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> excessively high cholesterol levels over a lifetime are correlated with heart disease

You're talking about blood cholesterol levels. Yet we're talking about dietary cholesterol. Totally different things, it's now well known that they're unrelated. The cholesterol in our bodies is produced by the liver by a completely different process. The old science is pretty foolish for assuming dietary -> blood cholesterol, as if we didn't have a digestive system. If your point was "stick to the settled science and don't believe the alternatives" you couldn't have picked a worse example.

To the original topic, dietary saturated fat does appear to increase the risk of heart disease by increasing LDL cholesterol. In other words, blood cholesterol is a problem but it's driven, at least partly, by saturated fat intake. High dietary cholesterol food like eggs do not increase serum levels, unless you deep fry them in butter.



They are related, dietary cholesterol does affect serum cholesterol: https://pubmed.ncbi.nlm.nih.gov/30596814/


Experimentally and experientially, saturated fat has no lasting impact on cholesterol levels. Those are genetically determined. https://www.ketogenicforums.com/t/dave-feldman-its-about-ene...

Serum levels of saturated fat are not related to dietary saturated fat intake. https://news.osu.edu/study-doubling-saturated-fat-in-the-die...

What puts a person at risk for chronic inflammatory diseases is excessive polyunsaturated fatty acid intake; in particular, arachidonic acid. Excerpt: "The Mediterranean diet is low in arachidonic acid and rich in healthy fats such as monounsaturated fats found in extra-virgin olive oil (EVOO), nuts and omega-3 fatty acids from fish, which has been shown to lower the risk of inflammation, heart disease, cancer, diabetes and obesity, and other degenerative diseases." https://advancedmolecularlabs.com/blogs/news/new-red-meat-st...

In the middle decades of the 20th Century the heart attack rate was extremely high. Much of that mortality is likely attributable to the release of heavy metals into the environment. Heavy metals such as lead tend to cause arterial plaques to rupture. Excerpt: It must be theoretically expected that there will be a synergistic (multiplicative) interaction between low Se intake (leading to undersaturation of the blood plasma with selenoprotein P), large exposure to toxic heavy metals (which may be expected to lead to simultaneous inhibition of selenoprotein P and extracellular thioredoxin reductase), a high dietary LA/oleic acid intake ratio and high rates of superoxide anion radical production from endothelial NADPH oxidase as causes of more rapid LDL oxidation - with a high rate of LDL oxidation leading in turn to high rates of atheromatosis development. Against this background it is not unreasonable to speculate that excessive exposure to a number of toxic metals from a wide range of different sources may have been one of the main causes of the post-war epidemic of coronary heart disease both in North America and Western Europe. These include lead from car exhaust and from drinking water (especially in the British Isles), as well as mercury and silver from dental amalgam fillings and cadmium from acid rain, commercial fertilizers and tobacco smoke...This hypothesis would appear to be in reasonably good agreement with what is known about the historical curves both for coronary heart disease mortality and for the use of lead as an additive in gasoline in Western Europe, compared to North America. The use of lead as an additive in gasoline started earlier and ended earlier in the United States than it did in the countries of Western Europe. And the epidemic of coronary heart disease has followed a similar time course with both its start and its culmination occurring earlier in the United States than in Western Europe." https://pmc.ncbi.nlm.nih.gov/articles/PMC3031257/




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