Andrew W. Campbell, MD, is the Editor in Chief of Alternative Therapies in Health and Medicine.
Corresponding author: Andrew W. Campbell, MD
In November of 2013, the American College of Cardiology (ACC) and the American Heart Association (AHA) announced their new clinical practice guidelines for the treatment of blood cholesterol in people at high risk for cardiovascular diseases caused by atherosclerosis that can lead to heart attack, stroke, or death. More specifically, the new guidelines recommended moderate or high statin doses for 4 groups of patients. These 4 groups are as follows:
- Individuals with clinical arteriosclerotic cardiovascular disease, also known as ASCVD, and defined as acute coronary syndromes, or a history of myocardial infarction (MI), stable or unstable angina, coronary or other arterial revascularization, stroke, transient ischemic attack (TIA), or peripheral arterial disease presumed to be of atherosclerotic origin, without New York Heart Association (NYHA) class II heart failure or receiving hemodialysis.
- Individuals with primary elevations of low-density lipoprotein (LDL) cholesterol ≥ 190 mg/dL.
- Individuals 40 to 75 years of age with diabetes and an LDL cholesterol level of 70 to 189 mg/dL without clinical ASCVD.
- Individuals without clinical ASCVD or diabetes who are 40 to 75 years of age with an LDL cholesterol level of 70 to 189 mg/dL and have an estimated 10-year ASCVD risk of 7.5% or higher.
Along with these 4 groups come lifestyle modifications—adhering to a heart-healthy diet, performing regular exercise, avoiding all tobacco products, and maintaining a healthy weight—which make up a critical component of ASCVD risk reduction, along with the use of statin drugs.
The ACC and the AHA define high-intensity statin therapy as a daily dose that will lower LDL cholesterol by more than 50% and moderate-intensity therapy as one that will lower LDL cholesterol by 30% to 50%. They go on to say, “All patients with ASCVD who are age ≤ 75 years, as well as patients > 75 years, should receive high-intensity statin therapy; or if not a candidate for high-intensity, should receive moderate-intensity statin therapy.”1 Of note is that in the recommendations of these guidelines, the usual medical thinking of the lowest dose for the effects of lowering cholesterol is now replaced with higher doses of statin drugs.1
All pharmaceutical drugs have side effects—some more than others. An examination of the medical literature will show the many side effects of statin drugs, also known as HMG-CoA reductase inhibitors. These include hepatoxicity, myopathy, renal failure, type 2 diabetes, memory loss, confusion, insomnia, peripheral neuropathy, erectile dysfunction, cancer, and mitochondrial dysfunction. More than 800 studies have compiled and documented the problems of those who are prescribed statin drugs. Neurotoxicity is becoming more evident from statin drugs as well. We know that the brain uses cholesterol, as it is a component of myelin. Demyelination of the central and peripheral nervous system causes a myriad of symptoms, medical problems, and disorders in patients. Yet according to Michael Roizen, MD, of the Cleveland Clinic and chair of its Wellness Institute, 15 million Americans take statin drugs and the ACC and AHA are recommending that several million more start using them.
Central to cardiovascular diseases and its related disorders is the important question: Do elevated levels of cholesterol cause ASCVD? The answer is simple: No. In a systematic review and meta-analysis, there were 32 observational studies of fatty acids from dietary intake with a total of 512 420 participants; 17 observational studies of fatty acid biomarkers with a total of 25 721 participants; and 27 randomized, controlled trials of fatty acid supplementation with a total of 105 085 participants. The current evidence does not support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids (PUFAs) and low consumption of total saturated fats.2 As reviewed in my editorial 1 year ago, we are chasing the wrong culprit.3 In that editorial, I gave the hard facts and studies, showing that cholesterol is not the cause, and the reader may wish to review that issue of this journal as it was dedicated to cardiovascular diseases.
It has been drummed into the television-watching American population that we should avoid saturated fats. Turn on the television and you are shown advertisement after advertisement of foods that are harmful to us: refined carbohydrates; sugars (mostly artificial); processed foods; and omega-6 vegetable oils, such as sunflower, corn, or soybean that we fry with. All the products advertised are simple to use, very tasty, and most will satisfy your hunger or thirst. One tablespoon (14.8 mL) of corn oil contains 7280 mg of omega-6 PUFAs; soybean contains 6940 mg. Other foods high in omega-6 PUFAs are cereals and whole grains. Omega-3 PUFAs are found mainly in oily fish, walnuts, and flax. If we would turn away from popular and advertised foods and drink, and instead pay more attention to healthy nutrition, much of the rise of inflammation and thereby cardiovascular diseases would be thwarted. Prying the fingers off of that sugar-coated doughnut; that chili with cheese hot dog; that double-patty, double-cheese cheeseburger; and that corn syrup- or aspartame-laden, large fizzy drink, after all these years of advertising on television, in magazines, and on billboards, will be very difficult. Yet, there is a glimmer of hope, as we have seen a recent law passed in New York limiting the size of fizzy drinks that can be purchased.
Inflammation may well be the key to reducing the rate of ASCVD in this country and worldwide. Inflammation is our immune response to a xenobiotic, which includes bacteria, viruses, and environmental toxins. We regularly ingest foods that cause an inflammatory response and expose our bodies to toxins in our environment. These bring about inflammation—the chronic inflammation that is known to be harmful. As a result, we have ASCVD, stroke, diabetes, obesity, and an alarming rise in autoimmune diseases. For example, a recent article by Burazor and Vojdani4 showed that the immune inflammatory response to oral pathogens could be part of the development of acute coronary atherothrombosis. Our focus should be directed more toward inflammation and how to reduce it.
Why not use nutrition and physical activity instead of a pill that can cause so many health problems? For example, we know curcumin and magnesium are anti-inflammatory and they have very few side effects, mostly related to taking too much of these 2 important nutrients.5-8 Walking, stretching, and resistance exercise for 30 minutes every day are known and overwhelmingly proven to improve cardiovascular health. Supplements are very helpful as well. In their book, The Great Cholesterol Myth, by Steven Sinatra, MD, and Jonny Bowden, PhD,9 there is an entire section devoted to what supplements are known and proven to be helpful in preventing cardiovascular disease. They include coenzyme Q10 (CoQ10), vitamin D3, omega fatty acids, niacin, resveratrol, and others.
Lowering cholesterol with statin drugs does not lower mortality from cardiovascular diseases. It is difficult to understand why it is, then, that we are now being given new guidelines by 2 conventional organizations—the ACC and AHA—which would increase the use of statins, both in dosage and by the number of patients taking them. The guidelines do mention nutrition and exercise, but they don’t give any alternatives to statin drugs. Michel de Lorgeril, MD, and Patricia Salen, BSc,10 reviewed 11 major statin drug trials from 1994 to 2009 and published their conclusions in JAMA, the New England Journal of Medicine, Circulation, the Lancet, the American Journal of Cardiology, and others. They conclude that the data in these trials should be re-examined by experts independent from the pharmaceutical industry, as they do not show any benefits from taking statin drugs. The ACC and the AHA should ask for the same if they are truly independent professional medical organizations dedicated to helping patients.
- Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63(25):PA. doi: 10.1016/j.jacc.2013.11.002.
- Chowdhury R, Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. Ann Intern Med. 2014;160(6):398-406.
- Campbell A. Editorial: Cholesterol and cardiovascular disorders. Alt Ther Health Med. 2013;19(suppl 1):4-6.
- Burazor I, Vojdani A. Chronic exposure to oral pathogens and autoimmune reactivity in acute coronary atherothrombosis. Autoimmune Dis. 2014; 2014(613157):1-8.
- Chainani-Wu N. Safety and anti-inflammatory activity or curcumin: a component of tumeric (Curcuma longa). J Alter Complement Med. 2003;9(1):161-168.
- Bengmark S. Curcumin, an atoxic antioxidant and natural NFkappaB, cyclooxygenase-2, lipooxigenase, and inducible nitric oxide synthase inhibitor: A shield against acute and chronic diseases. J Parenter Enteral Nutr. 2006;30(1):45-51.
- Dibaba D, Xun P, He K. Dietary magnesium intake is inversely associated with serum C-reactive protein levels: meta-analysis and systemic review. Eur J Clin Nutr. 2014:68(4): 510-516.
- Rosanoff A, Seelig M. Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals. J Am Coll Nutr. 2004;23(5):501-505.
- Bowden J, Sinatra S. The Great Cholesterol Myth: Why Lowering Your Cholesterol Won’t Prevent Heart Disease-and the Statin-Free Plan That Will. Beverly, MA: Fair Winds Press; 2012.
- de Lorgeril M, Salen P. Recent cholesterol lowering drug trials: New data, new questions. J Lipid Nutr. 2010;19(1):65-92.