What Causes Heart Attacks and Strokes?

Peter was worried about his cholesterol and was on a mission to do everything possible to lower it. Unfortunately, Peter died at the age of 51 from a massive heart attack. Prior to his death his doctor congratulated him for lowering his cholesterol from 225 to 186.

What went wrong?

Peter followed his doctor's recommendations to the "T". He avoided saturated fats, exercised three days week and faithfully took the prescription Zocor.

So why did this happen?

First and foremost, I want you to hear me loud and clear…

Peter was simply following the crowd who believe that lowering cholesterol will save them from having a heart attack or stroke.

Considering heart disease will claim the life of one out of two people, it is about time you learn the "real" causes of heart attacks and strokes.

So what are the real causes of heart attacks and strokes?

They are:

• High triglycerides
  

• Low HDL cholesterol
  

• Dietary deficiency of saturated fats and cholesterol. Yes, you read it right. Low intake of saturated fat is factor in increasing your risk of heart disease.

  The following facts on saturated fats are from Mary G. Enig, PhD president of the Price-Pottenger Nutrition Foundation.

  a) Saturated fatty acids raise HDL, the so-called good cholesterol, whereas the trans fatty acids lower HDL cholesterol.
  

  b) Saturated fatty acids lower the blood levels of the atherogenic lipoprotein (a), whereas trans fatty acids raise the blood levels of Lp(a)
  

  c) Saturated fatty acids conserve the good omega-3 fatty acids whereas trans fatty acids cause the tissues to lose the good omega-3 fatty acids.
  

  d) Saturated fatty acids do not inhibit insulin binding whereas trans fatty acids do inhibit insulin binding.
  

  e) Saturated fatty acids are the normal fatty acids made by the body and they do not interfere with enzyme functions such as the delta-6-desaturase, whereas trans fatty acids are not made by the body and they interfere with many enzyme functions such as delta-6-desaturase.
  

  f) Some saturated fatty acids are used by the body to fight viruses, bacteria and protozoa and they support the immune system whereas trans fatty acids interfere with the function of the immune system.
  

  g) Stearic acid, a naturally saturated fatty acid, is the preferred food for the heart whereas trans fatty acids replace these saturated fatty acids in the cell membrane, thus depriving the heart of its optimum energy source.
  

  h) Saturated fatty acids are needed for proper modeling of calcium in the bones whereas trans fatty acids cause softening of the bones.
  

  i) Saturated fatty acids from animal sources are carriers for vital fat-soluble vitamins whereas factory-produced trans fatty acids are devoid of these important nutrients.
  

• Excess dietary polyunsaturated fats. Polyunsaturated fat is found in vegetable oils like soyabean, corn, sunflower and safflower. Excess polyunsaturates have been shown to contribute to heart disease, cancer, weight gain and many other health problems.

• Excess Dietary carbohydrates (particularly fructose sugar)
  

• Thyroid insufficiency
  

• Excess estrogen
  

• Testosterone insufficiency
  

• Excess Catecholamines (epinephrine, norepinephrine and dopamine) Studies have found that the increased secretion of stress hormones when someone is angry (epinephrine, norepinephrine and dopamine) can damage the endothelium, a layer of thin, flattened cells that line the arteries and can accelerate the development of atherosclerosis.

  The damage of artery walls and plaque build-up in atherosclerosis is what is ultimately responsible for most heart attacks.

  Excess amounts of epinephrine, norepinephrine and dopamine, collectively known as catecholamines, also can disrupt the electrical rhythm of the heart.

  Catecholamines are also associated with platelet adhesion. Platelets assist in normal, healthy blood clotting, but they also can adhere to sites of endothelium damage, which can lead to blockages in veins and arteries. This sort of plaque buildup can lead to a complete blockage.

• Excess Cortisol
  

• Excess insulin (Syndrome X) Increased insulin levels have been found to be responsible for atherosclerotic lesions. Controlling insulin levels should be an important objective towards averting heart attack. Excess insulin has also been responsible for vasoconstriction and blood clotting, two more factors that contribute to arterial blockages.
  

• Oxidative stress to the heart and arteries
  Apples turn brown. Butter turns rancid. Iron rusts. All are everyday signs of oxidative stress -destruction caused by free radical molecules. But none of these nuisances compare to what these unstable molecules can do inside the body, especially to cells of the brain and the vessels of the heart.

  A single free radical can set off a chain reaction that can destroy an enzyme, a strand of DNA, or even an entire cell. Ongoing free radical damage leads to destruction of organ tissues and artery walls, and may be a contributing factor in the production of cancer cells.

• Excess and rapid growth of cells lining the arteries causing narrowing

• Platelet aggragation
  When there is a vascular injury, platelets rush to the site of the injury and form a plug (blood clot) commonly called a platelet plug. However, when there is an abnormal increase in platelet formation unwanted blood clots could develop causing them to lodge in an artery going to the brain leading to a stroke. If one finds itself in a coronary artery it can stop blood flow to the heart muscle and cause a heart attack.
  

• Excess prostaglandins
  Prostaglandins, it seems, can cause platelets in the blood to stick together, which can eventually lead to blocked blood vessels and prevent delivery of oxygen-rich blood to the tissues.

• Excess vasoconstriction
  Vasoconstriction increases the risk of blockage simply by reducing the diameter of the vessel. Hypertension, or high blood pressure, is a good indicator of vasoconstriction.

• Magnesium Deficiency
  

• Excess calcium (pushing out magnesium) in the heart, blood vessels and vasomotor nerves

• Trace mineral deficiencies

  Quite an exhaustive list, isn't it? (Note that elevated serum cholesterol is not on the list, and neither is excess dietary intake of cholesterol --- which is the point I have been making.

  Case History:

  Diane consulted with me in the beginning of 2004 for nutritional management of cardiovascular disease. Although her cholesterol levels were well within normal ranges, she was suffering with high blood pressure and elevated triglycerides. She also had a family history of strokes and heart attacks. At the age of 54, Diane wanted to be certain she was doing everything she can to prevent being a victim of a coronary episode.

  Diane was following the traditional diet of low saturated fats, and was taking medication to lower her blood pressure (calcium channel block).

  After a thorough cardiovascular evaluation, it was found that Diane had 11 of the probable causes of hearts and strokes increasing her risk of having a stroke or heart attack.

  Functional Diagnostic Testing provided valuable objective information helping me to formulate a personalized program. After 6 weeks, Diane's risk factors went from 11 to 4.

  ==========
  
  

  Clinical Indicators of Cardiovascular Disease
  
  

  Here is a list of clinical indicators of CVD risk. In other words, this is a list of factors indicating the likelihood that one or more of the above listed causes of CVD are at work in your body setting you up for a heart attack or stroke.

• Cardiac arrhythmia
  

• Elevated triglycerides (particularly elevated triglycerides to HDL cholesterol ratio) Elevated blood levels of triglycerides, but not cholesterol, have been associated with an impaired fibrinolytic system. Studies have implicated triglycerides in the progression of both coronary atherosclerosis.
  

• Elevated homocysteine: Homocysteine acts as a molecular abrasive by scraping the inner layer of blood vessels. Thus high levels of homocysteine have been correlated with damaged endothelium and the formation of atherosclerotic lesions. One study found that men with extremely high homocysteine levels were three times more likely to have an associated myocardial infarction.

• Elevated insulin: Hyperinsulinemia with normal blood glucose is a factor associated with the etiology of hyperlipidemias and is an independent risk factor for heart disease.
  

• Elevated cortisol levels: High levels of cortisol are associated with hypertension, and, interestingly, it has been found that simply having a family history of hypertension predisposes an individual to exaggerated cortisol excretion in response to stress.

  Patients with heart diseases exhibit higher cortisol levels than do controls.
  

• Elevated estrogen in respect to progesterone

• Low testosterone (in men)

  Higher levels of testosterone has been found to offer men greater than five-fold protection against atherosclerotic coronary artery disease. Chronically low testosterone levels, may actually precede coronary artery disease and thrombosis in men.

  Low testosterone is linked to higher levels of fibrinogen and plasminogen activator inhibitor which play a crucial role in blood viscosity, plaque formation, and platelet aggregation. Experimental studies also show testosterone capable of triggering vasodilation of the arteries--a relaxant effect believed to have a beneficial impact on angina and other cardiovascular impairments.

  A normal physiological level of testosterone may protect against the development of hyperlipidaemia, hyperinsulinism,

  --Quarterly Journal of Medicine.

  A normal physiological level of testosterone may protect against the development of hyperlipidaemia, hyperinsulinism, hypertension echoed British cardiologists in the Quarterly Journal of Medicine.

• High testosterone (in women): though testosterone may produces strong beneficial effects on an amazingly wide array of CVD risk factors in men, high levels of testosterone exert a detrimental influence on cardiovascular health in women.

• Lipid Perixoide: Lipid peroxides are the products of chemical damage done by oxygen free radicals to the lipid components of cell membranes. This test is an assay of total thiobarbituric acid-reactive substances (TBARS) in serum that measures total serum lipid peroxidation, an indicator of whole body free radical activity. High levels of lipid peroxides are associated with cancer, heart disease, stroke, and aging.

• Elevated C-reactive protein: Inflammation may be a crucial factor in the pathogenesis of atherothrombosis. C-reactive protein is a marker associated with production of inflammatory cytokines. These cytokines appear to encourage coagulation and damage to the vascular endothelium, increasing the potential threat to cardiovascular health.

  A recent study published in the New England Journal of Medicine found that plasma C-reactive protein (CRP), a marker for systemic inflammation, is a strong predictor of myocardial infarction and stroke. Men with CRP values in the highest quartile had three times the incidence of myocardial infarction and two times the incidence of ischemic stroke. Significantly, these relationships remained steady over long periods, and were independent of other lipid and non-lipid factors, including smoking.
  

• Mineral deficiencies

• Fatty acid imbalance

• Thyroid functional evaluation

  Do see the significance of the two lists you have just read?

  The knowledge you have in the first list puts you far above the vast majority of people in your understanding of CVD causes.

  As unbelievable as it may seem, we have a condition that kills more than 50% of all people, yet most doctors are almost entirely ignorant of the causes of this condition. How unbelievably absurd is that? You can be quite pleased that you have risen above the standards of mediocrity that characterize the healing arts professions.

  The real beauty is in the second list. Here, you have best clinical indicators that inform you completely about the 19 causative factors of CVD.

  Do you see how valuable this is to you and your loved ones? You have the ability to define and monitor the 19 causes of cardiovascular disease with best clinical indicators.

  Case History
  

  Peter is a 58 years old and he already had one heart attack. His triglycerides were over 1000, blood pressure in the stratosphere, and his pulse would bounce up to over 100 at the slightest provocation. Peter was found to have 14 of the 20 causes of cardiovascular disease.

  Functional Diagnostic Testing provided valuable objective information helping me to formulate a personalized program.

  Within three months, Peter's triglycerides came down below 200, the blood pressure was in the high normal and his pulse was steady and strong. Furthermore, Peter was able to eliminate four of his six medications prescribed by the Cardiologist, and is feeling better than he has in years. Overall, Peter's risk factors went from 14 to 6.

  ==========
  
  

  Overview of Risk Factors and Clinical Testing
  
  

  Dr. Grisanti's comments:
  Would you like to know if you are at risk to get a heart attack or stroke? Identifying your risk factors allows you to identify early stages of CVD 20 years or more before the typical physician will identify a pathology, and as much as 25-30 years before the heart attack or stroke.

  Remember, cholesterol "alone" is simply not acceptable. Don't buy into the Madison Avenue million dollar television ads telling you that lowering your cholesterol will save you from having a stroke or heart attack. Now that you know the truth, do something about it and demand that your physician properly evaluates your risk factors.

  It could mean the difference between life and death!

  In part 3 I will discuss the best and most researched treatment to reverse and prevent the 19 risk factors.

  References:
  

  Filipovsky J, Ducimetaere P, Eschwaege E, Richard JL, Rosselin G, Claude JR. The relationship of blood pressure with glucose, insulin, heart rate, free fatty acids and plasma cortisol levels according to degree of obesity in middle-aged men. J Hypertens 1996;14(2):229-35.

  Fredrickson M, Tuomisto M, Bergman-Losman B. Neuroendocrine and cardiovascular stress reactivity in middle-aged normotensive adults with parental history of cardiovascular disease. Psychophysiol 1991;28(6):656-64.

  Stahl F, Schnorr D, Pilz C, Dörner G. Dehydroepiandrosterone (DHEA) levels in patients with prostatic cancer, heart diseases and under surgery stress. Exp Clin Endocrin 1992;99:68-70.

  English KM, Steeds R, TH Jones, Channer KS. Testosterone and coronary heart disease: is there a link? QJM 1997;90:787-791.

  Phillips GB, Pinkernell BH, Tian-Yi J. The association of hypotesteronemia with coronary artery disease in men. Arterioscler Thromb 1994;14(5):701-706. Chute CG, Baron JA, Plymate SR, Kiel DP, Pavia AT, et. al. Sex hormones and coronary artery disease. Am J Med 1987;853-859.

  Sewdarsen M, Vythilingum S, Jialil I, Desai RK, Becker P. Abnormalities in sex hormones are a risk factor for premature manifestation of coronary artery disease in South African Indian men. Atherosclerosis 83:111-117.

  Alexandersen P, Haarbo J, Christiansne C. The relationship of natural androgens to coronary heart disease in males: a review. Athersclerosis 1996;125(1-13).

  Stampfer MJ, Malinow MR, Willet WC, Newcomer LM, Upson B, Ullmann D, et al. A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA 1992;268(7):877-881.

  Miller AL, Kelly GS. Homocysteine Metabolism: Nutritional modulation and impact on health and disease. Alt Med Rev 1997;2(4):234-254.

  Hiraga T, Shimada M, Tsukada T, Murase T. Hypertriglyceridemia, but not hypercholesterolemia, is associated with the alterations of fibrinolytic system. Horm Metab Res 1996; 28(11):603-6.

  Davignon J, Cohn JS. Triglycerides: a risk factor for coronary heart disease. Atherosclerosis 1996;124:S57-64.

  Frohlich JJ. Lipoproteins and homocysteine as risk factors for atherosclerosis: assessment and treatment. Can J Cardiol 1995:11(Suppl C): 18C-23C.

  Grau AJ, Buggle F, Beeher H,etal. The association of leukocyte count, fibrinogen, and c-reactive protein with vascular risk factors and ischemic vascular diseases. Thromb Res 1996; 82(3):245-255.

  Ridker PM, Cushman M, Stampher MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336(14):973-9.

  Assman G, Schulte H. Triglycerides and atherosclerosis: results from the prospective cardiovascular Münster study. Atheroscler Rev 1991; 22:51-63.

  National Institutes of Health:Conference Statement: Triglyceride High Sensity Lipoprotein and Coronary Heart Disease. JAMA 1993;269:505-510.

  Researched and Written on April 4, 2004

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