In this two part special edition of Catalyst (see video the right), Dr. Maryanne Demasi investigates the science behind the claims that high cholesterol causes heart disease.
Dr. Tener’s Comments:
For several decades, mainstream medicine has spent millions of dollars in advertising and propaganda creating and perpetuating the idea that high cholesterol is the cause of heart disease. As a result, millions of Americans (1 in 4 to be exact) are now taking a cholesterol lowering medication despite the fact that there is increasing evidence to suggest that these drugs can actually contribute to heart disease and other health related problems. The dangers associated with statin drugs are well established, with over 900 studies proving their adverse effects which include muscle damage (see case study below), anemia, increased cancer risk, diabetes, kidney and liver damage, cataracts and sexual dysfunction.(1) That these drugs have proliferated the market the way they have is a testimony to the power of marketing and the widespread greed and corruption that exists in our healthcare industry. In the two part special edition of Catalyst (see video above), Dr. Maryanne Demasi investigates the science behind statin drugs and exposes the disturbing truths behind an industry that appears to be willing to sacrifice our health for profit.
Goldberg Clinic Case Study: Muscle Weakness, Fatigue, Weight Gain | 2014
Patient presented with progressive muscle weakness, chronic fatigue and weight gain. Muscle weakness began after taking Zocor, a statin drug prescribed by his Medical Doctor to lower cholesterol. At the Goldberg Clinic, a comprehensive case history, physical examination and functional laboratory work was performed and key underlying factors were identified. Lab studies revealed significant elevation of Creatine Kinase, an enzyme reflective of muscle damage when elevated. Based on the data collected, an individualized program was developed for the patient to follow. In just a few months, the patient's Creatine Kinase level has dropped over 50%, his energy has improved considerably and he has lost 24 pounds.
Statin Drugs Impair Numerous Biological Functions
Despite its bad reputation, cholesterol is essential to our physiology. Cholesterol is a major component of every cell in our body and is vital for such physiological functions as transmission of nerve impulses, formation of vitamin D, the synthesis of steroid hormones (testosterone, estrogen, cortisol), and the formation of bile. Cholesterol also plays an essential role in the brain, which contains about 25% of the cholesterol in the body. Statin medications not only interfere with cholesterol production, but they dramatically impair the physiological pathways that are dependent on its existence. Every cell of the body is adversely affected.
Assessing Cardiovascular Disease Risk
Heart disease is one of the leading causes of death in the US, making it imperative for patients to understand the risk factors involved in order to avoid becoming a statistic. Unless exceptionally elevated, total cholesterol reveals little about heart disease risk. One of the best indicators for assessing risk for cardiovascular disease is the High Sensitivity C-Reactive Protein. This simple blood test is highly recommended as part of a comprehensive work-up for all patients at the Goldberg Clinic with an increased risk of cardiovascular disease. Following evaluation (case history, physical exam, laboratory testing), an individualized program is developed to address causes and create the proper conditions under which healing can occur. The High Sensitivity C-Reactive Protein (HsCRP) is commonly employed as a pre-post measure to monitor patient progress and to ensure a successful reduction in cardiovascular disease risk.
Before and After HsCRP results of patients at the Goldberg Clinic at risk for cardiovascular disease:
High Risk: Greater than 3. Normal: Less than 3. Ideal: Less than 1
1) Golomb BA, Evans MA. Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism. Am J Cardiovasc Drugs. 2008; 8(6):373-418.