Atherosclerosis: Diet and Drugs (Handbook of Experimental Pharmacology) [Hardcover]

Arnold von Eckardstein (Editor)

Book Description

Publication Date: August 5, 2005 | ISBN-10: 3540225692 | ISBN-13: 978-3540225690 | Edition: 1

This book gives an overview on important mechanisms involved in atherosclerosis and thereby presents targets some of which are used and others which may be useful for therapy and prevention of atherosclerosis. Since atherosclerosis is a multifactorial disease the scientifc approach must be multidisciplinary. Accordingly, the authors of this book represent different areas of methodology ranging from basic, clinical and population research as well as different fields of expertise ranging from metabolism to immunology and inflammation biology and to vascular biology.

Product Details

• Hardcover: 816 pages
• Publisher: Springer; 1 edition (August 5, 2005)
• Language: English
• ISBN-10: 3540225692
• ISBN-13: 978-3540225690
• Product Dimensions: 9.4 x 6.3 x 1.3 inches
• Shipping Weight: 2.8 pounds (View shipping rates and policies)
• Average Customer Review: 1.0 out of 5 stars  See all reviews (1 customer review)
• Amazon Best Sellers Rank: #3,292,155 in Books (See Top 100 in Books)

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1.0 out of 5 stars Is atherosclerosis a physics problem? And other questions . . ., April 20, 2011

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This review is from: Atherosclerosis: Diet and Drugs (Handbook of Experimental Pharmacology) (Hardcover)

While this book contains thirty articles from contributors who are each recognized authorities in their various disciplines, the simple fact that after more than 60 years of study, no one has been able to satisfactorily and convincingly explain the simple mechanism by which too many men and women living in the last half of the twentieth century and the first decade in the twenty-first century in the USA develop certain accumulations of so-called "fatty plaques" at selected locations in tissue areas known as the intima of the arterial walls of the coronary arteries, suggests that perhaps some of these scientists may not understand exactly what they are looking for. (1) It was the late Arnold Ehret who said that no matter how scientific sounding some explanation is, if it cannot be grasped by the average mind easily, it's suspect. (2) It was the late G. K. Chesterton who noted that long words are like long railway trains. They go rattling by us without hardly any wrinkle in grey matter [he illustrates with 'the social utility of the indeterminate sentence' -- if you haven't read it, it's worth buying the book just to read that one paragraph -- the book is The Romance of Othodoxy]. Chesterton's point: It's the short words that help us think. Concerning this book then: "triglycerides," is, unfortunately, one of Chesterton's long word. Fatty acids linked to one version of an alcohol molecule called glycerol, may well be the scientifically proper definition, but "triglycerides" is still just just a long word for fat. Indeed, triglycerides are actually "neutral" fat! ("Neutral" because the fat can be hydrolyzed at "normal" temperatures and normal pH? -- why do old physiology texts refer to triglycerides as neutral fat? Has that been forgotten?). (3) Does a section discussing "Atherogenic Dyslipidemia" in this book help us think? How in the world can the entire body be in a condition of dyslipidemia? Is such word usage like the otolaryngologist who pronounces that we have "acute purulent otitis media?" At first blush, it sure sounds impressive. But, what does it mean? Oh, a middle ear infection that came on quickly and produces puss [white blood cells fighting the infection]. But we want to know if it is a virus or a bacerial infection, don't we? And calling it "acute purulent otitis media" does not say one word about whether or not the source is a bacterium or a virus, does it? (4) So, if the patient has 330 mg/dl of triglycerides in his or her circulation, the concentration of patient's blood isn't tending to be water anymore, is it? Is that dyslipidemia? The serum is getting full of "neutral" fat, isn't it? Do you suppose that a change in the concentration of the serum from water to fat is going to affect how the cholesterol from former cell walls [from cells that have died (normal cell death = "apopotosis," right?)] can get out of the cell wall and be returned to the liver by the "correct" apolipoprotein [and we know they are also in the serum] so the liver can re-use the cholesterol molecule to make bile salts? (5) Does all the circulating triglyceride affect the diffusion of cholesterol from the arterial intima "back" into the serum? (6) Is diffusion a "physics" concept? (7) Is atherosclerosis a physics "problem?" (8) Doesn't all "chemistry" including "biochemistry" rest on physics? (9) Do the fatty plaques develop at venues of low arterial wall "stress?" (10) Isn't that counterintuitive? (11) Does the patient's blood pressure rise because the body needs to try to scour the triglycerides off the arterial epithelial cells so that normal processes (HDL returning the cholesterol from the peripheral cells to the liver) can work? (12) What about chylomicrons carrying dietary triglycerides? (13) Do they enter the circulation after they leave the thoracic duct? (14) Do they then also contribute to the blood becoming "too much like fat and not enough like water" until the fat can get deposited and out of the serum? This book has thirty articles (with many footnotes) taking up a total of almost 800 pages, yet we haven't got the answer. After 60 years of serious study, it honestly suggests that perhaps the authors, albeit well-intended, have been asking the wrong questions.