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 Interviews with Nutritional Experts: How Vitamin E Prevents Heart Disease  
 
Interview with Dr. David Janero
   as interviewed by Richard A. Passwater PhD

In recent columns, I have presented the evidence that vitamin E and other antioxidant nutrients are protective against heart disease. People -- especially scientists -- have trouble understanding this fact until they know "how" vitamin E accomplishes this feat.

One scientist -- a cell biologist and biochemist -- has done much to establish the necessary cellular evidence elucidating the protective mechanism. Dr. David Janero is a member of the senior staff in the Cardiovascular- Atherosclerosis Research Department of CIBA-GEIGY Corporation, Pharmaceuticals Division. He conducted his Ph.D. work in cell biology at the Yale University School of Medicine and was a National Institutes of Health Postdoctoral Fellow in biological chemistry at the Johns Hopkins University School of Medicine. Since 1983, he has held various research and development positions in the pharmaceutical industry. Dr. Janero and his research team have contributed to an increased understanding of the mechanisms of cardiovascular disease and have helped define the potential of both novel therapeutics and natural products (particularly vitamin E) to satisfy associated medical needs.

Their research findings are published in over 90 scientific reports and have been presented at many professional meetings, most recently at the Federation of American Societies for Experimental Biology conference "Vitamins E and C and Free Radical Reactions." I have asked Dr. Janero to explain how vitamin E protects against heart disease. I have set the stage in the previous column with Dr. Lester Packer, who explained how vitamin E stops free radicals including the lipid peroxidation process. Now Dr. Janero will help me continue the story. We discuss many of the ways in which vitamin E works to prevent heart disease, and then we look at the specific role of how vitamin E prevents low-density lipoprotein from becoming oxidized. This is the common ground that now has all cardiovascular researchers excited.

Passwater: You study heart disease from a different perspective than "traditional" heart researchers -- pathologists, cardiologists, and epidemiologists. You are trained as a cell biologist and biochemist, yet clinical cardiologists are learning from your work.

What does your cellular and biochemical perspective bring to heart disease research?

Janero: Modern cell biology uses concepts and technology from many disciplines, including physical sciences such as chemistry and physics, to help elucidate how the basic unit of life, the cell, functions in health and disease. The critical importance of cell biology to medicine stems from a principle elucidated over a century ago: all disease has a basis in abnormal cell function. Biochemistry provides ways of probing and explaining cell function in quantitative terms. Consequently, the combination of cell biology and biochemistry is a powerful experimental avenue for me as a researcher on the origins and mechanisms of cardiovascular disease. Cell biology and biochemistry provide essential information to the physician who must understand disease mechanisms in treating cardiac patients and optimize potential means of prevention/therapy. The link between modern medicine and modern therapeutics is the cell biology of disease.

Passwater: The timing seems good for new research approaches such as your laboratory's. Many theories on the development of atherosclerosis that once were thought to "hold water" are now considered full of holes. Would you give us a brief overview of the current theory of "spontaneous atherosclerosis?"

Janero: In the 1800's, anatomists recognized that

atherosclerosis is manifest as lipid-rich deposits in the walls of blood vessels, particularly certain arteries (hence, the alternative name "arteriosclerosis"). Such fat deposits reduce the vessel opening, thereby limiting the nutritive blood supply to whatever tissue or organ is downstream. Despite considerable research, the details of how atherosclerotic vessel disease develops remain elusive. Early thinking favored the concept that disruption or loss of the thin layer of cells lining the artery (the endothelium) precipitated atherosclerosis. Although rapid vessel blockage does occur after physical endothelial dosage, this accelerated form of vessel disease is distinct from "spontaneous" atherosclerosis.

Routine, spontaneous atherosclerosis is an injury response by the artery wall which develops chronically (over decades in humans) in the presence of extrinsic "risk factors" (e.g., high blood pressure, smoking, diabetes, excesses of certain blood lipids) that increase the likelihood of the first overt sign of atherosclerosis, the lipid deposit in the vessel wall termed the "fatty streak" because it consists of frothy-looking, lipid-laden "foam cells."

Although arteries in the body change structurally with time, this age-related differentiation is not pathologic and does not itself lead to atherosclerosis.

Passwater: Tell us a little about the structure of arteries.

Janero: Arteries are a type of blood vessel which receive nutrient-rich blood from the heart and conduct it to the major body organs. In humans, relatively large artery diameters mean that about 20% of the total circulating blood volume flows within these vessels. Generally, the artery wall contains an endothelial lining, one cell-layer thick, in direct contact with the circulating blood. Considerable connective tissue and smooth muscle are below the endothelium to support the artery and at the same time give the artery wall a fair degree of flexibility.

Passwater: Why did early researchers believe that cholesterol would just "zap" from the blood into the artery wall?

Janero: The mechanism by which certain cells in the artery wall (particularly so-called monocyte-macrophage cells) internalize circulating fat to form lipid-rich foam cells has been detailed only within the last 20 years or so. The research sought to explain a contradiction: lipid-laden foam cells tend to develop when blood low-density lipoprotein (LDL) levels are high, yet circulating LDL "fed" to isolated macrophages is not taken up by these cells.

Research on the cell biology of this seeming anomaly demonstrated that unregulated internalization of damaged or "modified" LDL particles through specific "scavenger receptors" on the macrophage surface leads to foam cell formation. The most pathologically relevant modification of LDL seems to be oxidation (i.e., free radical-mediated peroxidation of LDL polyunsaturated fatty acids). Therefore, oxidative lipoprotein damage can be considered a driving force for early lesion (i.e., fatty streak) formation [1].

Passwater: Conversion of smooth muscle cells of the artery wall into proliferating cells also seems important to the progression of atherosclerosis. What causes this conversion? Free radicals?

Janero: Smooth muscle proliferation is likely induced by small-molecule "messengers" released from nonmuscle cells (such as endothelial cells) in the artery wall. Growth factors within smooth muscle cells may regulate their proliferative response to exogenous chemical signals. It remains to be determined whether oxidants directly modulate the proliferative response.

Passwater: Do atherosclerotic lipid deposits appear mostly in specific arteries and/or at particular locations within arteries?

Janero: Atherosclerosis has a predisposition for critical arterial beds comprised of medium-sized arteries, e.g., the coronary and carotid arteries supplying heart muscle and brain, respectively, with nutritive blood. Potentially important predisposing factors in arteries may be the rather high oxygen tension of the blood flowing through them and the considerable hydrostatic pressure generated. But there is significant variability both along the length of the artery and around its circumference regarding the pattern of lipid deposition within the arterial wall. This variation is believed to reflect both blood-flow dynamics and the chronic, cumulative nature of the lipid build-up itself.

Passwater: Why might vitamin E protect against atherosclerosis?

Janero: The idea that vitamin E may help prevent the initiation and/or progression of spontaneous atherosclerosis is suggested by five main lines of largely experimental evidence:
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 About The Author
Richard A. Passwater, Ph.D. has been a research biochemist since 1959. His first areas of research was in the development of pharmaceuticals and analytical chemistry. His laboratory research led to his discovery of......moreRichard Passwater PhD
 
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