How Antioxidant Nutrients Protect Against Heart Disease

This article discusses the very latest findings on how antioxidant nutrients
prevent heart disease, and then forms the background for a series of articles
that explain in lay terms, “how” this occurs. An important point
of my new book, The New Supernutrition, is that heart disease is
not caused so much by what you eat as by what you don’t eat. [1]
It is difficult for the average person to understand that the nutrients
such as beta-carotene, vitamins A, C and E, and the mineral selenium are
more important to heart health than how much cholesterol is in their diet.
Merely presenting the evidence is not sufficient as the public needs some
easy-to-understand mental images so they can grasp the concept.



From time to time, I have pointed out current research showing that antioxidant
nutrients protect against heart disease. However, by the time I cover the
research findings, I have no space left for a scientifically correct —
but plain English — explanation of how these nutrients provide their protection.
I have had to be content with using general descriptions of how antioxidants
prevent the free-radical damage that causes heart disease.



This has served well for explaining how the nutrients prevent the damage
to the artery linings that starts the heart disease process. However, since
the public has been taught an oversimplified — and incorrect — concept
concerning cholesterol, the action of free radicals on the lipoproteins
that transport cholesterol in the bloodstream is hard for some to visualize.



Now I have been dealing with this “communications” problem for
more than twenty five years. The terms “free radicals” and “lipoproteins”
have become buzzwords that have helped many understand some pretty complicated
biochemical processes. The first time that the term “free radical”
was introduced to the general public was in an article about my 1960’s research
which appeared in the Ladies Home Journal . [2] Prevention
brought my free-radical research to the attention of the lay nutrition audience
in 1971. [3] And, I was first to describe high-density lipoprotein (HDL)
— the “good” cholesterol — and low-density lipoprotein (LDL)
— the “bad” cholesterol — in my 1977 book, Supernutrition
For Healthy Hearts
. [4] But now it is time to discuss the structures
of lipoproteins and lipoprotein receptors and the role of antioxidant nutrients.



More “New” Evidence

So much for the introduction to this series. By the way, there are so many
new and interesting topics to write about, that I won’t present the entire
series in consecutive installments. One thing I have learned from lecturing
is to make my point early or I will lose my audience. I often begin my lectures
with my point, which is opposed to the general practice of building up to
the point. This is how I will present this series. I will now present the
conclusion, and leave the background and explanations for the later sections.



Some of the high-lights are:


    1) Several new studies show that antioxidant vitamins prevent heart disease.



    2) We now know how HDL removes cholesterol from the interior of a
    cell, even though the HDL receptor is attached to the cell membrane.



    3) Lipoprotein(a) [Lp(a)] is one of the best markers of heart disease risk,
    and it in turn is controlled by vitamin C.



    4) We have identified a molecular “grappling hook,” a peptide,
    that LDL sinks into the free-radical damaged artery linings.




First, lets take a brief look at the new studies that show antioxidant nutrients
prevent heart disease.



Antioxidant Nutrients Prevent Heart Disease

My research in 1973 showed that dietary cholesterol didn’t cause heart disease.
[5] For those who are still skeptical, please read the confirming studies
in the thirteen cited references. [6-18] In 1974, I conducted an epidemiological
study that showed vitamin E protected against the artery damage that leads
to plaque (the so-called cholesterol deposits) and heart disease. [19-21]



In my study, where persons consumed 400 IU or more daily of vitamin E for
more than two years, their rate of heart disease was significantly lower
than normal. The amount of heart disease in any age group decreased proportionally
with the length of time that vitamin E had been taken. In fact, the length
of time was more important than quantity after a minimum of 400 IU daily
was taken.



Several researchers, including Dr. William Hermann of the Methodist Hospital
in Houston and Dr. Staurt Hartz of Tufts University, have now reported that
vitamin E supplements raise HDL. [22] A 1987 study has found that 500 IU
of vitamin E daily for three months produces a significantly improved HDL
level, Apolipoprotein A level, and Apolipoprotein A to Apolipoprotein B
ratio. [23]



Vitamin C has also been shown to raise HDL significantly. [24]



And, of course, selenium has been shown to be protective. [25] Epidemiological
studies have shown that persons with low-selenium diets have two-to-three
times greater risk of heart disease than those eating selenium rich diets.
[26] In a clinical study, patients with blockage of all three coronary arteries
had low blood selenium levels, while those with high blood selenium levels
were healthy and free of coronary heart disease. [27] Strikingly, those
with one diseased coronary artery had the next highest blood selenium levels,
and those with two blocked coronary arteries had the second lowest blood
selenium levels.



The role of antioxidant nutrients is not just in preventing the artery damage
that leads to atherosclerotic plaques, but in protecting against the formation
of blood clots when blood is squeezed through plaque-narrowed arteries.
Vitamin E reduces the stickiness of blood. Sticky blood due to high blood
platelet adhesion is what causes blood to clot in the coronary arteries
resulting in heart attacks. [28] Dr. Rudolph Riemersa of the University
of Edinburgh in Scotland and Dr. Fred Gey of the University of Berne in
Switzerland have found that men with higher-than-average blood levels of
beta-carotene, vitamin C and vitamin E –particularly vitamin E — were
less likely to have clinical symptoms of heart disease than those with lower-than-average
levels of these nutrients. [29]



Two months ago, I discussed the Harvard Physicians’ Health Study, in which
approximately 22,000 male physicians took either beta-carotene or a placebo
alternating with either aspirin or a placebo. Physicians who took the 50
milligrams (xx,000 USP) of beta-carotene every other day had about half
as many heart attacks, strokes, cardiac arrests, bypass operations or angioplasties
to remove embolisms. Among a sub-group of 333 physicians with a previous
history of heart disease, those taking a combination of aspirin and beta-carotene
suffered no heart attacks in six years of study! [30]



Lipoprotein(a)

As for LDL and HDL relationships, a better marker for heart disease risk
is the lipoprotein(a) [Lp(a)]. There is no correlation between Lp(a) levels
and cholesterol plasma levels, and in heart patients having normal blood
cholesterol levels, the only risk factor found is elevated Lp(a) or decreased
vitamin C and vitamin E levels.



Drs. Matthias Rath and Linus Pauling have published a revealing paper linking
heart disease, Lp(a) and vitamin C deficiency. Lp(a) shares with LDL its
lipid and apoprotein composition — mainly apoprotein B-100 (apo B), but
the unique thing about Lp(a) is an additional glycoprotein, apoprotein(a)
or apo(a). This difference will be discussed in a later installment of this
series.



Lp(a) levels are elevated in heart disease patients. Lp(a) blood levels
above 30 milligrams per deciliter of blood doubles the risk of coronary
heart disease. If, in addition, LDL is elevated,the risk is increased by
a factor of five. There is no correlation between Lp(a) levels and blood
cholesterol levels. In heart disease patients having normal blood cholesterol
levels, the only risk factor is found to be elevated Lp(a).



Lp(a) can be normalized by vitamin C. [31] Another 1990 report showed that
vitamin C reduces risk for heart disease. [32]



Oxidized LDL and Antioxidants

As discussed in last month’s column, the initiation of atherosclerosis results
from injury to the layer of endothelial calls which normally form the luminal
surface of blood vessel walls.



Such injury disturbs local vascular homeostasis resulting in platelet deposition,
aggregation and release of factors which promote smooth muscle proliferation
and eventual fibrosis. The damaged endothelium also becomes permeable to
lipoproteins, particularly oxidized LDL and macrophages which invade the
site of injury, accumulate cholesterol as cholesterylester, and develop
into foam cells and then fatty streaks.



Eventually, a rather complicated structure, the atherosclerotic plaque,
develops consisting of lipids (fats) complex carbohydrates, blood, blood
products, fibrous tissue and calcium deposits. A raised blood LDL-cholesterol
concentration has been recognized as a risk factor for heart disease because
it appears to be the donor of cholesterol deposited in the atherosclerotic
plaque. Raised LDL is associated more with heart disease incidence than
is blood cholesterol level, but HDL/LDL ratio correlates better, and better
yet, lipoprotein(a). The roles of these cholesterol carriers will become
clearer in later installments of this series.



The accumulation of LDL-borne cholesterol by macrophages is something of
a paradox, however, since the cell has few LDL-receptors and is able to
down regulate the receptor number when the LDL-cholesterol concentration
is increased. The resolution of this paradox may lie in one of two closely
related explanations. The first explanation is that the oxidation of LDL
produces a molecule which is no longer recognized by the LDL receptor but
by a non-regulated scavenger receptor. The macrophages can then accumulate
cholesterol from this oxidized LDL.



The second explanation is that oxidized LDL is attacked by the macrophages
and the macrophages are unable to digest the LDL particles and “die”.
The fat-filled “dead” macrophages accumulate and injure the arterial
lining resulting in plaque.



Antioxidants can prevent or slow the accumulation of cholesterol that is
due to the modification or oxidation of LDL. Antioxidant nutrients inhibit
the oxidation of human LDL. The synergistic protection of vitamins A and
C against LDL being oxidized has been shown. [33] Dr. K. Sato and colleagues
at the University of Tokyo has found that LDL is oxidized by a free radical
chain mechanism. Vitamin E halts this process within the fatty portions
of the LDL complex, while vitamin C is stops the free radical damage in
the watery medium. The two antioxidant vitamins act simultaneously and cooperatively
to reduce oxidation of LDL.



Dr. J. C. Fruchart and colleagues at the Pasteur Institute in Lille, France
found that when they gave volunteers with high LDL 1,000 IU of vitamin E
daily for two months, they produced fewer “dead” fat filled macrophages
and had lower blood cholesterol levels.



Antioxidant nutrients also protect the artery cell membranes lining the
arteries. A study at the University of Kentucky by Dr. B. Hennig showed
that when artery tissues were well-nourished with vitamin E, they were protected
from injury. [34] However, when they were vitamin E deficient, oxidative
stress caused many deleterious changes in the arteries. Related findings
have been reported by researchers at the Institute of Biochemical Science
in Italy. [35]



In the Harvard Physicians Health Study mentioned earlier, Dr. Gaziano noted
that beta-carotene discourages the formation of oxidized LDL, but there
is more to antioxidant protection than that. Dr. Daniel Steinberg of the
University of California at San Diego adds that “you’re dealing with
men in the study who have established atherosclerosis, so it may be that
oxidized LDL’s cytotoxicity is involved in thrombosis (clotting). Oxidized
LDL may be involved in fatty streak formation and precipitation of the coronary
event.” [36]





References

1. The New Supernutrition Passwater, Richard A.Pocket Books, NY (May 1991)

2. McGrady, Patrick Ladies Home Journal

3. Don’t Age Too Fast Kinderleher, Jane Prevention 23(12) 104-10 (Dec. 1971)

4. Supernutrition For Healthy Hearts Passwater, Richard A. Dial Press, NY
(1977)

5. Dietary Cholesterol Passwater, Richard A., Amer. Lab. 5(6): 10-22 (June
1973)

6. Oh, Suk Y. and Miller, Lorraine T. Amer. J. Clin. Nutr. 42(3) 421-31
(Sep. 1985)

7. Flaim, Evelyn, et al., Amer. J. Clin. Nutr. 34:1103-8 (June 1981)

8. Nutr. Rev. 43(9) 263-5 (Sep. 1985)

9. Keys, A., et al., Metabolism 14:759-65 (1965)

10. Kannell, William B. and Gordon, Tavia USDHEW Report 24 (1970)

11. Nichols, A. B., et al., Amer. J. Clin. Nutr. 29:1384-92 (1976)

12. Shekelle, R. B., et al., New Engl. J. Med. 304:65-70 (1981)

13. Drawber, Thomas R., et al., Amer. J. Clin. Nutr. 36:617-25 (Oct. 1982)

14. Porter, M. W., et al., Amer. J. Clin. Nutr. 30:490-5 (1977)

15. Slater, G., et al., Nutr. Rept. Internat. 14:249-52 (1976)

16. Kummerow, Fred A., et al., Amer. J. Clin. Nutr. 30:664-73 (1977)

17. Flynn, M. A., et al., Amer. J. Clin. Nutr. 32:1051-7 (1979)

18. Hirshowitz, B., et al., Brit. J. Plastic Surg. 23:529 (1976)

19. Heart Study of 50- 59 Year Olds. Passwater, Richard A., Prevention
28 (5) 111- 115 (May 1976)

20. Heart Study of 60- 69 Year Olds. Passwater, Richard A. Prevention 28
(4) 107- 113 (Apr. 1976)

21. Heart Study of 70- 79 Year Olds. Passwater, Richard A., Prevention 28
(2) 61- 68 (Feb. 1976)

22. Hermann, W., Ann. NY Acad. Sci. 462 (1982)

23. Cloarec, M. J., et al., Israel J. Med. Sci. 23(8) 869-72 (Aug. 1987)

24. Bazzarre, T., Nutr. Rep. Internat. 33:711-20 91986)

25. Selenium and Cardiovascular disease. Oster, O. and Prellwitz, W., Biol.
Trace Elements Res.
24:91-103 (1990)

26. …. Lancet II 175 (1982)

27. …. Clin. Chem. 30:1171 (1984)

28. Inhibition of cyclooxygenase-independent platelet aggregation by low
vitamin E concentration. Violi, F., et al., Atherosclerosis 82:247-52 (1990)

29. Fackelmann, K. A., Science News 23 (Jan. 12, 1991)

30. Gaziano, J. Michael, American Heart Association’s 63rd Scientific Sessions,
Dallas (November 1990)

31. Hypothesis: Lipoprotein(a) is a surrogate for ascorbate. Rath, M. and
Pauling, L., Proc. Natl. Acad. Sci. 87:6204-7 (1990)

32. Correlation of plasma ascorbic acid with cardiovascular risk factors.
Esk, C. et al., Clin. Res. 38:A747 (1990)

33. Free radical-mediated chain oxidation of low density lipoprotein and
its synergistic inhibition by vitamin E and vitamin C. Sato, K., et al.,
Arch. Biochem. Biophys. 279:402-5 (1990)

34. Hennig, B., Internat. J. Vit. Nutr. Res. 59:273-9 (1989)

35. Del Boccio, G., et al., Atherosclerosis 81:127-35 (1990)

36. Bankhead, Charles D., Medical World News 12-3 (Jan. 1991)


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to Ricahard A. Passwater, Ph.D. and Whole Foods magazine (WFC Inc.)

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