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Are you at risk of coronary heart disease or strokes? It is possible to minimize that risk by your own actions? In the author's experience, when people really understand what is going on in their bodies they take action. Perhaps it's my age but, some of my friends and relations are having heart attacks, strokes or have problems with walking distances without getting leg pains. Three particular events have pushed me into trying to find alternative solutions.

One friend had a slight stroke from which he has quickly recovered but the subsequent investigation showed 75% occlusion of one carotid artery and 55% occlusion in the other one. These arteries run in the neck and are major routes for blood going to the brain. He was advised to have the one with 75% occlusion cleared out by surgery because there was such a high chance of another stroke if this was not done. He duly went in for the operation but was told by the surgeon the next day that, after feeling the artery, it was decided that to try to clear it was too dangerous because the blockage went up too high. He was thus sewn up again and a couple of days later was home.

Another friend who was at school with me in the late 1940s and early 1950s, has had major bypass heart surgery but the replacement vessels are starting to fur up and he also has lung problems. A heart lung transplant was mentioned as an option, but in Australia where he now lives, at 61 he has been told he is too old. Apparently they have been so successful in cutting drink driving in Australia that the supply of organs for transplant has dropped dramatically.

A third is more of an acquaintance; he lives at the other end of the road to me, and I occasionally have a chat with him as he very slowly walks along the road. The pains in his legs get too bad if he walks fast or far.

These three have one thing in common – they all have a disease of the blood vessels called atherosclerosis. It is just in different places. I should add that they were all smokers.

What I wanted to know was
What can the individual do to help him/herself?
Is it possible to reverse this atherosclerotic process without surgery?

Or
Is it possible to stop the atherosclerosis getting worse and to reduce the chances of further events like strokes and heart attacks?

I know that various drug therapies are available to lower cholesterol and blood pressure and to decrease the chances of thrombosis, but what can an individual do for him/herself?

What is atherosclerosis?

Coronary heart disease, strokes and intermittent claudication are the three conditions talked about above. To the layman such names would seem to bear little relationship to each other, but they are mainly due to one thing – a disease of arteries known as atherosclerosis. The difference is the site at which the atherosclerosis occurs. The same disease of arteries can cause kidney failure when in the renal artery, impotence if in the artery to the penis and so on; the list is long because there are so many organs supplied by arteries.

Atherosclerosis is fatty growth on the inside wall of a blood vessel. The vessels principally affected are the arteries, the vessels carrying blood to the organs of the body – muscle, skin, kidneys, heart, brain, etc.

The atheroma, as each fatty growth is called, contains cholesterol, smooth muscle cells and fibrous tissue, and they start when we are quite young. By the age of 30 years most of us already have the start of atheromas in many arteries. The problem is they can continue to grow both along the vessel wall and across it. As they get bigger they start to get crystals of cholesterol in them and they harden the artery wall (sclerosis) making the artery less elastic and consequently putting up blood pressure. The growth narrows the artery so that the organ it is supplying gets a reduced blood flow. In the heart this reduced flow can mean that the heart muscle does not get enough oxygen and pain occurs called angina. In the legs this lack of blood causes pain when walking, called intermittent claudication.

Another problem is that the surface of the atheroma becomes changed or even ulcerated so that very small particles in the blood called platelets begin to stick to the surface of the atheroma. The job of the platelets is to stick together and make a plug to prevent blood loss from the circulation when there is any break in blood vessels walls, i.e. they are the first stage of a blood clot. Lots of platelets stuck together are called a thrombus, and the problem with a thrombus forming on the inside of an artery on an atheroma is that the thrombus can break away and block a smaller artery.

Blockage of an artery supplying heart muscle causes a heart attack, supplying the brain causes a stroke and supplying leg muscles causes pain in that muscle (note: a stroke can also be caused by a blood vessel bursting in the brain due to high blood pressure). The atheroma can of course occur in other organs and in the kidney; for instance, the reduced blood flow causes the release of a substance which acts to increase blood pressure.

Who gets atherosclerosis?

There are a range of well known risk factors for atherosclerosis, including smoking, eating a diet high in saturated fats and/or cholesterol, a family history of heart disease or strokes, having high blood pressure, psychosocial stress, and being obese (in particular having a waist measurement above 39 inches for men and 35½ inches for women is a very definite risk factor[1]).

These risk factors are additive. So, if you smoke, are overweight, in a stressful job which you cannot control well, have bacon and eggs for breakfast each morning, have little social support in your life and come from a family with a history of heart attacks or strokes then your life could be in serious danger even in your thirties.

Cholesterol

An obvious culprit is cholesterol because it makes up a large proportion of an atheroma. Cholesterol is an important component of all the cells in our bodies and is used by the body to make several hormones (chemical messengers) and consequently is very closely regulated. It is a component of our food and our bodies make it, principally in the liver. Because it does not dissolve in water, it is carried in the blood surrounded by a protein envelope. There are several different types of protein envelopes but the two most clinically important ones are called Low Density Lipoproteins and High Density Lipoproteins and they each contain many cholesterol molecules. They are normally referred to as LDL and HDL.

The job of LDL is to deliver cholesterol to all the cells in the body. When it arrives at a cell it is recognized by a receptor, the cell engulfs it, digests the protein envelope and uses or stores the cholesterol. In some people the cells do not have enough receptors for LDL and in these individuals the blood levels of LDL tend to be high, predisposing them to the development of atherosclerosis.

The function of HDL is to go around mopping up any loose cholesterol.

It has been known for a long time that very high levels of LDL are associated with atherosclerosis whereas high levels of HDL seem to provide protection. Consequently, LDL and HDL have come to be known respectively as bad and good cholesterols which is not strictly true. We need both but, for the good health of our arteries, LDL needs to stay fairly low, while we need to maximize our HDL levels.[2]

Maximizing HDL levels

Raising HDL is actually quite easy – exercise does it.[3] So if you want to decrease the rate at which your blood vessels are succumbing to atherosclerosis then start with regular exercise. This further benefits the blood vessels because it increases the speed at which blood moves along the vessels, which in turn increases the shear forces against the walls. Atherosclerosis appears first at places where the shear forces are low, like the inside curves of bends. Alcohol in moderate quantities also increases HDL and has the further benefit of decreasing the tendency of those platelets in blood from sticking together.[4],[5] Only moderate quantities have this effect, with high levels causing the opposite response.

Lowering LDL

Cholesterol is closely regulated, so that for instance if the intake of cholesterol goes up in our diet then the liver starts making less cholesterol and less LDL to carry it in and visa versa. Nevertheless, LDL cholesterol can be lowered to some extent by dietary methods.

However, what may be more important than the LDL cholesterol levels in our blood is whether LDL is in the form in which it can be incorporated into atherosclerotic plaques causing them to grow.5 It appears that LDL needs to undergo a chemical transformation before this can happen – a process known as oxidation. That oxidation is inhibited by certain antioxidants which can be obtained from our diet.

The Tables summarize the self-help ways that individuals can lower their LDL cholesterol levels, prevent the LDL being oxidised or have been shown to protect against heart disease or strokes.

Overall it is clear that a diet rich in vegetables, fruit, pulses, nuts, seeds and whole grain cereals and low in saturated fats (mainly from animal sources) will tend to minimize LDL cholesterol and prevent its oxidation. Meat consumption can include a moderate intake of fish and lean meat such as chicken breast. Considerable benefits can also be obtained with supplements of vitamin E and garlic and if necessary with vitamins B6, B12 and folate. Herbal solutions like Gingko Biloba and Padma 28 can also be of benefit.

Personality / Psychological Stress

There is an undoubted relationship between psychological stress and the development of atherosclerosis and resulting heart attacks and strokes. The process appears to be twofold.

Nutrition & Lifestyle Advice

Firstly, there is a blood pressure effect of stress. Each time the heart beats it pushes blood into our arteries which in turn swell up with this increased volume, and then recoil down, pushing blood through all the smaller blood vessels in the process. The blood pressure in the arteries which the doctor or nurse measures is the maximum (systolic) reached when the heart is pumping out blood and the minimum (diastolic) when the heart is refilling. When we are stressed, the heart beats faster and more forcibly and hence more blood is pumped by the heart and the blood pressure rises. We are all different in our response to stress, and those most at risk of developing atherosclerosis are the individuals with the most exaggerated heart rate and blood pressure responses. It is this type of finding which has led to proposals that white coat hypertension should be treated.[21] These are people whose blood pressure goes up dramatically when it is measured; if it goes up so easily, then what is it doing in response to the range of stressors in everyday life?

Secondly, stress causes hormones like adrenaline and cortisol to be released. This results in changes in the blood which increase the chance of those platelets sticking together to form a thrombus.[22] In other words, there is an increased chance of a heart attack or stroke in susceptible people. The same hormones cause a rise in LDL.

Anger, aggression and having a 'hostile' personality have all been identified as risk factors for atherosclerosis[23] and these are all associated with higher increased nervous system reactivity and adrenaline secretion with resulting increases in heart rate and blood pressure. Conversely, virtually the opposite behaviour, namely depression, has also been linked in as a factor in coronary heart disease.[23] In this case the body produces high levels of cortisol, and platelet function is affected, leading to an increased chance of thrombosis and hence a heart attack.

Recent studies are demonstrating that teaching patients with coronary heart disease to manage stress and modify lifestyle to minimize stressful situations are effective in decreasing heart attacks.[24]

Conclusion

By adopting dietary, exercise and lifestyle changes, the further development of atherosclerosis can possibly be stopped and certainly slowed down. There is also some evidence that atherosclerotic plaque sizes can be reduced by a small degree.

References

1. Egger G and Swinburn B. The fat loss handbook. Allen and Unwin. 1996.
2. Berger AJ. Commentary: How high density lipoprotein protects against heart disease. BMJ 319(21 Aug): 489. 1999.
3. Kokkinos P and Fernhall B. Physical activity and high density lipoprotein cholesterol levels: what is the relationship? Sports Med. 28(5): 307-14. 1999.
4. Constant J. Alcohol, ischaemic heart disease, and the French paradox. Coron Artery Dis. 8(10): 645-9 1997.
5. Whitney EN, Cataldo CB, and Rolfes SR. Understanding Clinical Nutrition. West Publishing Co. 1991.
6. Devaraj S and Jialal I. The effects of alpha-tocopherol on critical cells in atherogenesis. Current Opinion in Lipidology 9: 11-15. 1998.
7. Nieman DC, Butterworth DE and Nieman CN. Nutrition. Wm. C. Brown Publishers. 1992.
8. Harris WS. Nonpharmacologic treatment of hypertriglyceridemia: focus on fish oils. Clin. Cardiol. 22(6 Suppl): II 40-43. 1999.
9. Chisholm A, Mann J, Skeaff M, Frampton C, Sutherland W, Duncan A, Tiszavari S. A diet rich in walnuts favourably influences plasma fatty acid profile in moderately hyperlipaemic subjects. Eur. J. Clin. Nutr. 52(1): 12-16. 1998.
10. Prasad K. Dietary flax seed in prevention of hypercholesterolemic atherosclerosis. Atherosclerosis 132(1): 69-76. 1997.
11. Fraser GE. Nut consumption, lipids, and the risk of a coronary event. Clin. Cardiol. 22(7 Suppl): III 1-5. 1999.
12. Stephens SG, Parsons A, Schofield PM, Kelly F, Cheeseman K, Mitchison MJ, and Brown MJ. Randomised controlled trial of Vitamin E in patients with coronary disease. Lancet 347: 781-786. 1996.
13. Koscielny J, KlüBendorf, D, Latza R, Schmitt R, Radtke H, Siegel G. and Kiesewetter H. The antiatherosclerotic effect of Allium sativum. Atherosclerosis 144: 237-249. 1999.
14. Wilcken DEL. and Wilcken B. B Vitamins and Homocysteine in Cardiovascular Disease and Aging. Annals New York Academy of Sciences p361-70. 1998.
15. Croft KD. The chemistry and biological effects of flavonoids and phenolic acids. Ann. NY Acad. Sci. 854: 435-42. 20 Nov 1998.
16. Ishikawa T, Suzukawa M, Ito T, Yoshida H, Ayaori M, Nishiwaki M, Hara Y and Nakamura H. Effect of tea flavonoid supplementation on the susceptibility of low-density lipoprotein to oxidative modification. Am. J. Clin. Nutr. 66(2): 261-6. 1997.
17. Soleas GJ, Diamandis EP and Goldberg DM. Wine as a biological fluid: history, production, and role in disease prevention. J. Clin. Lab. Anal. 11(5): 287-313. 1997.
18. Peters H, Kieser M and Hölscher U. Demonstration of the efficacy of ginkgo biloba special extract Egb 761 on intermittent claudication – a placebo controlled , double-blind multicenter trial. Vasa 27(2): 106-10. 1998.
19. Smith PF, Maclennan K and Darlington CL. The neuroprotective properties of the Ginkgo biloba leaf: a review of the possible relationship to platelet activating factor. 1996.
20. Drabaek H, Mehlsen J, Himmelstrup H and Winther K. A Botanical Compound, Padma 28, Increases Walking Distance in Stable Intermittent Claudication. Angiology p863-7. 1992. Ingredients of Padma 28: spiral flag, iceland moss, chinaberry, myrobalan, cardamon, red saunders, sorrel, camphor, hardy orange, columbine, licorice, ribwort, knotgrass, golden cinquefoil, clove, gingerlilly, heartleaved sida, lettuce, valerian and marifold.
21. Spence DJ. Stress and atherosclerosis. Baillière's Clinical Neurology 6(2): 275-282. 1997.
22. Rozanski A, James A, Blumenthal JA and Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation 99: 2192-2217. 1999.
23. Dreary IJ, Fowkes FGR, Donnan PT and Houseley E. Hostile personality and risks of peripheral arterial disease in the general population. Psychosomatic Medicine 56: 197-202. 1994.
24. Ornish D et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA 280(23): 2001-7. 1998.

Author's Further Note

The problem with the research to date is that none have put the whole package together.

Wanted – a research programme which looks at the extent of atherosclerosis in particular arteries over a period of several years during which time patients carry out all the suggestions in the summary below. If just garlic can give a small regression then what about garlic, plus stopping smoking, plus vitamin E, plus exercise, plus a diet rich in fruit vegetables, nuts, seeds and grains, etc. The visualization of the inside of arteries by Magnetic Resonance Imaging or by Doppler ultrasound is now widely used, i.e. the technology is there.

Editor's Note

For further information regarding reducing risks of heart disease, readers are referred to the Cover Story Special Feature about Heart Disease in the previous issue No. 51 of Positive Health. For an excellent article summarizing research about Chelation Therapy, readers are referred to www.positivehealth.com From the Home Page, select Articles, then Heart, then Chelation Research Merits Priority Attention.