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Sadly, the truth is that saturated fat causally increase LDL cholesterol[1] which causally increases the risk for heart disease[2]. [1] Meta analysis of tens o
by anusername 6y ago
Sadly, the truth is that saturated fat causally increase LDL cholesterol[1] which causally increases the risk for heart disease[2].
[1] Meta analysis of tens of RCTs https://www.who.int/nutrition/publications/nutrientrequirements/sfa_systematic_review/en/ https://www.who.int/nutrition/publications/nutrientrequireme...
[2] There are plenty of Mendelian Randomization (MR) studies, studies on the effects of statins, etc.
- JPKab 6y agoIt's yet another garbage regression study observing populations. I'm fully aware that statins work to prevent heart attacks by lowering the LDL in the blood, but that's because they treat a symptom rather than the root cause triggering the body to use lipids to repair arterial walls in the first place. Why does the body deposit lipids on arterial walls? Because when arterial walls get damaged in any way, the body uses lipids to repair them. There is a specific sub-type of LDL that is not dietary in source, called VLDL. Source: https://www.healthline.com/health/vldl-vs-ldl https://www.healthline.com/health/vldl-vs-ldl VLDL is created by the liver in response to consumption of carbohydrates, fructose, etc. It is very important to note that VLDL is NOT created by the liver in response to consuming animal fats. The patty and cheese with no bun won't affect your VLDL amounts. The bun, the fries, and the soda? They will trigger your liver to produce VLDL. VLDL is the chief culprit in damaging arterial walls, and causing general inflammation in the body, when at unnaturally high levels. If you consume juice or soda on any kind of regular basis, your VLDL levels will spike afterwards. After VLDL damages those arterial walls, it, along with normal LDL, will be deposited on the walls and harden. The above explanation is why when people talk about having "high cholesterol", it is often useless in predicting heart attacks. The most important marker on a blood test for predicting heart attacks is the ratio of triglycerides to HDL in the blood stream. Notice that LDL isn't in the ratio. Why? Because the higher the amount of triglycerides in the blood, the higher the ratio, and the more VLDL a person has in their blood relative to HDL. Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664115/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664115/ My point is that: 1) Observational regression studies are often useless, because it's impossible to remove so many factors such as the "doesn't listen to doctors" effect where a person who goes against prevailing medical wisdom and eats red meat will engage in other behaviors that doctors advise against, like smoking. 2) It's not the meat in the meat and potatoes diet that is the root cause of heart disease. No, it's a horrible combination of the two: The potatoes trigger the release of VLDL, which damages and inflames the arteries, and the meat contains normal LDL that typically wouldn't lodge in arterial walls, but is used in conjunction with VLDL by the body to repair the now damaged walls. Eat just the meet? No VLDL. The LDL you consume in the meat doesn't damage the arterial walls. Just a note: In the past, I've been a vegan who consumed zero animal products. I didn't consume a single bite of animal products between 2002-2006. I'm not a blind defender of meat based diets, and I won't pretend that there aren't environmental implications of meat consumption. I just don't think it's useful to allow bad science to get people to eat less meat. I'm formally educated in statistics from studying Applied Economics, and I've worked professionally as a data scientist for 8 years now. I'm keenly aware of how bad these observational regression studies are. I'm not saying don't take them into account or use them, but they really need to be vetted when they conflict with longitudinal studies like Framingham.