When is high LDL cholesterol not dangerous?
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Mainstream medicine/ science says LDL is dangerous, Saturated Fats are bad, citing mountains of evidence. The alternative/ holistic side says that LDL is not dangerous, statins are bad.
My question is: When is high LDL not dangerous?Some will say it's not LDL that causes heart disease, but inflammation. But how to you measure and quantify inflammation?
Others will say it's PUFA, or sugar.
How do I know I am protected from developing heart disease? I am in my early 30s and have an LDL of 140-150.What truly causes heart disease? Is it PUFA?
Also, please consider the case of familial hypercholesterolemia. it seems that very elevated levels of LDL (over 300-400) are indeed dangerous.
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I believe it’s the oxidised cholesterol and yea elevated cholesterol with a lot of oxidative stress is probably a bad thing but Ray often says how cholesterol is protective.
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@GreekDemiGod said in When is high LDL cholesterol not dangerous?:
Mainstream medicine/ science says LDL is dangerous, Saturated Fats are bad, citing mountains of evidence. The alternative/ holistic side says that LDL is not dangerous, statins are bad.
My question is: When is high LDL not dangerous?"When is high LDL not dangerous"? When it isn't oxidized. HDL = "high density lipoproteins"; LDL = "low density lipoproteins"; VLDL= "very low density lipoproteins". Lipoproteins are known to oxidize. The amount of surface area on the molecule determines how much is exposed to oxidation. A bunch of tiny molecules (ldl, vldl) have more surface area than the same volume of large molecules (hdl). So ldl is more prone to oxidation than hdl.
However, this equation does not take into account how polyunsaturated/saturated the molecules are and how much oxidative stress the body is under. Saturated fat is stable, polyunsaturated fat is not stable so is more prone to oxidation.
It's a complicated topic.
Ray Peat on the topic: https://raypeat.com/articles/articles/cholesterol-longevity.shtml
"The recent discovery that the size of the LDL particle is a predominant factor in the development of atherosclerosis is one of those things that the editors and medical professors should find embarrassing.
Smaller lipoprotein particles have a greater surface area exposed to the oxidative factors in the serum, and so are more rapidly degraded into toxic substances. People with larger LDL particles are remarkably resistant to heart disease, and the drug companies are looking for a way to turn their lipoproteins into products. But the conditions that govern the size of the LDL particles are physically and chemically reasonable, and are causing confusion among the doctinaire.
There have been several studies in India showing that consumption of butter and ghee is associated with a low incidence of heart disease; for example, according to one study, people in the north eat 19 times more fat (mostly butter and ghee) than in the south, yet the incidence of heart disease is seven times higher in the south. A study in Sweden found that the fatty acids in milk products are associated with larger LDL particles (Sjogren, et al., 2004).
In a 35 day study, when butter (20% of the calories) was compared to various kinds of margarine (with more trans fatty acids) in a similar quantity, the LDL particles were bigger on the butter diet (Mauger, et al., 2003). But in a study of the habitual diet of 414 people, large LDL particles were found to be correlated with increased intake of protein, animal fat, and trans fatty acids (Kim and Campos, 2003).
In a study of the effect of dietary cholesterol on the atherogenicity of the blood lipids, 52 people were given either an egg diet (with 640 mg. of extra cholesterol per day) or a placebo diet for 30 days. Those whose LDL increased the most on the high cholesterol diet had the largest LDL particle size (Herron, et al., 2004). They concluded that "these data indicate that the consumption of a high-cholesterol diet does not negatively influence the atherogenicity of the LDL particle." A similar study in Mexico found that "Intake of 2 eggs/d results in the maintenance of LDL:HDL and in the generation of a less atherogenic LDL in this population of Mexican children" (Ballesteros, et al., 2004).
The estrogen industry tried to get into the heart disease business several times over the last half century, and they are still trying, but the issue of estrogen's harmful effects on LDL particle size is getting some attention. Estrogen clearly decreases the size of the LDL particles (Campos, et al., 1997). The LDL particles also get smaller at menopause, and in polycystic ovary syndrome, and in preeclamptic pregnancies, all of which involve a low ratio of progesterone to estrogen. But there are still journals publishing claims that estrogen will protect against heart disease, by reducing the atherogenic response in increasingly mysterious ways. Occasionally, people have argued not only that estrogen is the factor that protects women against heart attacks, but that androgens predispose men to heart disease. One of their arguments has been that androgens lower HDL, the "good" form of cholesterol. However, there are many studies that show that testosterone and DHEA (Arad, et al., 1989) are protective against atherosclerosis. The LDL particle size is increased by androgens, and postprandial triglyceridemia is decreased (Hislop, et al., 2001). "
Some will say it's not LDL that causes heart disease, but inflammation. But how to you measure and quantify inflammation?
Others will say it's PUFA, or sugar.
How do I know I am protected from developing heart disease? I am in my early 30s and have an LDL of 140-150.What truly causes heart disease? Is it PUFA?
Also, please consider the case of familial hypercholesterolemia. it seems that very elevated levels of LDL (over 300-400) are indeed dangerous.
Hypercholesterolemia points to hypothyroidism. It most likely has to do with cooking habits (polyunsaturated cooking oils) and possibly environmental toxin load (heavy metals accumulate in the thyroid gland). see here: https://environhealthprevmed.biomedcentral.com/articles/10.1007/BF02931255 Multiple toxins are known to increase oxidative stress; heavy metals, mercury in particular, are problematic. see here: https://www.mercuryfreekids.org/hg-poisoning-sources
Regarding cholesterol, see this Ray Peat article (again) https://raypeat.com/articles/articles/cholesterol-longevity.shtml
"Almost 100 years ago, some experiments in Russia showed that feeding rabbits cholesterol caused them to develop atherosclerosis, but subsequent experiments showed that rabbits are unusual in responding that way to cholesterol, and that even rabbits don't develop atherosclerosis from cholesterol if they are given a supplement of thyroid (Friedland, 1933). By 1936, it was clear that hypercholesterolemia in humans and other animals was caused by hypothyroidism, and that hypothyroidism caused many diseases to develop, including cardiovascular disease and cancer. There was already more reason at that time to think that the increased cholesterol was a protective adaptation than to think that it was maladaptive. " -
Here is an LDL discussion between Saladino and Fave that might be helpful: Paul Saladino podcast: When You Should Worry About LDL Cholesterol with Mike Fave
https://m.youtube.com/watch?v=j6ll4OhTHq0
They talk about true risk for cardiovascular disease, primary versus secondary prevention, lipid lowering drugs, and share their thoughts on a recent podcast episode with Peter Attia.
*Produced by Mountain Valley Media
00:06:08 Blood markers & imaging techniques of metabolic function
00:14:38 Gene mutations
00:20:28 LDL & Plaque burden
00:27:23 Money in statins
00:31:38 Downsides of lowering LDL
01:21:23 The downsides of popular cholesterol lowering drugs
01:41:07 Should we fear heart attacks?
01:45:23 PCSK9 Inhibitors
01:52:43 Risk profile of Statins
01:53:02 Risk vs. reward of Ezetimibe
02:04:02 Primary vs. secondary prevention
"You're changing your past every time you learn something because you become a different organism" Ray Peat
"Everything is changing thru time, whether it's a word, organism, thing. The world around it changes, and so its relationships change"Ray Peat
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@Sunniva Thanks, that video is hepful.
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@Sunniva said in When is high LDL cholesterol not dangerous?:
Here is an LDL discussion between Saladino and Fave that might be helpful: Paul Saladino podcast: When You Should Worry About LDL Cholesterol with Mike Fave
https://m.youtube.com/watch?v=j6ll4OhTHq0
They talk about true risk for cardiovascular disease, primary versus secondary prevention, lipid lowering drugs, and share their thoughts on a recent podcast episode with Peter Attia.
*Produced by Mountain Valley Media
00:06:08 Blood markers & imaging techniques of metabolic function
00:14:38 Gene mutations
00:20:28 LDL & Plaque burden
00:27:23 Money in statins
00:31:38 Downsides of lowering LDL
01:21:23 The downsides of popular cholesterol lowering drugs
01:41:07 Should we fear heart attacks?
01:45:23 PCSK9 Inhibitors
01:52:43 Risk profile of Statins
01:53:02 Risk vs. reward of Ezetimibe
02:04:02 Primary vs. secondary prevention
Looks great. Watching. Thank you.
