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.
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I found a paper, well, an abstract, discussing familiar hypercholesterolemia and diet from 1993:
https://pubmed.ncbi.nlm.nih.gov/8213496/
Check out the first few lines:
The principal goal of dietary treatment of heterozygous familial hypercholesterolemia (hFH) is the reduction of the plasma low density lipoprotein (LDL) cholesterol. This is best accomplished by enhancing the activity of LDL receptors and, at the same time, depressing liver synthesis of cholesterol. Both cholesterol and saturated fat down-regulate the LDL receptor and inhibit the removal of LDL from the plasma by the liver. Saturated fat down-regulates the LDL receptor, especially when cholesterol is concurrently present in the diet.
The paper is claiming LDL receptors are down-regulated by cholesterol and saturated fat, inhibiting removal of LDL from plasma via the liver.
Unfortunately paywalls all around these papers so I can't read it. Figurative paywalls around my attention span and understanding of such complex matters don't help.
It seems to be saying that saturated fat inhibits the LDL receptor, but especially when cholesterol is already present in the "diet." Return to Peat's article on cholesterol:
Stress accelerates the oxidation of the polyunsaturated fatty acids in the body, so people who consume unsaturated vegetable oils and fish will have some oxidized cholesterol in their tissues. The constant turnover of cholesterol in the tissues tends to lower the proportion of the toxic oxidized degradation products of cholesterol, but in hypothyroidism, the use of cholesterol is slowed, allowing the toxic forms to accumulate.
It really just looks like the self-perpetuating cycle over and over again. It's way over my head, but Peat seems to be suggesting the toxic forms accumulate because low metabolic rate.
Of course, the abstract later says:
The optimal diet for treatment of children and adults has the following characteristics: cholesterol (100 mg/day), total fat (20% of kcal, 6% saturated with the balance from omega-3 and omega-6 polyunsaturated and monounsaturated fat), carbohydrate (65% kcal, 67% from starch), and protein (15% kcal).
65% carb, 20% fat, 15% protein. But the fat ratio is reversed favoring mufa and pufa.
Another finding in the results related to pufas and hypertriglyceridemia: pufa to lower LDL.
https://pubmed.ncbi.nlm.nih.gov/233943/
https://www.jci.org/articles/view/107930
This really is a can of worms. But I'm interested in this because of the "genetic" markers that may or may not exist and have causation and all of the other factors shaping cholesterol ideology.
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@Corngold said in When is high LDL cholesterol not dangerous?:
Unfortunately paywalls all around these papers so I can't read it.
https://sci-hub.st/https://doi.org/10.1016/0002-9149(93)90010-a
Figurative paywalls around my attention span and understanding of such complex matters don't help.
Fair, we are said to "pay" attention. For new domains I found it helpful not to try and understand at that moment. I'd just read, sleep, be patient, go back and read it again.
These two aren't on sci-hub unfortunately.
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@GreekDemiGod said in When is high LDL cholesterol not dangerous?:
What truly causes heart disease?
Very good question.
Is it PUFA?
Certainly seems to prime for it. But why would there be conflicting studies and variability in real life.
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@GreekDemiGod said in When is high LDL cholesterol not dangerous?:
please consider the case of familial hypercholesterolemia. it seems that very elevated levels of LDL (over 300-400) are indeed dangerous.
Hi
See the interview of Chris Masterjohn by Chris Kresser on the first link
Chris Masterjohn interviewed by Chris Kresser. Transcript of a video. Part I
https://chriskresser.com/the-healthy-skeptic-podcast-episode-11/
Comment1 :
No need to read if you don't suffer from gene defect or leptin insensibility (inducing overweight).
No need to read if you already master the fake news from the cholesterol hypothesis (Ancel key) and the lipid hypothesis (induced by corn and soy oils).
OxLDL is the problem not LDL.
Interesting however if you want to "realize" that your health-practitioner is going to measure lipoproteins in the blood, not the kind, the amount and the state of your cholesterol.
I cite: "So the numbers that you’re getting are the amount of cholesterol that is contained within each lipoprotein. But the lipoprotein itself is not cholesterol; it’s basically a carrier or transporter."
Excerpt 1:
what happens in the lipoprotein particle in order to cause atherosclerosis is the polyunsaturated fatty acids in the membrane of the lipoprotein particle are oxidized, and this basically means molecular degeneration, the molecules are falling apart. And once they oxidize they become toxic and in order to protect the blood vessels from these toxic degenerated lipids, the immune system comes along and forms an atherosclerotic plaque. That’s basically a protective mechanism but over time if you get accumulation of these toxic lipids you get inflammation, other sources of oxidative stress, these plaques fall apart causes a clot and this is what ultimately leads to a clot in the blood and then a heart attack.
Excerpt 2:
So once we realize that it’s about the degeneration of these lipids, then we can start to understand what are the metabolic factors that effect the degeneration of lipids, and how do we move beyond our understanding of the amount of cholesterol in the blood to how do we protect these lipoproteins from degeneration.
Excerpt 3:
So what we really wanna understand about fats is that saturated and monounsaturated fat are the ones that are fairly stable and therefore they’re protective, and polyunsaturated fats are the risky ones because they’re so delicate.
Excerpt 4:
LDL receptor activity
The main way the liver regulates blood cholesterol levels is by expressing the LDL receptor making bile acids, and excreting those bile acids into the intestines. (...) The LDL receptor is going to respond to the needs of the body as well as the needs of that cell. Now the needs of the body are primarily communicated by thyroid hormone. And above thyroid hormone we seem to have leptin. (...) I know there’s things that control leptin, but in terms of communicating this abundance signal leptin is like the CEO of a company or the commander in chief of the armed forces. Thyroid hormone is like a general, so thyroid hormone is under the hierarchy of leptin but it’s the main signal that’s communicating this fact that times are abundant, it’s time to ramp up our energy, our virility, our fertility, time to reproduce and do all of these great things.
(...)
[When there is a problem], that signal is not getting where it needs to go there’s miscommunication in the body. I think that’s a major role in LDL receptor activity. (...)
Excerpt 5:
About hypercholesterolemia
There’s no totally safe, totally effective way to normalize LDL receptor activity in these folks. So what we can do is try to improve the things that we can most impact, and that’s the oxidation of the LDL particle to some degree, but to an even larger degree it’s preventing the inflammation and pro-clotting environment that comes downstream from the formation of the atherosclerotic legion. (...)
When I say antioxidants I do not mean something specific like blueberries. I mean the wide spectrum of antioxidants that are found in fresh, whole animal and plant foods. (...)
Source:
Chris Masterjohn on cholesterol, as possibly cause of heart disease, and the degenerative lipid hypothesis. 2015
Google search with:
Chris Masterjohn on cholesterol and interviewed by Chris Kresser and Transcript of a video. Part I
