The Consumption of Poultry und Bird Products may have a Connection with Chronical Respiratory and Blood Vessel Diseases

The influenza virus affects different animal species like humans, birds and pigs. That means that the receptor which lets the influenza virus into the respiratory and blood vessel cells is common in these species. This receptor consumed with food gets into gastro-intestinal tract and into the lymphatic system, antibodies against it are built and they react against it and falsely against human respiratory and blood vessel cells which have a common in structure receptor. So a chronic autoimmune disease is caused such as bronchial asthma, COPD, emphysema, autoimmune blood vessel diseases and perhaps also atherosclerosis, thus brain strokes, myocardial infarction and others.

It is largely spoken about the connection between cholesterol and atherosclerosis. There are two sources of cholesterol in blood: exogenous and endogenous. The exogenous or alimentary is 20% of all, and endogenous source is 80%. The endogenous is a result of the own organism’s production in connection with the building and demolition of cell membrane. In my opinion the high levels of cholesterol in blood is not the reason for atherosclerosis, but a result from it. By atherosclerosis by an autoimmune mechanism is demolished the endothelium membrane, and this leads to high cholesterol blood levels. The autoimmune demolition of endothelium membranes leads to accumulation of binding tissue and into it incorporate fat , because of its high level in blood, as a result from the demolition of cell membranes by autoimmunity. Therefore not cholesterol in food but consumption of meat leads to atherosclerosis.

Empirically is proven that vegetarians have lower levels of cholesterol and atherosclerosis. Why? In fact vegetables contain almost the same level of cholesterol as meat, because it is a part of their cell membrane. Usually medical doctors prohibit the consumption of pork and bird skin, because they are oilier. But according to the autoimmune theory it is not enough, because meat inclusive bird and eggs contain not only cholesterol, but also the so called influenza receptor. It is well known in microbiology that influenza virus develops wonderfully on the egg membrane, influenza virus affects also birds. The receptor for influenza virus in birds and eggs membrane has a very similar analogue in human respiratory and blood vessel cells. That is the reason why we all (humans and birds) get sick with influenza. The antibodies which our immune system builds against the bird receptor, which is found in bird’s meat, react to the human influenza receptor and cause respiratory and blood vessels deceases such as atherosclerosis resulting in peripheral vascular diseases, coronary vascular diseases and heart attacks and ischemic brain strokes.

Laboratory tests prove that not only so called autoimmune diseases such as lupus erythematosus, rheumatoid arthritis, Morbus Bechtereff, thyroiditis of Hashimoto, Basedoff disease contain an element of inflammation, but also degenerative diseases like atherosclerosis, diabetes, obesity, psychical disorders such as autism, psychoses, dementia, Parkinson syndrome, myasthenia gravis and many others. But until now no one has explained why. We all thought that cholesterol damages the blood vessel like a stone. It accumulates in the blood vessel interstitium and causes immune reaction and inflammation. But this idea does not make sense at all, does it?

Cholesterol is a building part of cell, so how could it damage the blood vessel? It is like hitting the vessel with a dilution of sugar or oil at a slow speed and expecting it would be damaged.

It is like aiming at rabbits with carrots. It could be deadly or?

The truth is the organism acquires high levels of cholesterol as a result from higher cell membrane demolition trough the autoimmune reaction caused by the antibodies built against the receptor proteins in meat. In the vessel accumulates binding tissue after the immune reaction and it binds cholesterol in its interstitium, thus causing atherosclerosis in all of its forms.

So in conclusion atherosclerosis is caused by autoimmune reaction. It is inflammatory reaction and high level of cholesterol is a result not a purpose for it.

In fact statin therapy of high level of cholesterol is completely purposeless, because it is like fighting with a biochemical substance which is not the reason for atherosclerosis, but a result from it. And statins have a lot of side effects. You can check it by yourselves.

Muscle pain and damage

One of the most common complaints of people taking statins is muscle pain. You may feel this pain as a soreness, tiredness or weakness in your muscles. The pain can be a mild discomfort, or it can be severe enough to make your daily activities difficult.

Oddly enough, most randomized controlled studies of statins indicate that people taking statins develop muscle pain at the same rate as people taking placebo. But up to 29 percent of the people who start taking statins report muscle pain and many discontinue statins because of it. Many of these people do well when they are switched to a different variety of statin.

Very rarely, statins can cause life-threatening muscle damage called rhabdomyolysis (rab-doe-my-OL-ih-sis). Rhabdomyolysis can cause severe muscle pain, liver damage, kidney failure and death. The risk of very serious side effects is extremely low, and calculated in a few cases per million of patients taking statins. Rhabdomyolysis can occur when you take statins in combination with certain drugs or if you take a high dose of statins.

Liver damage

Occasionally, statin use could cause an increase in the level of enzymes that signal liver inflammation. If the increase is only mild, you can continue to take the drug. Rarely, if the increase is severe, you may need to try a different statin.

Increased blood sugar or type 2 diabetes

It's possible your blood sugar (blood glucose) level may increase when you take a statin, which may lead to developing type 2 diabetes. The risk is small but important enough that the Food and Drug Administration (FDA) has issued a warning on statin labels regarding blood glucose levels and diabetes.

Neurological side effects

The FDA warns on statin labels that some people have developed memory loss or confusion while taking statins. These side effects reverse once you stop taking the medication.

The only way to heal atherosclerosis is the restriction of meat in the diet.

This article suggests that atherosclerosis is also connected with inflammatory reaction. So why not an autoimmune inflammatory reaction?

Inflammatory reactions in the pathogenesis of atherosclerosis.

Fan J¹, Watanabe T.

Abstract

Atherosclerosis and its complications constitute the most common causes of death in Western societies and Japan. Although several theories or hypotheses about atherogenesis have been proposed during the past decades, none can completely explain the whole process of the pathogenesis of atherosclerosis because this disease is associated with multiple risk factors. In spite of this, the concept that atherosclerosis is a specific form of chronic inflammatory process resulting from interactions between plasma lipoproteins, cellular components ( monocyte/macrophages, T lymphocytes, endothelial cells and smooth muscle cells ) and the extracellular matrix of the arterial wall, is now well accepted. Histologically, atherosclerotic lesions from the early-stage (fatty streak) to more complicated lesions possess all the features of chronic inflammation. It has been demonstrated that atherogenic lipoproteins such as oxidized low density lipoprotein ( LDL ), remnant lipoprotein (beta-VLDL) and lipoprotein [ Lp ] ( a ) play a critical role in the pro-inflammatory reaction, whereas high density lipoprotein ( HDL ), anti-atherogenic lipoproteins, exert anti-inflammatory functions. In cholesterol-fed animals, the earliest events in the arterial wall during atherogenesis are the adhesion of monocytes and lymphocytes to endothelial cells followed by the migration of these cells into the intima. It has been shown that these early events in atherosclerosis are triggered by the presence of high levels of atherogenic lipoproteins in the plasma and are mediated by inflammatory factors such as adhesion molecules and cytokines in the arterial wall. The development of genetically modified laboratory animals ( transgenic and knock-out mice and transgenic rabbits ) has provided a powerful approach for dissecting individual candidate genes and studying their cause-and-effect relationships in lesion formation and progression. The purpose of this article is to review the recent progress regarding the inflammatory processes during the development of atherosclerosis based on both human and experimental studies. In particular, we will address the mechanisms of atherogenic lipoproteins in terms of inflammatory reactions associated with hypercholesterolemia. Understanding the molecular mechanisms responsible for inflammatory reactions during atherogenesis may help us to develop novel therapeutic strategies to control, treat and prevent atherosclerosis in the future.

These articles also suggest the connection between atherosclerosis and immunity, why not autoimmunity

 

The immune response in atherosclerosis: a double-edged sword

• Göran K. Hansson
•  & Peter Libby

Abstract

Immune responses participate in every phase of atherosclerosis. There is increasing evidence that both adaptive and innate immunity tightly regulate atherogenesis. Although improved treatment of hyperlipidemia reduces the risk for cardiac and cerebral complications of atherosclerosis, these remain among the most prevalent of diseases and will probably become the most common cause of death globally within 15 years. This Review focuses on the role of immune mechanisms in the formation and activation of atherosclerotic plaques, and also includes a discussion of the use of inflammatory markers for predicting cardiovascular events. We also outline possible future targets for prevention, diagnosis and treatment of atherosclerosis.

Adaptive immunity and atherosclerosis.

Andersson J¹, Libby P, Hansson GK.

Abstract

Atherosclerosis involves the formation of inflammatory arterial lesions and is one of the most common causes of death globally. It has been evident for more than 20 years that adaptive immunity and T cells in particular regulate the magnitude of the atherogenic pro-inflammatory response. T cells also influence the stability of the atherosclerotic lesion and thus the propensity for thrombus formation and the clinical outcome of disease. This review summarizes our current understanding of T cells in atherogenesis, including which antigens they recognize, the role of T cell costimulation/coinhibition, and their secretion of pro- and anti-inflammatory mediators. Furthermore, we outline future areas of research and potential clinical intervention strategies.