Xinggang Wang Profile picture
Sep 26, 2021 13 tweets 4 min read Read on X
1/11 LDL-C is not the main cause of atherosclerosis! We all know that endocrine disorders will produce endocrine diseases, metabolic diseases, cardiovascular diseases, and even tumors! Many hormones in our body are steroid hormones. Many of these hormones come from cholesterol. Image
2/11 Why “demonize” a basic nutrient in the human body? What is the differences of cholesterol in aorta, coronary artery, carotid artery, middle cerebral artery, arteriole and vein? And why is the incidence in these blood vessels so different?
3/11 Why atherosclerosis is much more severe in the muscular arteries than that of aorta and smaller arteries? Not obvious in the veins? Is cholesterol the main cause? There is basically no concentration difference of various components in the blood in these continuous pipes!
4/11 One said: “Do you drink too much water, which leads to physical obstacles? Can you say that water is toxic? The so-called “model” of mice with high-fat diet is completely different from human atherosclerosis in pathology.
5/11 Granulation tissue repair induced by vascular media injury / dysfunction is the main mechanism of human atherosclerosis.This new theory subverts the traditional atherosclerosis hypotheses and can perfectly explain the characteristics of human atherosclerosis.
6/11 Traditional hypotheses prefer schematic diagrams, lack human pathological evidences, and cannot explain clinical practice. 10 References as follows:
7/11 1. Haemodynamics of atherosclerosis: a matter of higher hydrostatic pressure or lower shear stress? Cardiovasc Res 2021;117(4):e57-e59.
doi.org/10.1093/cvr/cv…
2.Myofibroblast Forms Atherosclerotic Plaques. bioRxiv 2020:2020.07.20.212027.
biorxiv.org/content/10.110…
8/11
3.Medial Injury/Dysfunction Induced Granulation Tissue Repair is the Pathogenesis of Atherosclerosis. arXiv 2020:2010.06683.
arxiv.org/abs/2010.06683
4.Atherosclerotic Plaque Healing. New England Journal of Medicine 2021;384(3):293-293.
nejm.org/doi/10.1056/NE…
9/11
5.Spontaneous Coronary-Artery Dissection. NEJM 2021;384(11):1077-1077.
nejm.org/doi/10.1056/NE…
6.Hypertension Aggravates Atherosclerosis: A Matter of Pressure Remodeling of Myofibroblasts or LDL Accumulation? JACC 2021;77(20):2619-2620.
doi.org/10.1016/j.jacc…
10/11
7.
Promising Etiological Treatments of Artery Diseases
dx.doi.org/10.13140/RG.2.…
8.
Macrophages Transform into Foam Cells by Phagocytosing Tissues Formed by Myofibroblasts
dx.doi.org/10.13140/RG.2.…
11/11
9.
Steroid Hormones Affect Vascular Diseases through Myofibroblasts
dx.doi.org/10.13140/RG.2.…
10.
Atherosclerosis
dx.doi.org/10.13140/RG.2.…

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More from @xinggang_wang

Sep 15, 2022
1/6 Some say that "low-density lipoprotein cholesterol (LDL-C)" is the culprit of atherosclerosis. However, a general survey of people (not just inpatients) found that LDL-C has nothing to do with coronary heart disease. The lower the LDL-C, the higher the all-cause mortality.
2/6 Some say that "inflammation" is the cause of atherosclerosis. I say that it is only a risk factor, because in patients with vasculitis, if myofibroblast remodeling is not repaired enough, they would form aneurysm instead of atherosclerosis.
3/6 Some say that "thrombus" is the cause of atherosclerosis, but I don't think so, because venous thrombosis is easy to form and blood flow is slow, but "venous atherosclerosis" in situ is very mild.
Read 6 tweets
Mar 30, 2022
1/4 One: A person has myocardial infarction whose low density lipoprotein (LDL-C) is 8.1mmol/L. There are no other risk factors except high LDL-C. Therefore, LDL-C causes atherosclerosis.

I: What causes the high LDL-C ?
zotero.org/groups/4523215…
2/4 Is it a criminal when something is present? For example, BNP is high in patients with heart failure. Does BNP lead to heart failure? An old man fell and you helped him. Did you say you fell the old man?
3/4 The increase of LDL-C is the compensatory response of the body to the metabolic disorder of LDL-C. It Is the metabolic disease that leads to the dysfunction of vascular smooth muscle cells, which leads to the vascular tunica media dysfunction.
Read 5 tweets
Dec 1, 2021
1/5 If you cannot see the essence, you like making nonsense... People who can see the essence of things in a few seconds and people who cannot see the essence of things all their life are destined to be different lives. Some people live to be 100 years old.
2/5 They still think that human nutrients such as lipids are the cause of atherosclerosis. They never consider why atherosclerosis of the same blood vessel in less than 1cm away is so different.
3/5The atherosclerosis of the epicardial artery proximal to myocardial bridging is very serious, while the coronary atherosclerosis in the myocardial bridging is very mild. After a lifetime of angiography, they saw countless such images, and they would not consider this problem.
Read 6 tweets
Nov 9, 2021
1/3 I want to ask: Is there injury to the endocardium? Is there injury to the intima of the aorta? Is there any injury to the smaller artery? This is a continuous pipeline. Why do lipids selectively deposit in large muscular arteries,
2/3 there is no lipids deposition under the endocardium, and there is less lipid deposition under the intima of aorta and smaller arteries? Do lipids have eyes? Lipid with larger molecules can be deposited under the intima.
3/3 Can smaller molecules such as water, sugar and amino acids be deposited under the intima to form dissection? Should intimal injury form dissection or lipids deposition?
Read 4 tweets
Nov 7, 2021
1/4 Q: How is intimal injury caused? Is there only lipid deposition after injury? Why can't smaller molecules such as water, sugars and amino acids be deposited? According to the knowledge of physics and chemistry, dissection should be formed instead of lipids deposition!
2/4 How to explain with the authority hypotheses?

A: Low shear stress and turbulence lead to intimal damage. We only care about lipids, not about the deposition of water, sugar and amino acids!
3/4 Q:Where the shear stress is low, the blood flow velocity is low, and the blood flow velocity at the turbulent position is high. How to explain this contradiction? Are there only lipids in the blood vessels? Don't think about anything else? Are these the authority hypotheses?
Read 5 tweets
Nov 7, 2021
1/5 Some people say that lowering LDL-C below 1.4 will reduce MACE events by 20%. If I give an example, I would let them respond without words immediately. For example, patients with acute heart failure, BNP also decreased after reducing heart failure.
2/5 Can you say that heart failure is treated because of reducing BNP? Markers and causality are two different things! LDL-C is related to atherosclerosis, but it is not causality , because the lower the LDL-C, the milder their metabolic diseases are.
3/5 It is because lipid-lowering drugs divide the risk of atherosclerotic diseases, so there will be such a result. Correlation and causality are not the same thing! It is similar to BNP, because BNP can stratify heart failure!
Read 7 tweets

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