Dietary cholesterol has long been vilified as one of the major causes of cardiovascular disease. This pervasive belief has profoundly shaped healthcare policy for more than 50 years. However, we are now seeing that the association between dietary cholesterol and heart disease is not as clear or definitive as we have been led to believe. Careful review of the early studies has shown inconsistencies and contradictions in the data. Some of the studies do show a link between dietary cholesterol and heart disease, while others do not. This results in a confusing dilemma for both physicians and their patients.
Cholesterol was first isolated from gallstones in 1758 by French doctor Francois Poulletier de La Salle. In 1815, French chemist Michel Eugene Chevreu isolated and purified this sterol and name it cholesterol. John Gofman at University of California at Berkely developed the technique of ultracentrifugation to separate the lipoproteins. The more lipid the fraction had, the faster it would float. The fractions were named high density lipoproteins (HDL), low density lipoproteins (LDL) and very low density lipoproteins (VLDL). The high-density fractions correlated with the alpha lipoproteins, the low-density fractions correlated with the beta lipoproteins, and the very low density with the prebeta lipoproteins. That’s really how we got “Apo B” and “Apo A”, the proteins or apolipoproteins associated with each fraction. Then Gofman observed that people who had higher levels of the beta lipoproteins, or the low-density lipoproteins, had more frequent coronary disease while ones with higher levels of the HDL had fewer coronary events.
In 1852, Irish Physician Richard Quain observed fatty material deposition in the blood vessels. In 1854, Dr. Rudolf Virchow described atherosclerosis as a disease that was due to excess cholesterol deposition. Cholesterol became associated with heart disease in 1913 when Nikolai Anitschkow discovered that feeding rabbits purified cholesterol led to atherosclerosis. This study had very little effect on research because the scientist did not see a connection between this work on rabbits and human health and disease. In 1973, Joe Goldstein genetically classified the types of cholesterol-carrying lipoproteins in the blood. Joseph Goldstein and Arno Motulsky found familial hyperlipidemia linked to premature heart disease. Michael Brown and Goldstein found genetics behind the inability to remove LDL. This research made him one of the founders of modern cholesterol research.
The Seven Countries Study by Ancel Keys began in 1956. It examined the connection between lifestyle, diet and heart disease in men from different countries; it was the first study of its kind. Keys measured the association between saturated fat and coronary heart disease controlling for total caloric intake and sugar. Saturated fat remained statistically significantly associated with heart disease in that model. Proponents argue this study had several flaws:
- The saturated fat in the study included hydrogenated trans fats. The data linking trans fats with heart disease did not come out until years later in the 1980s.
- Discrepancies have been reported with the data analysis; suggesting that not all of the data were used in the final analysis, thus skewing the results.
- It has been reported that the lead investigator looked back at the data years later and noticed sugar actually had a stronger association with heart disease versus saturated fat. If trans fats were then excluded, the association between dietary saturated fat and heart disease became even weaker.
It is important to note that scientific inquiry does not take place in a vacuum. At the same time Keys was attempting to demonstrate saturated fat was dangerous, one of his contemporaries, John Yudkin, a diabetes expert, was convinced sugar was the real culprit with regard to heart disease. He and Keys debated this issue; Keys won the popular opinion at the time and the American Heart Association declared that butter, eggs and beef increased coronary disease risk.
The Keys Study led to the Framingham Study, which has been ongoing since 1948. The purpose of this study was to identify common factors that contribute to cardiovascular disease by following its development over time in a large sample of participants free of heart disease. The data revealed that higher risk factors for heart disease include cigarette smoking, cholesterol level, obesity, blood pressure and EKG abnormalities. Lower Risk Factors included regular physical activity and higher HDL
The study attributes heart disease to many factors other than dietary intake of saturated fat; it does not say that those with high cholesterol have higher mortality rates. In fact, according to Dr. David Diamond about the Framingham Heart Study, the study concludes: “If your cholesterol is below 300, there is no significant association between your cholesterol and heart disease.” William Castelli, MD, a former director of the Framingham Heart Study—the one that originally implicated cholesterol as a problem in cardiovascular disease (CVD) —noted that low serum cholesterol means that we have three times the chance of having a stroke. High cholesterol has been shown not to be significantly correlated with heart attacks since 40 percent of the people who have heart attacks have cholesterol that is lower than average.
One thing most people can agree upon is that inflammation is a significant component to virtually every degenerative condition; heart disease is no exception. Studies have shown that patients who have had a heart attack tend to have higher levels of c-reactive protein (CRP), an important biomarker for inflammation. Elevated levels of CRP are also associated with higher rates of atherosclerosis and stroke.
These studies bring us back to some of the basic tenets of health that we have known for a long time. Our diets should consist of whole, unprocessed foods with high amounts of vegetables, fruits—supplying us with antioxidants and fiber. Including anti-inflammatory foods, such as turmeric, ginger, rosemary, cayenne, blueberries and green tea, in your diet can help. Fat is not the enemy as long as we have enough antioxidants to keep the LDL from being oxidized. Dr Sinatra and others have reported that the size of the atherogenic LDL particles are actually more important than the concentration. LDLs vary in size based on our genetics; the large neutral particles are less problematic than the small dense ones. They even suggest these parameters may be considered the “new good and bad” cholesterol, instead of the traditional HDL and LDL cholesterol.
Beyond the Basic Lipid Panel
Since the basic cholesterol test may be leading us down inaccurate or incomplete paths, here are some of the more specific recommended tests to consider when evaluating risk for heart disease.
- Lipoprotein subclasses: Smaller LDL particles can cause plaque formation faster than larger LDL particles
- Apoliprotein B(apoB – LDL particle number): A higher ApoB number indicates an increased risk for heart disease
- Lp(a): A lipoprotein associated with increased coagulation and increased risk for heart attacks and stroke
- Lp (PLA2): A marker for inflammation in the arteries; elevated levels are risk factors for ischemic stroke and heart attack
- HS-Cardio CRP: A high sensitive cardio c-reactive protein and a biomarker for inflammation
- Fibrinogen: An inflammation biomarker and clotting factor
- Insulin: associated with atherosclerosis
- NT-proBNP: A hormone released from the heart muscle in response to ongoing stress or strain on the heart
- Vitamin D: Low levels are associated with an increased risk of heart disease, stroke, diabetes, hypertension and heart failure
- Omega 3 and Omega 6 fatty acids: Lower omega 3 and higher omega 6 have been associated with increased risk of heart disease
- HEMOGLOBIN AIC: A marker for average blood sugar over a three-month period of time
- Apo A1: The major component of HDL; higher levels tend to reduce risk of heart disease