I have been advocating the use CT heart scans to yield a coronary calcium score (CCS) to assess risk for heart disease (heart attack, angina, need for bypass surgery or stent implantation) for over 20 years after Dr. John Rumberger at the Mayo Clinic demonstrated how coronary calcium provided a reliable gauge of coronary atherosclerosis and Dr. Arthur Agatston of The Miami Heart Institute (and author of the South Beach Diet) developed the Agatston scoring system for coronary calcium. Since those early days, CCS has, time and again, stood up to scrutiny and, even today, remains the best predictor of overt heart disease, superior to cholesterol testing, stress tests, and other methods to gauge cardiovascular risk. Dr. Rumberger demonstrated that coronary calcium occupies 20% of total atherosclerotic plaque volume and thereby provides a virtual dipstick to quantify the severity of coronary disease. Dr. Agatston’s scoring system helped demonstrate (via hundreds of clinical studies) that, the higher the score, the greater the risk for heart attack and other events.
Problem: If you have a positive CCS (i.e., any score above zero), the average rate of annual increase in the CCS is 25% per year if you do nothing. (This is a bit of an oversimplification, as a score of 5 that increases to 10–a small increase–is a 100% increase, while a score of 1005 that increases to 1010–the same small increase–is less than a 1% increase. If we lump everyone together, however, the average rate of increase is 25% per year.)
What if you engage in what my colleagues call “optimal medical therapy”? This includes high-dose statin cholesterol drugs to reduce LDL cholesterol to 70 mg/dl or less, a baby aspirin per day, a low-fat and low saturated fat diet, and exercise? Some add a beta blocker such as metoprolol or atenolol. On this regimen, CCS scores increase 25% per year or more. In other words, from the perspective of CCS progression and the increased cardiovascular risk it predicts, statins have virtually no effect. This has been shown in men, this has been shown in women.
This is not to say that statins, despite their substantial adverse effects such as alteration of bowel flora composition that pushes you towards weight gain and type 2 diabetes, have no positive effects. They have been shown to modestly reduce the burden of “soft” plaque, i.e., the elements in coronary arteries prone to rupture and cause heart attack. But even this observation is flawed. Consider:
- The diet widely advocated by doctors with reduced total and saturated fat with greater whole grain content–Is a style of eating that provokes formation of small LDL particles, causes exaggerated postprandial (after-meal) VLDL particles via the process of liver de novo lipogenesis, adds to insulin resistance, promotes glycation (irreversible glucose-induced modification of proteins, including small LDL particles that are especially glycation-prone), and has other effects that promote or cause heart disease. In other words, my colleagues are guilty of promoting a pattern of eating that promotes formation of atherosclerotic plaque, including soft rupture-prone elements, then coming to your rescue with prescription drugs.
- The failure to address insulin resistance–Insulin resistance drives growth of coronary atherosclerosis, as well as hypertension, more small LDL and VLDL particles, accumulation of visceral fat (including pericardial fat surrounding the heart) that drives inflammation, phenomena that also lead to greater soft plaque. Having coronary disease in the absence of insulin resistance is uncommon (in non-smokers). Addressing insulin resistance is as simple as eliminating foods such as wheat, grains, and sugars that cause it, followed by addressing common nutrient deficiencies that make it worse: vitamin D, omega-3 fatty acids, magnesium, iodine.
- Failure to address endothelial dysfunction–The same phenomena causing insulin resistance also causes abnormal constrictive behavior in the coronary and other arteries, a process called “endothelial dysfunction,” since it is the paper thin, single cell layer of endothelial cells lining arteries that controls their “tone.” Endothelial dysfunction is associated with abnormal constriction of arteries that adds to arterial damage and atherosclerosis.
- Failure to address dysbiosis and small intestinal bacterial overgrowth (SIBO)–Dysbiosis confined to the colon and SIBO that has ascended up the upper gastrointestinal tract are both associated with entry of bacterial breakdown products into the bloodstream, a process labeled “endotoxemia.” Endotoxemia explains how gut flora can be responsible for diseases in other parts of the body such as psoriasis in the skin, Parkinson’s disease in the brain, and coronary disease in the heart. It also worsens insulin resistance and endothelial dysfunction, both of which add further to soft atherosclerotic plaque accumulation.
Following a program that addresses all the above factors, as we do in the Wheat Belly and Undoctored programs, can stop or reduce CCS in the majority. While we have not quantified (e.g., via intracoronary ultrasound or quantitative CT coronary angiography) changes in the soft component of atherosclerotic plaque on the program, the virtual absence of coronary events, even over 15+ years of implementing these strategies, suggests that we have indeed inactivated and/or regressed even the soft elements of plaque, in addition to stopping or reduce CCS.