Monday, August 15, 2011

Is it LDL cholesterol unquestionably and unequivocally a causal risk factor for myocardial infarction?

It is my pleasure to share the following point of view of Dr. David Diamond, researcher, scientist and professor from the University of South Florida – and our colleague from THINCs – about low density lipoprotein and its relationship with the incidence of myocardial infarction:
“If only it were that simple, then reducing LDL by any means would reduce and even eliminate MI from occurring, and enable people to live longer. However, serum cholesterol levels had been reduced with treatments long before statins were developed, first with corn oil, and then GI surgery and cholestyramine and then there were the statins, including Baycol and Torcetrapib, which reduced LDL and even raised HDL. Baycol and Torcetrapib were very effective as LDL reducing agents, but they were also very effective at killing people, which is why they are no longer on the market. So lowering LDL levels, alone, is not sufficient to reduce the incidence of MI and to enable someone to survive the treatment.
The question should be, why are elevated levels of LDL associated with MI? The answer is that LDL is not "bad cholesterol" which is destined to harm blood vessel walls and "clog arteries" as drug company ads incorrectly state. Part of the problem is that LDL gets glycated by glucose, which distorts the lipoprotein sufficiently that it can't bind to the LDL receptor. The glycated LDL molecule then accumulates in the blood and becomes oxidized. It is the oxidized LDL that contributes to the deterioration of the blood vessel wall, not the native (normal) LDL. How do you stop sugar from glycating LDL? Keep blood sugar low through exercise and a low carb diet - 2 rather simple strategies which have never been compared head-to-head to statins in a clinical trial for reducing CHD, perhaps because the outcome would be unappealing to the drug companies that sponsor this research.
The other way of looking at LDL and MI is that when LDL becomes oxidized and glycated it becomes ineffective at doing what it's supposed to do, which is to kill bacteria (yes, LDL is a part of the immune system) and to build new cells. In response to the increasing concentration of oxidized (ineffective) LDL, the liver makes more LDL, thereby raising the concentration of total serum LDL. This is actually why total LDL levels can correlate with MI incidence, but it's actually the synergy between high sugar diets and oxidized LDL (and high blood pressure) which causes to damage to artery walls.
So, it's not that LDL is inherently atherogenic. The LDL molecule is an essential part of optimal health, serving to work with white blood cells to kill pathogens and to rebuild damaged tissue. It is the oxidization of LDL, which is precipitated by stress, smoking, lack of exercise and a high sugar diet, that is atherogenic. The literature on this work is vast, but I cite at the end of this little article some papers showing that ox-LDL levels are a much better indicator of CHD than native LDL (1, 2, 3).
I have reviewed only a small part of the thousands of medical papers and dozens of books I've read on this subject. Based on my reading, and the findings of experts in the field, there is good reason to be skeptical about the claims that statins have enhanced cardiac health in the absence of substantial side effects. In my recent talk** I reviewed well-documented evidence published in highly respected medical journals of more extensive adverse side effects of statins than is typically reported in the drug company sponsored research papers. For a relatively small reduction of cardiac events in the treated population, the cost of statins financially and in terms of insufficient improvement in overall health and survival is unjustified.”
* David Diamond, Ph.D, is Professor from the Depts of Psychology and Molecular Pharmacology and Physiology, Center for Preclinical and Clinical Research on PTSD. Director, USF Neuroscience Collaborative, 4202 E. Fowler Ave (PCD 4118G), Tampa, FL 33620. His homepage is
** The web article that summarizes his talk and includes the on-line video is at
1. Margareta Kristenson, Bo Ziedén, et al. Antioxidant state and mortality from coronary heart disease in Lithuanian and Swedish men: concomitant cross sectional study of men aged 50. BMJ 1997;314:629–33
2. Christa Meisinger, Jens Baumert, et al. Plasma Oxidized Low-Density Lipoprotein, a Strong Predictor for Acute Coronary Heart Disease Events in Apparently Healthy, Middle-Aged Men From the General Population. Circulation 2005;112;651-657
3. Huiling Huang, Weiyi Mai, Dan Liu, et al. The oxidation ratio of LDL: A predictor for coronary artery disease. Disease Markers 24 (2008) 341–349

In the acidity theory of atherosclerosis we support a link between LDL oxidation and acidic pH presenting different studies showing this relationship (1).
1. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at

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