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.

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?

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.

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.

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!

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.

1. Q: How does atherosclerosis form?

Authority: Intimal injury / intimal dysfunction, lipid deposition, inflammation, low shear stress, turbulence!

Q: Why can't these hypotheses explain the characteristics of human atherosclerosis, prone sites and non prone sites? 2.Authority: I don't know. These are authority hypotheses!

Q: Are there any evidences of human pathology?

Authority: There is no pathological evidence from human, but pathological evidences from mice and rabbits. The human atherosclerosis is proved by drawing schematic models!

1/4 The time of clinical study can be 1 day, 1 year, 2 years, 3 years, 5 years or 10 years. If a drug is very unreliable, basically useless, or even increases mortality after long use, they will set the experimental time relatively short. 2/4 For example, the clinical trials of PCSK9 inhibitor will not exceed 3 years. In these 3 years, they will try to exclude the cases that are not conducive to good results. Even so, the trumpet is getting smaller and smaller.

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. 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?

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. Why “demonize” a basic nutrient in the human body? What is the difference 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?