https://lmgtfy.com/?q=Atherosclerosis

"When plaque (fatty deposits) clogs your arteries, that’s called atherosclerosis."

~ American Heart Association (https://www.heart.org/en/health-topics/cholesterol/about-cho...)

"Atherosclerosis is a disease in which plaque builds up inside your arteries....Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood."

~ https://www.nhlbi.nih.gov/health-topics/atherosclerosis

"Atherosclerosis refers to the buildup of fats, cholesterol and other substances in and on your artery walls (plaque), which can restrict blood flow."

~ https://www.mayoclinic.org/diseases-conditions/arteriosclero...

-sclerosis is a hardening. E.g arthrosclerosis for a hardening of joints.

The hardening in atherosclerosis is caused directly and exclusively by atheroma.

https://www.mayoclinic.org/diseases-conditions/arteriosclero...

An atheroma, or atheromatous plaque ("plaque"), is an abnormal accumulation of material in the inner layer of the wall of an artery; it is present in the arteries of most adults.[1] The material consists of mostly macrophage cells,[2][3] or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.

https://en.wikipedia.org/wiki/Atheroma

"Plaque" and "atheroma" are synonyms in the context of cardiovascular health.

Also, both quotes together go to show the ongoing misconception. Nowhere in the first quote are macrophages and other WBCs mentioned (but they are in the second, luckily). I guess this is what happens when you use quotes from different sources, too.

"While the early stages, based on gross appearance, have traditionally been termed fatty streaks by pathologists, they are not composed of fat cells but of accumulations of white blood cells, especially macrophages, that have taken up oxidized low-density lipoprotein (LDL)."

So whilst it may be more accurate to say they are white blood cells that fed on LDL (and presumably contain fatty substances as a result) there is a long tradition of calling them fatty substances, and there is at minimum a connection to fat.

It seems misleading to try to discount the role of the fat to me. They don't sound like they are just normal white blood cells. Is there any doubt that the fat plays a causative role? I know a couple of cardiologists who say it is clear. Do you have some references for the idea that fat is not relevant?

Regarding the mechanism of atheroma formation, I don't have a list of references handy, but maybe this is a good start: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3152836/

Also of interest would be the role of high insulin and/or glucose and the damage they can cause to the arterial walls (inflammation is a necessary condition in the formation of atheroma).

Which part of that paper disputes the importance of fat?

Immune cells kill using peroxides, superoxides and other free radicals. Anyone with an over-active immune system that's triggered easily — allergies, chronic stress, sub-optimal sleep, genetics, exposure to pollutants, metal ions etc¹ — you're better off reducing immune system activity.

So yes, eat less fat but also focus on the immune system. A study found 29% of Japanese babies less than 1 year old had fatty streaks and they were not spending the first 11 months chugging slurpies and McDs.⁴

TL;DR: Dietary fat and adipose tissue/adipocytes involved in AS are two different things⁵, and try not to get oxidized to death by a glitchy immune system while busy chasing fats or the latest fad diet. Fats are just one piece of the puzzle.

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¹Mechanisms of LDL oxidation: http://sci-hub.tw/10.1016/j.cca.2010.08.038

²This means sleeping better, reducing stress, taking anti-oxidants, reduce insulin triggers i.e., reduce food with IF/ADF/CR³ and reduce carbs

³Intermittent Fasting/Alternate-Day Fasting/Calorie Restriction. This study finds ADF to be superior to CR; if you can stick to it, that is: Differential Effects of Alternate-Day Fasting Versus Daily Calorie Restriction on Insulin Resistance — http://sci-hub.tw/10.1002/oby.22564

⁴https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812791/ - conjecture is the mothers were smokers, see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644569/ for more info. Pollution should be focused more strongly when it comes to heart health, the evidence is clear.

⁵Any excess energy gets stored as fat, so reduce fat intake but increase protein or carb intake to compensate? No dice, the body will generate fat for you in the form of adipose tissue which will lead to AS in the presence of an unregulated immune system.

I've done elimination diets and had blood tests to determine foods I react to. I've also met with nutritionists to create meal plans. But over the long term I tend to gravitate back to foods that my family and friends tend to eat which includes stuff that jacks up my immune system (kid didn't finish her mac and cheese? I'm on it!...visit my Italian mom? pasta time!)

So how do you keep to what you know you should do when other people in your life are doing things to the contrary?

That said, if I was in your position and if I couldn't tackle the problem in any of the standard ways, I'd take an NSAID like aspirin¹ on "cheat" days to temporarily suppress the immune system as an experiment and see how that works. I found a 1982 issue² of The Lancet where someone had the same idea and reports success with this strategy but I'm not even close to a medical professional and this is just one data point so YMMV, caveat emptor etc, etc.

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¹But not ibuprofen or other NSAIDs, those seem to worsen the problem — https://www.thedailybeast.com/research-shows-link-between-ns.... Aspirin however has its own set of side-effects (bleeding risk, may interact with medication you are already taking etc) so strict diet is still the safest, long-term solution for now.

²http://sci-hub.tw/10.1016/s0140-6736(82)90024-1: 650mg Aspirin, 5-15 mins before meals, not after. Again, this is NOT medical advice, it is just one data point.

https://peterattiamd.com/the-straight-dope-on-cholesterol-pa...

my TL;DR (as a non-doctor): LDL "cholesterol" (actually proteins carrying cholesterol and "fat" (triglycerides) in blood) has a tendency to get "stuck" in artery walls. That causes inflamation, which attracts macrophages which also get stuck, and so on until you get plaques ("clogged arteries") and one plaque breaks off and causes a heart attack. Consuming saturated fat / cholesterol is problematic because it causes a decrease of LDL-sensitive receptors and consequentially more LDL in blood. If I understand correctly, the later part of the previous statement is considered settled science ("we know how it actually works" - 1985 Nobel Prize was awarded for this), while the first part (diet) seems to be somewhat debated and has mostly statistical justification ("evidence suggests") and also depends on an individual's genetics.