel Keys. Panelists presented the lipid hypothesis as the cause of the heart disease epidemic and launched the Prudent Diet, one in which corn oil, margarine, chicken and cold cereal replaced butter, lard, beef and eggs. But the television campaign was not an unqualified success because one of the panelists, Dr. Dudley White, disputed his colleagues at the AHA. Dr. White noted that heart disease in the form of myocardial infarction was nonexistent in 1900 when egg consumption was three times what it was in 1956 and when corn oil was unavailable. When pressed to support the Prudent Diet, Dr. White replied: "See here, I began my practice as a cardiologist in 1921 and I never saw an MI patent until 1928. Back in the MI free days before 1920, the fats were butter and lard and I think that we would all benefit from the kind of diet that we had at a time when no one had ever heard the word corn oil."
But the lipid hypothesis had already gained enough momentum to keep it rolling, in spite of Dr. White's nationally televised plea for common sense in matters of diet and in spite of the contradictory studies that were showing up in the scientific literature. In 1957, Dr. Norman Jolliffe, Director of the Nutrition Bureau of the New York Health Department initiated the Anti-Coronary Club, in which a group of businessmen, ranging in age from 40 to 59 years, were placed on the Prudent Diet. Club members used corn oil and margarine instead of butter, cold breakfast cereals instead of eggs and chicken and fish instead of beef. Anti-Coronary Club members were to be compared with a "matched" group of the same age who ate eggs for breakfast and had meat three times a day. Jolliffe, an overweight diabetic confined to a wheel chair, was confident that the Prudent Diet would save lives, including his own.
In the same year, the food industry initiated advertising campaigns that touted the health benefits of their products—low in fat or made with vegetable oils. A typical ad read: "Wheaties may help you live longer." Wesson recommended its cooking oil "for your heart's sake" a Journal of the American Medical Association ad described Wesson oil as a "cholesterol depressant." Mazola advertisements assured the public that "science finds corn oil important to your health." Medical journal ads recommended Fleishmann's unsalted margarine for patients with high blood pressure.
Dr. Frederick Stare, head of Harvard University's Nutrition Department, encouraged the consumption of corn oil—up to one cup a day—in his syndicated column. In a promotional piece specifically for Procter and Gamble's Puritan oil, he cited two experiments and one clinical trial as showing that high blood cholesterol is associated with CHD. However, both experiments had nothing to do with CHD, and the clinical trial did not find that reducing blood cholesterol had any effect on CHD events. Later, Dr. William Castelli, Director of the Framingham Study was one of several specialists to endorse Puritan. Dr. Antonio Gotto, Jr., former AHA president, sent a letter promoting Puritan Oil to practicing physicians—printed on Baylor College of Medicine, The De Bakey Heart Center letterhead.9 The irony of Gotto's letter is that De Bakey, the famous heart surgeon, coauthored a 1964 study involving 1700 patients which also showed no definite correlation between serum cholesterol levels and the nature and extent of coronary artery disease.10 In other words, those with low cholesterol levels were just as likely to have blocked arteries as those with high cholesterol levels. But while studies like De Bakey's moldered in the basements of university libraries, the vegetable oil campaign took on increased bravado and audacity.
The American Medical Association at first opposed the commercialization of the lipid hypothesis and warned that "the anti-fat, anti-cholesterol fad is not just foolish and futile. . . it also carries some risk." The American Heart Association, however, was committed. In 1961 the AHA published its first dietary guidelines aimed at the public. The authors, Irving Page, Ancel Keys, Jeremiah Stamler and Frederick Stare, called for the substitution of polyunsaturates for saturated fat, even though Keys, Stare and Page had all previously noted in published papers that the increase in CHD was paralleled by increasing consumption of vegetable oils. In fact, in a 1956 paper, Keys had suggested that the increasing use of hydrogenated vegetable oils might be the underlying cause of the CHD epidemic.11
Stamler shows up again in 1966 as an author of Your Heart Has Nine Lives, a little self-help book advocating the substitution of vegetable oils for butter and other so-called "artery clogging" saturated fats. The book was sponsored by makers of Mazola Corn Oil and Mazola Margarine. Stamler did not believe that lack of evidence should deter Americans from changing their eating habits. The evidence, he stated, " . . was compelling enough to call for altering some habits even before the final proof is nailed down. . . the definitive proof that middle-aged men who reduce their blood cholesterol will actually have far fewer heart attacks waits upon diet studies now in progress." His version of the Prudent Diet called for substituting low-fat milk products such as skim milk and low-fat cheeses for cream, butter and whole cheeses, reducing egg consumption and cutting the fat off red meats. Heart disease, he lectured, was a disease of rich countries, striking rich people who ate rich food. . . including "hard" fats like butter.
It was in the same year, 1966, that the results of Dr. Jolliffe's Anti-Coronary Club experiment were published in the Journal of the American Medical Association.12 Those on the Prudent Diet of corn oil, margarine, fish, chicken and cold cereal had an average serum cholesterol of 220, compared to 250 in the meat-and-potatoes control group. However, the study authors were obliged to note that there were eight deaths from heart disease among Dr. Jolliffe's Prudent Diet group, and none among those who ate meat three times a day. Dr. Jolliffe was dead by this time. He succumbed in 1961 from a vascular thrombosis, although the obituaries listed the cause of death as complications from diabetes. The "compelling proof" that Stamler and others were sure would vindicate wholesale tampering with American eating habits had not yet been "nailed down."
The problem, said the insiders promoting the lipid hypothesis, was that the numbers involved in the Anti-Coronary Club experiment were too small. Dr. Irving Page urged a National Diet-Heart Study involving one million men, in which the results of the Prudent Diet could be compared on a large scale with the those on a diet high in meat and fat. With great media attention, the National Heart Lung and Blood Institute organized the stocking of food warehouses in six major cities, where men on the Prudent Diet could get tasty polyunsaturated donuts and other fabricated food items free of charge. But a pilot study involving 2,000 men resulted in exactly the same number of deaths in both the Prudent Diet and the control group. A brief report in Circulation, March 1968, stated that the study was a milestone "in mass environmental experimentation" that would have "an important effect on the food industry and the attitude of the public toward its eating habits." But the million-man Diet Heart Study was abandoned in utter silence "for reasons of cost." Its chairman, Dr. Irving Page, died of a heart attack. UNQUOTE.
Source: http://www.westonaprice.org/knowyourfats/oiling.html |
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QUOTE: ...In several models, we show that PGE2 produced by the arterial wall facilitates arterial thrombosis. Next, we detected PGE2 in mouse atherosclerotic plaques. We demonstrate that this plaque-produced PGE2 is not altered and is still able to activate EP3. In addition, we present evidence that PGE2 can leave the plaque and activate EP3 on blood platelets. Consistent with these findings, we observed that atherothrombosis induced in vivo by mechanical rupture of the plaque was drastically decreased when platelets lacked EP3. In conclusion, PGE2 facilitates the initiation of arterial thrombosis and, hence, contributes to atherothrombosis... UNQUOTE. Source: J Exp Med. 2007 Jan 22; [Epub ahead of print]. Title: "Vascular wall-produced prostaglandin E2 exacerbates arterial thrombosis and atherothrombosis through platelet EP3 receptors." Authors: Gross, S., et al. |
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Atherosclerosis. 1994 Nov;111(1):65-78.
"Iron induces lipid peroxidation in cultured macrophages, increases their ability to oxidatively modify LDL, and affects their secretory
properties."
Fuhrman B, Oiknine J, Aviram M.
Abstract: The present study demonstrates for the first time that iron ions can induce lipid peroxidation in intact macrophages without causing cell death. Macrophage lipid peroxidation increases cell-mediated oxidation
of LDL, enhances the release of interleukin 1 and inhibits the release of apolipoprotein E from the macrophages. When cultured macrophages
were exposed to ferrous ions (50 microM FeSO4) for 4 h at 37 degrees C, cellular lipid peroxidation (measured by analyses of malondialdehyde (MDA), conjugated dienes (CD), and lipid peroxides (PD)) increased 2-4-fold in comparison with non-treated cells. This
process was iron-dose dependent, reached its maximum after 4 h of incubation, and was accompanied by 68% and 53% reductions in the
content of the cellular linoleic (18:2), and arachidonic acid (20:4), respectively, and by 29% and 36% reductions of cellular vitamin E and
vitamin A, respectively. Cell viability (measured by trypan blue exclusion, by [3H]thymidine incorporation into DNA, by analysis of the release of lactate dehydrogenase (LDH) or [3H]adenine), and cell
morphology (studied by scanning electron microscopy) were not significantly affected by the iron-induced oxidative stress. Manitol and dimethylthiourea (DMTU), but not catalase or superoxide dismutase
(SOD), significantly inhibited iron-induced cellular lipid peroxide formation, suggesting that hydroxyl radical, but not superoxides or hydrogen peroxides, mediated the iron-induced cellular lipid peroxidation. Incubation of LDL (0.2 mg of protein/ml) with oxidized macrophages resulted in LDL lipids peroxidation, as evidenced by an 8-fold increase in the LDL associated MDA in comparison with LDL that was incubated under similar conditions with non-oxidized macrophages.
Furthermore, oxidation of LDL by oxidized macrophages in the presence of copper ions (10 microM CuSO4) was 2-fold higher in comparison with oxidation of LDL by non-oxidized macrophages. The release of
apolipoprotein E from oxidized macrophages decreased by 50%, whereas macrophage release of beta-glucuronidase and of interleukin-1 beta
increased by 83% and by a factor of 6, respectively. This study demonstrates for the first time that iron ions induce oxidation of the cellular polyunsaturated fatty acids in intact macrophages and that this cellular lipid peroxidation can subsequently induce LDL
oxidation. |
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QUOTE: Doctors at the University of Maryland Medical Center had a mystery on their hands. A 51-year-old physician colleague who looked the picture of health—no cardiovascular risks, a marathon runner who had exercised vigorously each day for 30 years—had just flunked a calcium screening scan of his heart. The patient had expected a score indicating a healthy cardiovascular system. Instead, the images indicated a high score: a build-up of calcium in his coronary arteries put him at high risk for blocked blood vessels and a possible heart attack. The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range... The researchers conclude that the physician’s intense, long-term exercise regime... contributed to his cardiovascular disease. "In this particular individual, we think that oxidative stress was an important contributor," says the study’s senior author, Michael Miller, M.D., director of preventive cardiology at the University of Maryland Medical Center and associate professor of medicine at the University of Maryland School of Medicine. "But we also found that this individual has exercise-induced hypertension, which I think is vastly under-diagnosed." Oxidative stress is a byproduct of the normal cellular metabolism of oxygen. It refers to cell, tissue or organ damage from a class of molecules associated with oxygen metabolism, including unstable molecules called "free radicals." Oxidative stress plays a role in many heart, lung, blood and sleep disorders, including atherosclerosis, or hardening of the arteries, hypertension, heart failure, asthma and sleep apnea... ...the patient was given vitamins C and E just before exercise and was tested again for endothelial response. These vitamins are known as antioxidants and may protect cells from free radical damage. This time, the test revealed a partial reversal of the blood vessel constriction after one hour, and normalization after two hours... UNQUOTE. Note that the vitamins C and E appeared to help, and that the only mechanism known is that they neutralize the free radicals generated from unsaturated fatty acids, especially polyunsaturated ones? Why don't the researchers mention this? They may not know, but why are they not doing the research? It won't take anyone more than a few minutes of research to see what C and E do, and they should already know that unsaturated fatty acids can generate free radicals whereas saturated ones will not. Source: http://www.sciencedaily.com/releases/2007/03/070315091100.htm |
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Different cause, same underlying biochemical mechanism for "heart disease:"
QUOTE: ...Pollutant particles are coated in chemicals sensitive to free radicals, which cause the cell and tissue damage known as oxidation. Oxidation leads to the inflammation that causes clogged arteries... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/01/080121084718.htm |
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Metab Syndr Relat Disord. 2004 Jun;2(2):124-8.
Title: "Polyunsaturated Fatty acids, insulin resistance, and atherosclerosis: is inflammation the connecting link?"
Authors: Dubnov and Berry.
Abstract: We discuss the concept that the two essential (not produced by the body and obtained exclusively through the diet) polyunsaturated fatty acid families-n-6 and n-3-may play a role in the pathogenesis of insulin resistance through inflammatory pathways. Linoleic acid, the major n-6 fatty acid, is metabolized into pro-inflammatory arachidonic acid, which, in turn, gives rise to leukotrienes and protaglandins. N-3 fatty acids, found in plants and in fish, reduce the levels of arachidonic acid, thereby lowering inflammatory mediator concentrations and increasing insulin sensitization. We discuss these findings and their implications for insulin resistance and their possible effect on coronary heart disease. |
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Title of report: "Heart Disease Discovery: New Mechanism Links Activation Of Key Heart Enzyme And Oxidative Stress."
QUOTE: A study, led by University of Iowa researchers, reveals a new dimension for a key heart enzyme and sheds light on an important biological pathway involved in cell death in heart disease...
The UI researchers and colleagues from Vanderbilt University in Nashville, Tenn., focused on calmodulin kinase II, or CaM kinase II, a well-studied enzyme critical to many fundamental processes including heartbeat and thought.
Scientists know that CaM kinase's activity is sustained by adding a phosphate group -- a process known as phosphorylation. The new study proves that oxidation -- adding oxygen -- also can sustain the enzyme's activity, and like phosphorylation, the mechanism can be reversed to inactivate the kinase.
"Our results suggest that oxidation of CaM kinase is a dynamic and reversible process that may direct cell signaling in health and disease," said Mark Anderson, M.D., Ph.D... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/05/080501125455.htm |
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QUOTE: ...Atherosclerosis (hardening of the arteries) is an inflammatory disease in which the walls of the blood vessels are thickened and become less elastic. It can cause blood clots and other cardiovascular diseases. It is not known precisely what causes atherosclerosis, but the immune system probably plays an important role. Research scientists suspect that various oxidised forms of what is known as bad cholesterol, LDL (low-density lipoprotein), contribute to the development of the disease. A research team from Karolinska Institutet, in cooperation with Lund University, has now shown that a particular type of naturally occurring antibodies, anti-PC, which are targeted against the lipid portion of the LDL molecule, play an important role in the development of cardiovascular disease. The findings show that individuals who have low levels of anti-PC are at increased risk of cardiovascular disease. The risk is particularly high in men who develop stroke, with an almost fourfold increase... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/07/080731073547.htm
Note that while they seem to know what they're talking about here, they don't mention that dietary saturated fatty acids have absolutely nothing to do with this process. Dietary polyunsaturated fatty acids, on the other hand, certainly can lead to oxidized LDL. The molecular-level evidence makes this point clear. |
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QUOTE: ...Marauding molecules cause the tissue damage that underlies heart attacks, sunburn, Alzheimer's and hangovers. But scientists at the Stanford University School of Medicine say they may have found ways to combat the carnage after discovering an important cog in the body's molecular detoxification machinery.
The culprit molecules are oxygen byproducts called free radicals. These highly unstable molecules start chain reactions of cellular damage - an escalating storm that ravages healthy tissue... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/09/080911150053.htm |
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QUOTE: Aspirin has become one of the most widely used medications in the world, owing to its ability to reduce pain, fevers, inflammation, and blood clotting. In animal studies, aspirin has also been shown to prevent atherosclerosis, though none of its known mechanisms of action would seem to account for this...
Using cell culture and mouse models, Sampath Parthasarathy and colleagues observed that aspirin –specifically its active byproduct salicylate�?can greatly increase the expression of two proteins: paraoxonase 1 (PON1) and apolipoprotein A1 (ApoA1); in the mouse studies, low dose aspirin supplements could increase PON1 and ApoA1 levels by 7- and 12- fold, respectively.
Both of these proteins are beneficial components of the HDL complex, the "good cholesterol" that helps prevent atherosclerosis; ApoA1 removes bad cholesterol from the bloodstream while PON1 is an antioxidant that breaks down toxic lipid peroxides... UNQUOTE.
Note that toxic lipid peroxides are not likely to be a problem if your only source of dietary fat was fresh coconut oil.
Source: http://www.sciencedaily.com/releases/2008/09/080922155916.htm |
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