Skip to main content

Heart Disease - How Dangerous Is it?

English

 

 

 

 

 

 

Heart disease, or cardiovascular disease (CVD), is the leading cause of death in the western world, resulting in approximately 1 in every 4 deaths in the US.[1] The World Health Organization also lists heart disease as the leading cause of death worldwide, with 85% of CVD deaths resulting from heart attack or stroke.[2] Formation of atherosclerosis is considered the first step in developing CVD. The major risk factors for developing atherosclerosis are thought to be high low-density lipoprotein (LDL), diabetes/prediabetes, smoking, being overweight or obese, physical inactivity, family history of heart disease, poor diet, aging, and high blood pressure.

There will be a follow-up to this article, which will discuss nine lifestyle factors you have direct control over that could drop your CVD risk by as much as 90%. For now, let’s focus on the development of CVD and the factors that contribute to it.

Heart Disease

To begin discussing this topic, we should first review the mechanisms behind developing CVD, so that we can discuss ways to prevent it as well as reverse it once an individual has developed it. As mentioned previously, the development of CVD begins with atherosclerosis. This is the term used by medical professionals to describe the process of plaque (fat, cholesterol, etc.) formation and the subsequent hardening of the walls of the arteries. The arteries are composed of three main layers, with the innermost being called the vascular endothelium. The endothelium is only one cell thick and is semipermeable. Atherosclerosis starts when an LDL particle slips beneath the endothelium and gets trapped there, between the endothelium and the internal muscular layer of the artery. When the LDL particle is trapped and eventually becomes oxidized by free radicals, it damages the endothelium. These damaged endothelial cells send out signals for help, resulting in inflammation. Inflammation causes specific white blood cells to come to the area to help the cells in distress; some of these white blood cells ingest the oxidized LDL particles. After ingesting the oxidized LDL particles, the white blood cell becomes a “foam cell” filled with the cholesterol and lipids. These foam cells inside the endothelium become known as plaque and are the initial process in atherosclerosis. As atherosclerosis develops, it causes the vessel wall to protrude in both directions (out of the vessel and inside the vessel) and narrows the diameter of the vessel over time. The result of this (at its latest stages), is turbulent blood flow and slower blood flow through the area, which can cause clot formation or tissue death if blood flow is impeded to areas “downstream.” This is how angina and, eventually, heart attacks occur. This is also a cause of kidney failure, as the small blood vessels in the kidneys rely on constant blood flow. The term “fatty streaks” are used to describe areas of the vessels where the initial stages of atherosclerosis are forming—these fatty streaks are seen in children of western cultures as young as 2 years old![3]

So, the question then should be: “What causes CVD?” For decades, conventional medicine believed high cholesterol (primarily LDL) was the sole culprit. One of the most influential scientists behind this theory was Ancel Keys and his “Seven Countries Study,” which reviewed the dietary habits and life expectancy of several countries around the world and concluded that cholesterol was a major factor in heart disease. Cholesterol is a naturally occurring molecule found in all animal cells, so it is primarily found in animal products like meat, dairy, and eggs. This focus on cholesterol also led to the terminology of “good” v. “bad” cholesterol—high-density lipoprotein (HDL) being good and LDL being bad. However, this labeling is not entirely correct, since both are required to sustain life. Partly due to this fact, the cholesterol focus has become a centre for controversy in the last several years. Critics state that Ancel Key’s conclusions from the study were erroneous. They argue that there are plenty of evidences around the world of cultures that consume high-fat, high-animal-product diets which do not have CVD—the Masai and Inuit being the most popularly referenced. The alternative theory they propose is that a diet high in refined carbs and processed oils is responsible for CVD, and there is some evidence to support this.[4] As another evidence of cholesterol not being an important factor in CVD is an often-cited study of 136,905 patients who were admitted to the hospital due to a heart attack (aka myocardial infarction). The study found that “Almost 75 percent of heart attack patients fell within recommended targets for LDL cholesterol…”[5] This study was published in January 2009; at the time, the LDL cholesterol cut-off for acceptable CVD risk was 100–130 mg/dL. Furthermore, almost half of the patients who had heart attacks had LDL cholesterol below 100 mg/dL, which is considered optimal. The thinking is that since the cholesterol levels of these patients was considered acceptable, and some even optimal, then cholesterol levels must not matter. Thus, cholesterol is not the real culprit for CVD. It should be noted, though, that many of these patients had previous histories of heart disease and were likely taking medication (e.g. statins) to lower their cholesterol scores since that is the standard of care. The conclusion of the study were recommendations to revise the LDL cholesterol guidelines even lower—for example, from 100–130 mg/dL in nonrisk patients to below 100 mg/dL. This would result in more patients qualifying for pharmaceutical intervention sooner and in greater numbers. Unsurprisingly, one of the lead authors of the study, Dr. Gregg C. Fonarow, has close ties to many pharmaceutical companies which would benefit from more patients using their products.[5] Having said that, the data in the study is still valid, whatever the conclusions may have been. If we look at other cultures that have very low rates of heart disease, the majority of them have LDL cholesterol levels in the 70–80 range; this means that levels around 100–130 mg/dL are 1.4–1.8 times higher than in cultures where there is virtually no heart disease.[6][7][8] CVD is a chronic illness which takes decades to develop, and having LDL cholesterol in the 100–130 range for decades would likely still cause it to form, such that by the time you are in your fifth decade of life, your chances of having a cardiovascular event have increased dramatically.

Heart Disease

Now, let’s look at the argument in favour of cholesterol and saturated fat being an important factor for developing CVD. First, let’s look at the argument regarding Inuit and Masai cultures as examples of high-animal-product diets and CVD. A well-referenced and thoughtful article about both of these cultures and their diets, written by Thomas Campbell, MD, shows that the low Inuit CVD rate is a myth and the Masai studies are not clear—for or against.[9] One of the most important studies demonstrating CVD being very closely linked to LDL cholesterol is a study which selected for genetically low LDL-cholesterol–producing men due to a gene mutation and assessed their rate of CVD when compared to men without the gene mutation lowering LDL cholesterol.[10] The study had a total of 12,887 men separated by race (black and white), who were then further separated into those who have a genetic mutation and those who did not have the mutation. The black subjects with the gene mutation had a 28% reduction in their average LDL cholesterol, and the white subjects with the gene mutation had a 15% reduction in average LDL cholesterol. All groups underwent an initial examination to determine hypertension, diabetes, and tobacco use (three major risk factors for CVD). The risk factors where present in similar ratios among all four groups. What were the results? In the black subjects with the mutation, there was an 88% reduction in the incidence of coronary heart disease (atherosclerosis in the arteries of the heart)! In the white subjects with the mutation, there was a 50% reduction in incidence. Less lifetime exposure to high LDL cholesterol showed a dramatic improvement in the risk of developing coronary heart disease. This study shows that LDL cholesterol levels are closely linked to CVD. Although high LDL levels are not the only factor in developing CVD, it must be present.

Having said that, is your LDL cholesterol the most important factor in whether you develop CVD or not? The short answer is no. Plenty of patients have a normal/acceptable LDL number and still have a cardiovascular event. Low-density lipoprotein particle number (LDL P) is a much better indicator of risk. LDL P shows the total number of LDL particles in your blood rather than looking at how many molecules of cholesterol there are inside the LDL particles. Since LDL particles are what get stuck in the arterial walls and start the process of atherosclerosis, the exact number any person has is the more important factor. Conventional testing that measure total cholesterol, LDL and HDL, do not show how many LDL particles are present, which can be deceiving because a person can have normal/low LDL and still have high LDL P. You can think of it as the difference between counting the number of cars on a highway v. counting the number of people in each car (you want to count the number of cars). Apo B is another value which tests for LDL particle number. Other lab values which can be helpful in guiding risk assessment are markers for inflammation. High-sensitivity C reactive protein (hsCRP) is a general measurement of inflammation throughout the body and is a late indicator of CVD. More specific blood tests for inflammation in the arterial walls are MPO and Lp PLA2. Since these tests measure inflammation in the atherosclerotic part of the arteries, they are great ways to assess specific risk. Another important test is F2 IsoPs, which is a measurement of free radicals in the body. Free radicals are thought to be the reason why stuck LDL particles become oxidized: so, the higher the F2 IsoPs value, the higher your risks of developing atherosclerosis. Having these tests done might prove very beneficial and should be considered if you are concerned about your risk of CVD.

In conclusion, heart disease is the number one cause of death worldwide, with multiple risk factors contributing to its development. In western cultures, atherosclerosis was shown to begin to develop at a very young age but takes decades to become heart disease. High LDL cholesterol, while not the only concern in developing CVD, must be present to develop atherosclerosis. In the next article, the focus will be on how to maximize your chances of living a longer, healthier life by making different choices every day.