Short answer: cholesterol is essential for cell membranes, steroid hormones and bile acids. That does not conflict with the evidence that LDL-containing apoB particles play a causal role in atherosclerotic cardiovascular disease.
The earlier version of this article argued that we had effectively been misled about LDL and that there was “no connection” between bad cholesterol and cardiovascular disease. That statement is not consistent with the totality of genetic, mechanistic, epidemiological and randomized-trial evidence.
Dietary cholesterol is not the same as blood LDL
One useful point from the original article remains true: eating cholesterol and having a high concentration of LDL particles in blood are not the same thing. The body synthesizes cholesterol, and dietary cholesterol often has a smaller effect on blood LDL than people once assumed.
But that observation does not imply that LDL in blood is harmless. Diet can affect LDL through several mechanisms, including saturated fat intake, energy balance, body weight and replacement nutrients.
Why LDL is considered causal
The European Atherosclerosis Society consensus reviewed evidence from pathology, genetics, Mendelian randomization, epidemiology and randomized clinical trials and concluded that LDL particles cause atherosclerotic cardiovascular disease. Risk relates to both the concentration of apoB-containing particles and the duration of exposure.
This is stronger evidence than a simple correlation. People with genetically lower lifelong LDL have lower risk, people with familial hypercholesterolemia have much higher risk, and multiple different drug classes that lower LDL reduce cardiovascular events.
What about dissenting reviews?
The 2018 paper previously highlighted on this page argued against the mainstream interpretation of LDL. Scientific disagreement is worth reading, but one narrative review should not be presented as if it overturns the much larger evidence base. Its conclusions are not reflected in current European dyslipidaemia guidelines.
Can lowering LDL change plaque itself?
Yes, although the effect is usually modest and takes time. Meta-analyses of intravascular imaging studies show regression of coronary atheroma with intensive lipid-lowering therapy. The more important clinical point is that LDL lowering reduces heart attacks, strokes and other major vascular events.
Stress still matters, but through different pathways
Chronic stress can influence cardiovascular risk through blood pressure, sleep, smoking, diet, inflammation and other pathways. It should not, however, be used as a replacement explanation for the retention of apoB particles in the arterial wall.
Bottom line
Two statements can be true simultaneously: cholesterol is biologically necessary, and excessive lifetime exposure to LDL-containing particles promotes atherosclerosis. The useful debate is about individual risk, treatment thresholds, absolute benefit and the best way to lower risk, not whether LDL has any causal role at all.
Sources
- European Atherosclerosis Society consensus: Low-density lipoproteins cause atherosclerotic cardiovascular disease.
- 2025 ESC/EAS Focused Update on dyslipidaemias.
- Meta-analysis of 60 randomized trials: LDL reduction and cardiovascular risk over time.
- Meta-analysis of atherosclerotic plaque regression with lipid-lowering therapies.
Medical information
This article may contain published medical evidence, clinical context, personal observations, or hypotheses. These are not equivalent levels of evidence. See the Editorial & Medical Review Policy and Medical Disclaimer. This content is educational and does not provide an individual diagnosis or treatment plan.
The article is certainly very bright, but I would listen to the story with a certain degree of skepticism. For example, the theory that all vessels (except those for muscles) constrict under stress. Then how to explain that in most cases atherosclerosis can be detected in the aorta, through which blood is directed to the entire body, including the muscles? And what about peripheral artery disease, when atherosclerosis mainly damages the vessels of the legs? In my opinion, you is too fond of advancing your own hypotheses. Although, regarding the fact that fat and cholesterol as such are not the main cause of sclerosis, I agree.
But, in my opinion, more than low self-esteem, this process depends on the intake of carbohydrates and too frequent food intake.
Thank you for your thoughtful feedback, Janis. Indeed, the physiology of blood vessels and the development of atherosclerosis are multifaceted processes that aren’t fully understood.
Regarding the constricting of blood vessels under stress, it’s a generalized statement and does not apply uniformly to all vessels. Certain factors, like the presence of atherosclerotic plaques, the type of vessel, and individual physiological responses, can all affect how vessels react to stress.
As for your question about atherosclerosis in the aorta and peripheral artery disease, you’re correct that these conditions seem to contradict the theory. Atherosclerosis can indeed be widespread and affect various types of arteries throughout the body, not just those in the heart or brain.