Cardiovascular Disease – In the News – Part 1

by Judith A. DeCava, C.N.C., L.N.C.

Have you heard? The rates of death from cardiovascular disease in the US have dropped! This improvement has been attributed to the “major medical advances in the prevention and treatment of cardiovascular disease.” In reality, increased survival rates appear to be due to progress in emergency technologies that prevent only immediate death.

The overall incidence of heart attacks, for example, has not declined and has actually increased among women. People are having as many, or more, heart attacks. Heart disease, strokes, and peripheral arterial disease (all cardiovascular diseases) are still the leading causes of death and major causes of disability. “The absolute number of deaths from these conditions continues to increase.” Increase! “The epidemic of obesity and associated diabetes is expected to further increase the prevalence of cardiovascular disease in the 21st century.” Though emergency care may have advanced, preventing and treating the causes of cardiovascular disease have been flops.

Over the past 15 years, there has been a dramatic increase in the use of “cardiac procedures” in the US such as bypass surgery and angioplasty. But this has not affected the heart attack rate. Doctors are quicker to intervene when there are even mild symptoms although sometimes these procedures “may be unnecessary.” Lots of data “show that opening a narrowed artery will not reduce your chances of having a heart attack.” It may help while having a heart attack, but it doesn’t get to the cause. Within 6 months of having angioplasty, 50% of patients are already showing signs of “re-clotting” with plaque buildup. Plugging-in pieces of arteries doesn’t solve the underlying problem either. Many people believe that bypass or angioplasty saved their lives, “but the benefit of most procedures is [solely] control of symptoms.” There “is no evidence to show that artery-opening procedures will prolong life.” Doctors ordered more cardiac tests and procedures between 1993 and 2001 than ever before. But the rates of heart attacks over that period were no better than before. And there is no sign of let-up.

What causes cardiovascular disease? We are told that high cholesterol, high blood pressure, diabetes, obesity, tobacco, secondhand smoke, and physical inactivity all increase risk. Some people with some of these “warning signs” develop heart disease, but others don’t. “This observation indicates that yet-unrecognized factors must also influence risk.” No kidding! A review of more than 40 trials conducted over a period of 3 decades showed that risk-factor reduction had “limited, if any impact on reducing mortality and morbidity [illness].” Not everybody who is obese or smokes or is inactive has a heart attack. About half of heart attack victims didn’t have high cholesterol. Diabetes does double risk for cardiovascular disease, which kills up to 80% of diabetics. Elevated blood sugar, not only in diabetics, increases risk of heart attack. Elevated blood sugar is often a result of over-consuming refined carbohydrates and trans fats. Could these be causes?

We used to be told that having a heart attack was due to a sort of plumbing problem—that coronary arteries slowly became narrowed with plaque like a pipe becomes corroded with rust and other gunk. In time an artery became so clogged that blood flow to the heart got shut off with a blood clot. Now we’re told that only a minority of heart attacks occur this way since most of the time heart attacks don’t occur in the part of the artery that is most obstructed. Rather, most heart attacks (60 to 70%) occur where plaque breaks off and a clot forms over the area. If the clot cuts off the flow of blood to the heart, the person has a heart attack. If the clot cuts off blood to the brain, the person has a stroke. Problem plaques are soft, vulnerable, and comprised of an assortment of inflammatory cells, LDL cholesterol, and blood. They are topped with a thin, fibrous cap that can rupture at any time, spilling their contents into the bloodstream. But not all plaques rupture and not all ruptures lead to heart attack. Heart disease is now believed to involve an inflammatory process by which coronary arteries are subjected to a constant cycle of irritation, injury, healing, and re-injury that makes plaque likely to rupture. The demand on the immune system from perpetual inflammation can result in immune system compromise or dysfunction. In other words, normally inflammation would proceed along a programmed agenda ending in repair, but, instead, there’s an inability to properly complete this function.

The medical tendency is to seek ways of interfering with or stopping the inflammation, but there is another angle that should be considered. What if inflammation is the process used by the body to repair damaged cells—like biochemistry books say? What if plaques were the body’s attempt to reinforce and support a weakened or injured blood vessel wall? And that cells involved in the inflammatory process, LDL cholesterol, platelets, and other cells were used to build this patchwork? Suppose that if a body was able to make good, strong patches and that the inflammatory process—aided by nutrients needed for healing and for improving the strength, integrity, and elasticity of the blood vessel walls—was able to accomplish its repair. Then risk for a heart attack would greatly diminish. It’s known that small, vulnerable soft plaque—poor patching—is more likely to rupture than large, calcified, strong plaque—good patching. On the other hand, if the body doesn’t get the nutritional support it needs, then the patches may not be able to bolster the weakened areas, may be soft, and break away. The blood vessel walls wouldn’t get the reinforcement and repair needed and would be subject to re-injury, more inflammation, and spasm. Arteries are more prone to injury when required nutrients are deficient, and they can be irritated and weakened by various toxins.

Air pollution and other toxins have been linked to cardiovascular risk. Sitting in traffic for as little as an hour might almost triple your risk of having a heart attack within a few days. Public-transit riders and even bicyclists are also at risk. Toxic particles in the air can constrict arteries, cause inflammation (due to tissue insult and injury), and disrupt heart rhythms. Poor nutrition can increase the susceptibility to tissue injury and compromise the body’s ability to deal with toxic insult.

Some scientists already think atherosclerosis may not be a disease, but “possibly the body’s way of repairing or bolstering weak or damaged arteries.” Some even propose that the body uses cholesterol as part of the process that attempts to repair damaged arteries. Especially if deprived of needed nutrients, the body uses LDL (so-called “bad”) cholesterol) to aid the repair work. Atherosclerosis may be more about efforts to heal than harm. [i]


Because vulnerable plaque is mostly made of inflammatory cells, the search is on to find blood tests that identify increased amounts of these “risk markers.” CRP is one of them. “People with a high CRP are more likely to have unstable plaques, which are more prone to rupture.” Researchers hope that by lowering CRP heart attacks can be prevented. But this may not work! First, to get an accurate reading, you must have the high-sensitivity form of the test. Second, a few studies “purportedly” showed that lowering CRP levels with statin drugs can lower the rate of heart attacks in people with severe heart disease. The goal is to give statins to as many people as possible, which can cause more harm than help. The authors of 2 such studies have “strong financial ties to the cardiac drug industry.” Statins (including Crestor, Lipitor, Mevacor, Pravachol, and Zocor) are widely prescribed. They lower cholesterol and have anti-inflammatory effects. But scientists like John Abramson, MD, (Harvard Medical School) remain unconvinced that the studies proved that reduced CRP levels account for the reduced incidence of heart attacks and stroke. And the recommended higher doses of statins increase potential for “serious adverse reactions.” Third, a recent large study found CRP doesn’t predict risk any better than “traditional major risk factors.” Routine measurement of CRP “is not warranted for risk assessment.” Fourth, CRP levels fluctuate—you need several tests to get a fix on your usual level. Fifth, elevated CRP can signal inflammation in your body, but it doesn’t tell you WHERE.

CRP increases during numerous inflammatory flare-ups such as occurs in sinusitis, lupus, or rheumatoid arthritis; during chronic inflammation as occurs in periodontal disease or osteoarthritis; when taking hormone replacement therapy; when overweight; with high blood pressure; and with diabetes—among other things. Small elevations occur with age, second-hand smoke exposure, and air pollution. Your genes can affect CRP levels. So a CRP test will not necessarily predict cardiovascular disease! Still, more and more doctors are using CRP tests to determine who should go on statin drugs. Millions of people at low risk for heart disease will be targeted for statin prescriptions if the only indication for such ‘treatment’ is elevated CRP. “CRP is a weak risk factor.” Most Americans currently on stain drugs don’t have heart disease. The drugs interfere with the natural inflammation and repair process, disrupt cholesterol production, and depress adrenal function.

Foods and nutrients affect CRP levels. Fiber reduces it. A healthier diet lowers it. A diet high in fruits, vegetables, legumes, poultry, tea, and whole grains resulted in lower CRP than a diet high in refined grains, red meat, butter, processed meat, dairy, sweets and desserts, trans fats, pizza, eggs, and soft drinks. Non-foods in the latter diet (refined grains, processed meats, sweets, desserts, trans fats, soft drinks) no doubt contributed to the higher CRP. Adherence to a Mediterranean diet resulted in a 20% reduction in CRP. High intake of vegetables and fruit lowers CRP. Dietary intake of vitamin C complex, omega-3 fatty acids, carotenes, B vitamins, vitamin E complex, magnesium, arginine, and other nutrients have all been linked with lower CRP. The average American diet is loaded with trans fatty acids that up CRP, and is low in omega-3 fatty acids which reduce CRP. Low fat diets don’t reduce CRP. Foods cooked at high temperatures (like frying or grilling) can increase CRP. Sure enough: “A comprehensive dietary program can be as effective as a statin drug in reducing both LDL-cholesterol and C-reactive protein levels.” Physical activity can also reduce CRP. So why not suggest that people eat a healthful, whole-food diet, lose weight, and exercise instead of giving them potentially dangerous drugs? [ii]


We’ve long been told that a high-fat diet leads to more cholesterol in the blood, which sticks to artery walls, causing heart disease. But there is plenty of evidence that this is wrong. Still hanging on to the theory, the latest view is that atherosclerosis comes from a combination of poor fat/cholesterol regulation and inflammation.

Health recommendations are often based on “surrogate endpoints” along with “a heavy dose of assumptions.” For example, ‘estrogen drugs lower cholesterol in women; therefore it must save them from heart disease.’ That was wrong, like many other assumptions are wrong. The idea that a low-fat diet (below 20% of total calories) reduces the risk of heart attack was challenged following the results of the 8-year Women’s Health Initiative study which involved thousands of healthy women over age 50. No distinctions were made in the types of fat consumed—good or bad—as long as they kept the total intake below 20%. Yet even the highly motivated women couldn’t get their fat intake that low—best they could do was 24% in the first year and 29% in subsequent years. Nevertheless, the low-fat diet didn’t prevent heart disease, stroke, or other cardiovascular disease.

So, total fat intake may not be a major determinant of cardiovascular disease. For one thing, most studies that looked for links between fat intake and cardiovascular disease didn’t take into account the association between fats and refined-sugars, which often occur together in ‘non-foods.’ Fats were blamed when refined carbohydrates could have been the culprit. If natural fats are a problem, this may be due to impaired capacity to properly process fats. The typical American diet is low in nutrients needed to process fats such as vitamin C complex, magnesium, B vitamins, chromium, potassium, choline, betaine, and more. Other people have a reduced or disturbed functioning of the liver, gallbladder and/or pancreas—they can’t digest fats properly. But good, natural fats don’t cause cardiovascular disease. Overall, low-carbohydrate eating plans (such as those popularized by the South Beach and Zone diets) “don’t appear to raise the dieter’s risk of heart disease despite higher intake of fat and protein.”

However, research does indicate that certain types of fat contribute to atherosclerosis. These include trans fatty acids (partially-hydrogenated fats), heated unsaturated oils (resulting in the formation of toxic lipid perioxides), and oxidized (rancid) cholesterol (made during high-temperature cooking of meat, dairy products, or other animal fats). “Thus, the type of fat consumed appears to be more important than the total amount consumed.” Cardiovascular disease is becoming epidemic in Third World countries where it used to be rare. What changed? Not the amount of fat, but the type of fat. Refined vegetable oils are replacing animal fats for cooking. Consumption of trans fats and refined carbohydrates has escalated. And there is heavy use of pesticides and confinement livestock systems.

Though scientists still link total blood cholesterol with the risk for cardiovascular disease, “there is no connection between fat intake and cholesterol—in fact, quite the reverse.” Dr. William Castelli, director of the Framingham study, observed, “the more saturated fat and cholesterol one ate, the lower the person’s blood cholesterol.” Actually, saturated fats protect against the harmful effects of trans fats! A recent study compared the effects of two diets on 120 overweight people with high blood cholesterol. For 6 months, 60 of them ate a low-fat/low-cholesterol diet. The other 60 ate a low carbohydrate diet that allowed unlimited amounts of animal foods and eggs; 68% of their calories came from fat. Total cholesterol levels went up a little, but it was mostly the so-called “good” HDL cholesterol that went up. (Cholesterol will increase temporarily when there is a significant change [increase] in fat intake.) After 6 months, the low-carb dieters had lower triglycerides and lost more weight than the low-fat dieters. Risk for heart attack went down.

Remember, half the people who have heart attacks never had high cholesterol levels and had an HDL in the “normal range.” So perhaps it can be assumed that high cholesterol is not a sure sign of cardiovascular disease. Sounds more like a crap shoot with 50/50 odds! Ah, but the story is that it’s not the total cholesterol that’s important, but the ratio of HDL to LDL cholesterol. The higher the relative levels of HDL, the lower the risk. Well, maybe. Alan Fogelman, MD, at UCLA, says HDL can transform in people who already have inflammation in their arteries, raising rather than lowering the risk of heart attack or stroke.

Another add-on is that there are two types of LDL, one more dangerous than the other. The smaller the LDL particle, the deadlier it’s supposed to be. So there’s type “A” (big and relatively harmless) and type “B” (small and bad). But researchers found that a 20%-fat diet produced around 50% “bad” Bs in the blood, whereas a 45%-fat diet produced only 20% Bs. Furthermore, the lower-fat diets actually converted many of the ‘harmless’ As into ‘deadly’ Bs. Another study showed that a low-fat diet in children raises the ‘bad’ Bs. Oops. That didn’t work! Low-fat diets do not increase the light, fluffy, beneficial LDL

In 2005, results of a 5-year study of nearly 30,000 middle-aged people were announced. The study looked at fat intake and deaths (especially from cancer and heart disease). Only female cancers seemed to be affected by high-fat diets. No links were found for heart disease or for death in general. High fat intakes were not only not associated with higher death rates, but the highest fat intakes resulted in the fewest deaths—and vice versa! The advice to keep total dietary fat below 30% and saturated fat below 10% doesn’t seem right!

Researchers from the UK found that high cholesterol levels protected people who had chronic heart failure, leading to dramatic reductions in death rates. The higher the level of cholesterol, the higher the chance for survival. One of the researchers said: “In contrast to what you might imagine, having a high level of cholesterol might be good for you.” Scientists at the University of Michigan concluded that the new goals for even lower cholesterol levels have no scientific validity but may only be arbitrary.

If neither natural fats nor cholesterol are culprits, what is? Mary Enig, PhD, points out: “It’s a little known fact that, before 1920, coronary heart disease was rare in developed countries like America, but it rose dramatically over the next 40 years. If, as we have been told, heart disease results from the consumption of saturated fats, one would expect to find a corresponding increase in animal-fat consumption. Actually, the reverse is true. In America, for example, during the period from 1910 to 1970, there was a significant decline in the proportion of traditional animal fat in the national diet.” Dr Enig has shown that the rise of heart disease corresponds with the introduction of refined polyunsaturated plant oils into the American mainstream diet around the early 1900s. One reason polyunsaturated oils cause problems is that, when they are heated, as in food processing, they produce extremely reactive chemicals that can damage blood vessels, initiating atherosclerosis. The most harmful process is hydrogenation used to transform poly-unsaturated plant oils into solid fats. Hydrogenated oils contain large amounts of toxic trans fats which have found their way into processed foods of all kinds.

Harvard researchers reported on their analysis of at least a decade’s worth of data on trans fat intake and heart disease. “TFAs [trans fatty acids] have a major role in heart disease,” announced Professor Walter Willetts. “The magnitude of the association with CHD [coronary heart disease] is considerably stronger than for saturated fat.” Saturated fats have been blamed for causing cardiovascular disease. Yet, until the mid-1980s, scientists did not discriminate between saturated fats and trans fats when they analyzed diets. So the harm caused by trans fats was blamed on saturated fats. And all that early research has been the basis for dietary recommendations since then. Assumptions!

Scientists are finally admitting that individuals are different in the way they respond to fats, that not everyone eating substantial amounts of fat or saturated fat will get high blood cholesterol levels. They allow that many factors influence risk for cardiovascular disease, all of which should be taken into account. Wait! Weren’t we all advised to lower fat and cholesterol intake? Many people assume—probably because that’s what they were told—that the cholesterol in the foods they eat (meat, eggs, full-fat milk products, butter, etc.) contributes directly to the amount of cholesterol in their blood. Nope. Cholesterol in foods can increase blood cholesterol to some degree, more in some people than in others. But most cholesterol in the blood comes from what the body itself produces, depending on its needs. If cholesterol levels are high, there’s a darned good reason. It’s the reason that needs to be determined. Cholesterol itself is not bad. We need it for health and survival.

At least we’re now told not to go on a very low-fat diet, one in which less than 20% of calories comes from fat. As fat intake goes down, carbohydrate intake goes up. The carbs craved are usually refined—sweets, snacks, bakery products, soda, and the like. This can raise triglyceride levels, lower HDL, damage blood vessels. We need natural fats. [iii]

To aid proper digestion of fats, for 3-6 months: With Your Two Largest Meals:
1 Cholacol OR 2 Cholacol II
1 Multizyme
2 Betafood—chew

To support liver health and function, can add, before two meals: 3 Cataplex B, 1 Choline (180 only), and 1 Livton Complex (120) only.

What about nutrients that may help prevent cardiovascular disease? Look for Part 2

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© 2007, Judith A. DeCava