Atherosclerosis is Just One type of vlekjes Arteriosclerosis None of these methods, however, produced anything resembling human atherosclerosis. While arteriosclerosis refers to hardening and degeneration of the arteries in general, atherosclerosis is a specific type of arteriosclerosis in which a plaque rich in lipid-loaded white blood cells, cholesterol, fatty acids, calcium, various debris — called an atheroma — invades the innermost layer. If you are not familiar with the anatomy of a blood vessel, you can see a diagram of it here. The research in Anitschkov's day suggested that, while various types of arteriosclerosis occurred in humans, atherosclerosis was a much more important cause of death. Anitschkov thus concerned his research with what caused atherosclerosis. The mechanical injuries to blood vessels or nerves produced a local repair process that involved the proliferation of cells, their congregation around the damaged area, and a resultant thickening of the vessel wall. The results were local rather than systemic, however, and never produced a lesion resembling an atheroma. Injections of adrenalin produced much more interesting changes that were much more relevant to humans. They produced necrosis (death) of cells in the media followed by extensive calcification.
Clinically, given enlargement of the arteries for decades, symptomatic atherosclerosis is typically associated with men in their 40s and women in their 50s to 60s. Sub-clinically, the disease begins to appear in childhood, and rarely is already present at birth. Noticeable signs can begin developing at puberty. Though symptoms are rarely exhibited in children, early screening of children for cardiovascular diseases could be beneficial to both the child and his/her relatives. 15 While coronary artery disease is more prevalent in men than women, atherosclerosis of the cerebral arteries and strokes equally affect both sexes. 16 Marked narrowing in the coronary arteries, which are responsible for bringing oxygenated blood to the heart, can produce symptoms such as the chest pain of angina and shortness of breath, sweating, nausea, dizziness or light-headedness, breathlessness or palpitations. 14 Abnormal heart rhythms called arrhythmias (the heart is either beating too slow or too fast) are another consequence of ischemia. 17 Carotid arteries supply blood to the brain and neck. 17 Marked narrowing of the carotid arteries can present with symptoms such as a feeling of weakness, not being able to think straight, difficulty speaking, becoming dizzy and difficulty in walking or standing up van straight, blurred vision, numbness of the face, arms, and legs, severe.
The injury was primarily seen as either a mechanical or a toxic factor, and was sometimes believed to be injury to the nerves rather than injury to the blood vessels. Researchers carried out a multitude of experiments on rabbits and other animals, including the following: Mechanical damage to the blood vessels including ligating, pulling, pinching, and wounding them, and cauterizing them with galvanic wire or silver nitrate. Increasing blood pressure by constricting the blood supply through the aorta, damaging the kidneys, or hanging rabbits up by their feet. Severing or irritating certain nerves. Injecting rabbits with adrenalin. Injecting rabbits with a multitude of toxic factors, including digitalin, strophanthin, adonidin, ergotin, theocin, barium chloride, hydrastin, nicotine, caffeine, formalin, ergosterol, and various salts of acids and heavy metals. Injection of diphtheria toxin and many other bacteria cultures or bacterial byproducts. Most of these methods caused substantial damage to the arteries and resulted in a "regenerative thickening" of one or another type. So the response-to-injury concept is quite real.
The cellular biology
As we will see below, these are all correct! Atherosclerosis is largely driven by the degeneration of lipids which infiltrate the blood vessel and thereby cause dermatitis inflammation. Inflammation from other sources may accelerate the process or further the degeneration of the atherosclerotic plaques once they are formed, but the initiating factor for fatty plaques appears to be the degeneration of lipids — especially the degeneration of polyunsaturated fatty acids (pufa). In order to begin looking at the evidence, we must go back a ques century in time to the cholesterol-fed rabbit. The cholesterol-fed rabbit model came on the heels of extensive investigations into what would later be termed the "response-to-injury hypothesis.". Around the turn of the twentieth century, research into the cause or causes of heart disease was in full throttle.
A 1933 compilation edited. Arteriosclerosis: a survey of the Problem (New York: Macmillan) contained twenty reviews of investigations into the matter, including statistical relationships, the distribution of the disease in wild animals, the distribution in humans according to race and climate, nutritional influences, the physical and chemical nature. Nikolai anitschkov, who developed the cholesterol-fed rabbit model, wrote the 50-page review of experimental animal models. 1, much of this research was published in German, so Anitschkov's review is an invaluable resource. According to Anitschkov, early ideas about the origin of arteriosclerosis — a general term for hardening and damage to the arteries, of which atherosclerosis is a specific type — saw the diseases as a response to injury.
The Great Cholesterol Con: The Truth About What really causes heart Disease and How to avoid It by malcolm Kendrick, md (2007). So is the theory that cholesterol causes heart disease just a myth? Or are the skeptics truly waging a war against the preponderance of the evidence? In this Article: The truth is that each of these authors makes important points. Were there never any good evidence that cholesterol was involved in heart disease, there would be no national Cholesterol Education Program, no statin empire, and Daniel Steinberg could never have written a book plus over 200 scientific papers on the subject.
On the other hand, were there never anything seriously wrong with the mainstream dogma on the issue, ravnskov, colpo, kendrick, and many other authors could never have built their careers around pointing out the gaping holes in the theory. There is no one cause of "heart disease." "Heart disease" is a heterogeneous compliation of diseases of the heart and blood vessels with many different causes. Some of these include disturbances of the rhythm of the heart, calcification of the middle portion of the blood vessels and calcification of the heart valves, and congestive heart failure. The question i address in this article is whether and in what sense cholesterol is involved in atherosclerosis, the development of fatty and calcified plaques in isolated, raised lesions, which can cause heart attacks by rupturing, clotting, and blocking arteries. In 1933, the famous proponent of the cholesterol-fed rabbit model nikolai anitschkov declared that atherosclerosis had been shown to be of an "infiltrative" character rather than a "degenerative" character and was driven by lipids (fatty substances) rather than by inflammation. He did not deny inflammation was involved, but believed that it was secondary to lipid infiltration. Many opponents continue to claim that the root cause driving heart disease has nothing to do with lipids and everything to do with inflammation and that it is degenerative rather than infiltrative in character.
Inflammation in, atherosclerosis Macrophage, functions cayman
When the cap ruptures, the blood clots, blocking the artery and causing a heart attack. This is called the lipid hypothesis. But is this drole true? Books and web sites devoted to debunking this theory have come out of the woodwork over the last decade; books defending it have followed suit. Consider the following titles to see just how controversial the idea really is: The Cholesterol Myths: Exposing the fallacy That Saturated Fat and Cholesterol cause heart Disease by Uffe ravnskov, md, phD (2000). The Great Cholesterol Con: Why everything you've been told about cholesterol, diet, and heart disease is wrong! By Anthony colpo (2006). The Cholesterol Wars: The skeptics. The Preponderance hond of the evidence by daniel Steinberg, md, phD (2007).
The response-to-Injury rabbit never developed Atherosclerosis — why not? August 23, 2008 by, chris Masterjohn, the pop science version of cholesterol goes something like this: when you eat fatty foods, especially foods rich in animal fat, the saturated fat and cholesterol in these foods wind up citroen in your blood and stick to your arteries. Since saturated fats are solid outside your body, they will be solid inside your body too — depsite the 30-degree increase in average temperature. Arteries are much like pipes. When they get caked up with grease, blood flow is impaired, and a heart attack ensues. None of the prominent scientists who promoted the idea that cholesterol is a critical factor in the development of heart disease ever believed anything remotely resembling this nonsense. From the beginning, they recognized that atherosclerotic plaque accumulates behind the layer of the artery in contact with the blood, called the endothelium, and that the cholesterol and fat within it is engulfed in white blood cells. The theory these scientists promoted looked something like this: when the cholesterol level in the blood increases, it penetrates the arterial wall and gets stuck; white blood cells circulating in the blood then enter the arterial wall and gobble up the cholesterol; the accumulation.
is asymptomatic for decades because the arteries enlarge at all plaque locations, thus there is no effect on blood flow. 12 even most plaque ruptures do not produce symptoms until enough narrowing or closure of an artery, due to clots, occurs. Signs and symptoms only occur after severe narrowing or closure impedes blood flow to different organs enough to induce symptoms. 13 Most of the time, patients realize that they have the disease only when they experience other cardiovascular disorders such as stroke or heart attack. These symptoms, however, still vary depending on which artery or organ is affected. 14 Typically, atherosclerosis begins in childhood, as a thin layer of white-yellowish streaks with the inner layers of the artery walls (an accumulation of white blood cells, mostly monocytes/macrophages) and progresses from there.
3, plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. 7, the narrowing of arteries limits the flow of oxygen-rich blood to parts of the body. 7, diagnosis is based upon a physical exam, electrocardiogram, and exercise stress test, among others. 8 Prevention is generally by eating a healthy diet, exercising, not smoking, and maintaining a normal weight. 4 Treatment of established disease may include medications to lower cholesterol such soda as statins, blood pressure medication, or medications that decrease clotting, such as aspirin. 5 A number of procedures may also be carried out such as percutaneous coronary intervention, coronary artery bypass graft, or carotid endarterectomy. 5 Atherosclerosis generally starts when a person is young and worsens with age. 2 Almost all people are affected to some degree by the age.
Macrophages in, atherosclerosis : From
For the journal, see, atherosclerosis (journal). Atherosclerosis is a disease in which the inside of an artery narrows due to the build up of plaque. 7, initially, there are generally no symptoms. 1, when severe, it can result in coronary artery disease, stroke, peripheral artery disease, or kidney problems depending on the arteries affected. Symptoms, if they occur, generally do not begin until middle age. 3, the exact cause is not known. 1, risk factors include abnormal cholesterol levels, high blood pressure, diabetes, smoking, obesity, family history, and brief an unhealthy diet.