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ARTEREZ is Targeting the Multi-Factorial 'Root-Causes' Of Cardiovascular Disease While Exposing the Cholesterol Hypothesis Myth.  How Did it all Get Started?

METAMORA, Mich., May 21, 2019 /PRNewswire/ -- In 1908, a Russian scientist (Alexander Ignatowski) thought that eating too much protein would speed up the aging process in humans. To test this hypothesis, he fed rabbits meat, milk and eggs and found 'fatty streaks' accumulated in the arteries. In 1913, Nikolai Anichkov, repeated the experiment with egg yolk and produced 'fatty streaks'; this gave birth to the "cholesterol hypothesis" and was hailed as one of the "greatest discoveries in cardiology of the 20th century."

The rabbit is an herbivore and the egg yolk diet is therefore foreign to its metabolic system, thereby accumulating as a 'fatty streak' or 'foam cells' in the arteries. Prolonged feeding of cholesterol is toxic because the rabbit does not have a functional enzyme (cholesterol hydroxylase) to flush it out of the system. Humans are omnivores equipped with cholesterol hydroxylase to process diet cholesterol to bile and prevent accumulation.

The industrial revolution marked an increasing incidence of coronary heart disease due to sedentary lifestyle and a high-fat, highly-processed diet. However, in 1955, Ancel Keys, a University of Minnesota nutritionist, embraced the "cholesterol hypothesis"; that dietary cholesterol poses higher risk of heart disease in humans, like rabbits. Thus, in 1961, Keys and the American Heart Association (AHA) drafted a dietary guideline to reduce cholesterol, particularly limiting eggs to 'not more than 3/week'. (Note: reversed in 2015, citing no evidence to link dietary cholesterol to heart disease).

The focus on cholesterol-lowering inspired Akira Endo of Japan (Sankyo) in 1971 to screen for drugs that inhibit cholesterol synthesis (statins), targeting the enzyme 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG CoA) reductase. The first statin, Compactin, was effective in vitro but was subsequently dropped because it was proven toxic and failed to lower plasma cholesterol in rats and mice. The 2nd statin, Lovastatin, discovered in 1979 by Merck, also failed to lower cholesterol in animals and was dropped. However, per the recommendations of Michael Brown and Joseph Goldstein (Merck consultants and Nobel Prize winner for their discovery in 1973 of the genetic cause of familial hypercholesterolemia, FH), Lovastatin was resurrected and tested clinically on FH patients. Lovastatin lowered cholesterol in FH patients and was approved by the FDA in 1987.

In 1985, Ancel Keys and the AHA lobbied to legislate a "war on cholesterol", which resulted in an AHA/NIH partnership. In 1987, they established the National Cholesterol Educational Program (NCEP); the same year Lovastatin was approved. To assess the cholesterol-lowering effect of Lovastatin, the "lipid panel" was introduced by William Friedewald of the NIH. The lipid panel calculates blood cholesterol (LDL, HDL) and fats (triglycerides) and an initial Lovastatin goal of <130 mg/dL LDL. Subsequently, more statins were developed to achieve the LDL target goal. Gimmicks to highlight the utility of the 'panel' include designating LDL as 'bad cholesterol' and HDL as 'good cholesterol', which inspired 'HDL-boosting' drugs and triglyceride drugs such as antihypertensives.

Dr. Tunac and Arterez pose this important question – is the 'cholesterol hypothesis' and all drugs targeting components of the lipid panel a 'wishful thinking' academic exercise given that cardiovascular disease and related healthcare costs continue to increase in the US and worldwide? Cardiovascular disease (CVD), particularly coronary heart disease (CHD), remains the No. 1 disease killer in the world despite record numbers of statins being prescribed year after year.  By 2030, 23.6 million people are predicted to die from CVD (World Heart Federation report).

Arterez, LLC is a Michigan-based bio-pharmaceutical company focused on the development of first-in-class diagnostic panels as well as a triple compound oral therapy targeting the multi-factorial root causes of cardiovascular disease including the repair and maintenance of the Endothelial Glycocalyx, while minimizing the damaging effects of oxidation and reducing inflammation.

For more information, contact Mike Brennan,, 248-931-9091 or visit 

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