Tried with paleo (meat and veggies) as I thought the carbs were the culprit and I decreased the frequence of the accidents.
Finally I went carnivore and within a week I had zero symptoms. I was strict carnivore for 8 weeks (lost 8kgs) then I tried reintroducing other food but without great success.
These days I eat mainly butter, eggs and steak and I've been good for 2.5 years now (I was eating organs too at first but I don't really feel any difference if I don't eat them). Eating the occasional sweet from a bakery makes me feel a bit bloated. Eating some fruit For 1.5 years eating vegetables would cause the diarrhea to reappear, after 1.5 years I can eat vegetables occasionally without problems. It's like a "limit" got reset or something.
The other thing cholesterol is used to make, also quite nice to have, is bile. Used for fat digestion and such. A lot of bile. From a lot of cholesterol. Seems like a waste though, to excrete all that finely synthesized bodily chemical. BUt aha, the body realizes this and so resorbs it. THus there is a cycle and recycle of cholesterol and bile. Aha! What if we can trick the body to not resorb it and just release it. Such a drug has been developed. Well, hard to call it a drug. There is no fanciness, no elegant molecular binding to an esoteric receptor, no, nothing of the sort. It's called metamucil, and as the name tells us, it mostly works by being a big chonky mucinous blob of very impressively thick goop. The "magic" of how it works is literally the bile gets trapped in the thick goop and excreted. And thus we've bled off some bile from the cholesterol recycling loop, and thus, cholesterol. And that's why this weird blobby old person fiber supplement is cholesterol magic.
Certain famous men in the past smoked pipe all day and lived very long lives. E.g. Winston Churchill and Bertrand Russell. Do you have any theories on why smoking didn't harm them as much. Do you think back then there might not have been some interaction factor that's prevalent today, etc.?
Cholesterol is the principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. — https://en.m.wikipedia.org/wiki/Cholesterol
I thought it was obvious, hence the original broad quote, but the bizarre Wikipedia response made me think that perhaps I wasn’t clear enough. Hence the clarification with my follow up.
What’s the evidence for the claim “cholesterol by itself isn’t harmful?”
I thought it was obvious, hence the original broad quote, but the bizarre Wikipedia response made me think that perhaps I wasn’t clear enough. Hence the clarification with my follow up.
So for clarification on your view - do you think that high levels of LDL-C (proxying for ApoB) increase risk of CVD?
What I think is that your behavior is quite strange, to create a fake profile just to post a link "debunking" the author. Do you have something personal against her?
And then when you got corrected, in place of recognizing you said something wrong, you double-down your irrational behavior: "shadow boxing against an imaginary interlocutor". Yeah because the original interlocutor makes stupid questions.
By "imaginary interlocutor" I was referring to a misreading of the parent reply, not mine. This was the person who said: "Anyone else have alternative takes on cholesterol based on personal experience?"
The question is then whether when that person said "alternative takes on cholesterol" they meant "alternative takes on the function of an individual molecule of cholesterol" and not "alternative takes on the significance of high serum cholesterol". Considering their next two bullet points refer to high and low levels of serum cholesterol, I thought it was fairly obvious.
Apparently it wasn't for some people, and those same people are then claiming that making this clear is some sort of dodge/goalpost shift/deceptive behaviour. But it clearly isn't. If you read the above, where someone was obviously referring to high serum cholesterol, and in response someone says "cholesterol by itself isn’t harmful", is it reasonable to quote that claim and ask for evidence, by which you mean "I want evidence that high serum cholesterol isn't harmful"? If it is reasonable, which I believe it is, then no deception, goalpost shifting or correcting has actually taken place here.
The full pathway and supporting evidence can be found here: https://academic.oup.com/eurheartj/article/41/24/2313/573522...
If a patient is already accumulating arterial wall damage then it might be necessary to limit serum cholesterol through dietary changes or statins or something. But I would claim that those interventions usually come too late, and that most of the damage can be prevented through other interventions thus making serum cholesterol levels less relevant.
It's like if you have a truck driving around full of toxic waste. Maybe that's cause for concern, but if you can take other measures to ensure it won't crash and spill the cargo then maybe it's fine.
These factors may increase the effect of high LDL-c on CVD, but I’m not sure on what basis we should assume that those without them aren’t at risk from high LDL-c.
Some people live a long time with high(er) fat diets and no heart disease; Cardiologist Dr William Davis[1] selling his heart-scan plan using non-invasive CT scan / calcium measuring as a proxy for atherosclerotic plaque buildup claims that cholesterol is "virtually worthless" for predicting heart disease, and that taking statins or cutting the fat in your diet measurably "does nothing" to affect that measure of plaque buildup. Your suggestion is that cutting fat should do something. He claims his plan of removing wheat, grains, using fish oil, fixing inflammation and insulin resistance, various vitamins and minerals, can measurably stop plaque developing and it can reduce. That seems like it should be a very testable claim.
I haven't read his books, don't know the details of his plan, but if calcium is a solid proxy for plaque buildup, and a CT scan can measure it stay the same in people who switch to low-fat diets, and measure it drop in some people who don't but instead remove grains, that suggests plaque buildup from LDL only takes place in some individuals who eat fat, not all. Arterial wall injury or inability to repair damage are they possible reasons? Or the inflammation and insulin resistance he mentions?
[1] https://drdavisinfinitehealth.com/2019/03/why-you-should-get...
CAC scores (which it sounds like what you’re referring to) only look at calcified plaque, but not soft plaques. So there’s a whole category of risk that is missed by them. People’s CAC only tends to go up when they’re in a very late stage of atherosclerosis, and calcified plaques also tend to be more stable than soft plaques, so if two individuals had the same mass of plaque, but one’s was soft and the other’s one’s hard (sorry for the “carry on cardiology”) then we’d actually expect the individual with the CAC score of zero to be at greater risk of a CVD event.
It’s my interlocutor’s burden to show that arterial wall damage and/or an individual’s inability to repair damage is required for ASCVD to take hold, and so far they’ve yet to meet it. That’s what I’m looking for, basically.
From what I could gain in the paper you linked in another comment, they write that apoB with less LDL in it goes more easily into the arterial wall, apoB with more LDL in it causes more damage once in the arterial wall, and those two effects cancel out, so overal more LDL is worse.
These things don't add up to a coherent picture. If eating less fat reduced LDL, that should reduces plaque buildup (by your claims and your study's claims) and that should reduces heart disease risk, and that should show up in the CAC scans. And apparently it doesn't. If eating more fat increases LDL and that increases heart disease risk, that should show up in Dr Davis' CAC scans and he should think that worsens heart disease risk, and he doesn't.
> "But this being the case does not serve as evidence that arterial wall injury or an inability to repair damage is required in order for high serum cholesterol to be a risk."
It doesn't, and I don't make that claim. So I have no more comment. Agree that it's multifactorial (or appears that way).
[1] https://myheart.net/articles/ct-coronary-artery-calcium-hear...
Your Dr Davis just appears to be one person saying something is the case, without providing any evidence for it. I don’t see why we should believe his claims that serum cholesterol is irrelevant over the incredibly robust evidence I’ve brought to the table.
I agree that the two things don’t add up, but why wouldn’t we then just favour the higher quality evidence? Seems like Davis is a quack with historical form for just making things up without any evidence in order to sell a product: https://www.healthyeating.org/blog/detail/rdn-s-book-review-...
I don't think Dr Davis has said serum cholesterol is irrelevant, the statement I linked is that dietary fat removal doesn't stop CAC score increasing.
Why we should believe him is that he's got a feedback loop with a measuring machine. Science is about settling abstract arguments by testing them against the real world, right? So you can dismiss Paul Mason by saying he's an idiot, he can't read, he's looking at old studies, and he's a sports medicine doctor so he's not treating heart disease anyway, but Dr Davis is actually a cardiologist and he gets a patient with a heart problem, he takes actual measurements (CAC score) then gives advice to change their life, then sees them again for followup over years and years, measures again and sees the results. The measurement is not based on whether he is smart or stupid, it's not affected by which studies he's citing.
He's a quack selling a book? The US Bureau of Labour says Cardiologist is the highest paying job in the USA[2]. He could just as easily be shilling low-fat books instead of low-carb books so that makes no sense that he would be shilling a book which goes against his findings instead of one which goes with his findings. Why does he need to shill any product - his financial incentive is do do more treatments, more stents, more bypass surgery, prescribe more statins for pharma kickbacks.
Could he be totally wrong, and his patients are dying en-masse, and others are leaving him to go to another cardiologist for bypasses, and other patients are eating something different and lying to him - I'd actually believe it, yes, but who knows. If we go with that he appears to have found something which reduces his patients' need for surgical intervention over years and decades, then it seems that the biggest things to affect heart disease risk are metabolic syndrome et al, and they appear to have far more effect on serum fats than dietary fat intake does, and far more effect on fats-causing-plaque-buildup than dietary fat does. Less fat in the blood is better, is something your links claimed, and that can also be something Dr Davis would agree with through insulin resistance improvements; as I asked in my other comment, I have no idea what the link there actually is.
At this point serum LDL seems important, dietary fat intake might be but it seems less important/effective as a way to modulate serum levels than fixing other diesease processes does?
[1] It says: "Results A total of 23 759 symptomatic patients, of whom 12 771 (54%) had a CAC score of 0, were included. Overall, the prevalence of obstructive CAD was relatively low across all age groups, ranging from 3% (39 of 1278 patients) in those who were younger than 40 years [..] In patients with obstructive CAD, 14% (725 of 5043) had a CAC score of 0, and the prevalence varied across age groups from 58% (39 of 68) among those who were younger than 40 years" - how can there be 39 people with CAD under fourty in total and also (__ of 68) under fourty with CAD and zero score? Where did the 68 come from?
[2] https://cardiovascularbusiness.com/topics/healthcare-managem... (I don't know why they don't say "CEO" but whatever, it's a high paying job, he doesn't need to be shilling anything).
Your response was "Some people live a long time with high(er) fat diets and no heart disease". But this is not evidence that atherosclerosis only takes place in individuals with arterial wall injury or without the ability to repair damage. That could equally be evidence that some people are genetically less predisposed to arterial retention, regardless of arterial wall injury, for example. There are plenty of hypotheses that negate your proposed one that are equally likely on the evidence you've provided. So this whole thread is just a tangent that doesn't engage with the core question. That said, here goes:
My point on CAC was that your entire argument hinges on being able to look at a CAC score and say "this score is a reliable indicator of whether a person has coronary artery disease". But if you're under 40 and actually have CAD, there's a 58% chance that when you get your test results back, it will show 0 CAC (even though you have CAD!). So demonstrably, CAC is a poor proxy for CAD, and so a lynchpin proposition in your argument is clearly false. Whether the numbers look different when read a different way is irrelevant. The above is true, and demonstrates how CAC is not a reliable metric.
> I don't think Dr Davis has said serum cholesterol is irrelevant, the statement I linked is that dietary fat removal doesn't stop CAC score increasing.
Literally from the article you linked: "Can you look at your cholesterol and say “Oh, my cholesterol is 240. I must have heart disease.”? No, of course not — cholesterol is virtually worthless when it comes to predicting heart disease"
So he says exactly that, unless you're willing to quibble over a semantic difference between "virtually worthless" and "irrelevant".
> Why we should believe him is that he's got a feedback loop with a measuring machine
It's not just "why should we believe him", it's "why should we believe him over meta-analyses of RCTs, and other high quality data?" Look at where "expert opinion" and "case reports" (which is the evidence you're citing, if we're being generous) sits relative to the MAs of RCTs that I'm bringing to the table on the hierarchy of evidence (https://en.wikipedia.org/wiki/Hierarchy_of_evidence). It's not clear to me why you're throwing out robust evidence with comparatively low risk of systematic bias and relying on bottom-tier evidence instead. Can you please explain to me why this is a superior epistemic framework?
> He's a quack selling a book?
Yes. I'd take a quack to be anyone wearing the coat of science while violating the standards of modern science. Whether or not he stands to gain (or cares about) the money his book makes isn't relevant to that claim, it's based entirely on the nature of what he has to say/publish.
Indeed, going back to the previous point, dismissing the enormous body of high quality evidence showing LDL cholesterol is a causal agent in atherosclerosis by referring to serum cholesterol measurement as "virtually worthless" merely because of his own personal experience, with the plethora of biases that entails, is textbook quackery. The fact that he's published a pop science book that blames many of the ills of the world on wheat with no evidence to back up such an assertion is just the cherry on top.
So I don't need to speculate why he's a quack, and his salary doesn't alter my point. Maybe he does it because being a number one bestseller satisfies his ego in a way nothing else can. Maybe having that accolade means he can charge more for his cardiology services, so there's an indirect financial benefit. Maybe he genuinely believes wheat is the devil's food? I don't really care, my point is that his output suggests he's not a sound practitioner of the scientific method.
Your entire argument here seems to boil down to "there's this guy who sees patients and he says they're not leaving his practice and they're getting better, how would he have patients if everything he says about heart disease wasn't true?" This is wild, the kind of arguments I see from homeopathy advocates. We should always aim for the evidence base most likely to be free from bias. That is not one clinician's account of how they do things.
From your study link: "Introduction .. Coronary artery calcium (CAC) that is assessed by computed tomography is reliable in evaluating the future risk in both asymptomatic and symptomatic patients with stable coronary artery disease (CAD)".
They call it "unmatched".
OK it isn't perfect, that doesn't make it poor. Still instead of "can it miss something", the other way around - if the CAC score measures something is it always definitely plaque buildup? Because then repeated CAC scores have the potential to be good for telling if plaque buildup is changing over time in response to dietary changes in people with non-zero scores and CAD.
Fine with him saying cholesterol is worthless, yes.
> ""why should we believe him over meta-analyses of RCTs, and other high quality data?""
Because when someone you don't like cites multiple meta-analyses of RCTs you handwave it away with a Twitter thread where he "runs away from an argument chef's kiss". I know of Ben Goldacre's Bad Science, I see plenty of HN links about the reproducibility crises in science about the ways of p-hacking and manipulating data, about the broken incentives to publish and get funding, about the complexities of statistical analysis, things I can't argue through. Medical experts are incentivised to push treatments, academic experts are incentivised to push dodgy results, it's not easy for people who like and care about this stuff to say what's "high quality data" or isn't, let alone me. One can't handwave away measuring the amount of plaque buildup in the heart and say "that's not a measure of the amount of plaque buildup in the heart" as easily. If people change X and their heart health measurably improves, and X isn't reducing dietary fat, that should mean something.
> "Your entire argument here seems to boil down to"
My argument was less about Dr Davis himself and more as a way to bring the CAC score in and to say Dr Davis says the CAC score isn't affected by removing dietary fat. That's a testable claim. That's much nicer than "this expert says that expert is wrong" or "this paper says that paper is wrong". You don't believe Dr Davis, well, presumably somewhere is a researcher or practitioner who has done many CAC measurements and has studied whether cutting dietary fat changes the score or not, at this point I am not going to look for it.
I am interested in the things you've said and linked, and my opinions have changed, but I think I'm well past what I am able to follow or interested to continue.
Ok, that's unfortunate but obviously your prerogative! I will try to post some more lay-friendly links in this response that may convey my points more straightforwardly.
> if the CAC score measures something is it always definitely plaque buildup? Because then repeated CAC scores have the potential to be good for telling if plaque buildup is changing over time in response to dietary changes in people with non-zero scores and CAD.
No, it can measure plaque density. Additionally, since calcified plaques are more stable than soft plaques, it can actually go up while risk goes down. We see this occur on some statin regimes, where we have boatloads of data showing statins reduce risk, yet we can see CAC scores go up as soft plaque is stabilised into calcified plaque.
I'm not saying CAC is without its merits, but you are stretching credulity beyond breaking point to suggest that because one cardiologist claims that reducing dietary fats doesn't show a reduction in CAC scores, it therefore disproves the lipid hypothesis. CAC has too many caveats to use it to make such bold inferences, even if we get to the wild epistemic standards required to think one cardiologist's claims are sufficient to overturn decades of well-conducted research. Additionally, as I've stated elsewhere, it still wouldn't be evidence that arterial wall damage or inability to repair damage is required for ASCVD, which, let's remember, is the reason we're even talking about this in the first place.
There's quite an interesting discussion about the pros and cons of the CAC here. Suffice to say, it's not suitable to stand up the kind of arguments you're making: https://www.youtube.com/watch?v=gxIeRUbHauw
> Because when someone you don't like cites multiple meta-analyses of RCTs you handwave it away with a Twitter thread where he "runs away from an argument chef's kiss"
No, that's not why I dismiss Mason's claims. I dismiss Mason's claims because he says "this meta analysis says this" and then when you look at the MA it says nothing of the sort. It's false to claim that I'm handwaving away the evidence itself.
> I know of Ben Goldacre's Bad Science, I see plenty of HN links about the reproducibility crises in science about the ways of p-hacking and manipulating data, about the broken incentives to publish and get funding, about the complexities of statistical analysis, things I can't argue through. Medical experts are incentivised to push treatments, academic experts are incentivised to push dodgy results, it's not easy for people who like and care about this stuff to say what's "high quality data" or isn't, let alone me. One can't handwave away measuring the amount of plaque buildup in the heart and say "that's not a measure of the amount of plaque buildup in the heart" as easily. If people change X and their heart health measurably improves, and X isn't reducing dietary fat, that should mean something.
I think it's really worth taking a second to think about what you're saying here. Some points of order first:
- The reproducibility crisis is about some fields of science re-running individual studies and finding that when they do so, they cannot reproduce the original findings.
- p-hacking is about altering the methodology of a study post-hoc to generate statistically significant findings when such findings were not present under the original methodology.
- the objection of the complexities of statistical analyses, I presume, is an objection based on the fact that when using statistical analyses to try to account for confounders and systematic bias, sometimes these analyses are poorly conducted and thus fail to mitigate these biases.
- "Medical experts are incentivised to push treatments" is presumably an objection that individuals publishing papers may have an implicit or explicit bias that causes them to over or understate the significance of a given finding, or record data incorrectly.
So your argument appears to be: "Ok, so you've provided evidence that LDL is a risk for CVD based on over 200 prospective cohort studies (that is, the results have been successfully produced literally hundreds of times), mendelian randomisation studies, and randomised controlled trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events. However, I believe it's likely that if we were to re-run those studies again, we would not be able to reproduce those results.
“I'm also concerned that p-hacking and systematic bias is so consistently prevalent within all of these studies that it affects the summated findings so profoundly, and consistently in the same direction, that we cannot trust the findings to be accurate. Additionally, the individuals conducting these studies are all incentivised to push treatments and therefore we should believe it to be more likely than not, without any evidence to actually demonstrate this, that these individuals are biasing the results because of these incentives.
“It's not easy for lay people like me to ascertain whether these data from the top of the evidence hierarchy (that is, the evidence least likely to be affected by bias) are high quality, so we have to find a source of evidence that is less likely to be affected by such bias. To achieve this, I propose that we throw all the above data out, and instead trust the claims of a single cardiologist, who's written a blog post on his website about how serum cholesterol is irrelevant when it comes to cardiovascular disease risk.
“After all, p-hacking can't take place when the evidence is so poor that there are no p-values, calculations of statistical significance, or even recorded data from which one could calculate p-values.
“After all, you can't make errors in your statistical analyses if you don't perform any statistical analyses.
“After all, your attempts to control for bias can't go wrong if you don't attempt to control for bias.
“After all, 'One can't handwave away measuring the amount of plaque buildup in the heart and say "that's not a measure of the amount of plaque buildup in the heart" as easily. If people change X and their heart health measurably improves, and X isn't reducing dietary fat, that should mean something,' despite the fact that there are studies that do measure plaque buildup in the heart and show that it is affected by serum cholesterol. I believe that we can handwave it away when it's published in a peer reviewed journal, but we can't do so when it's a blog post on a cardiologist's website. This is the most reliable way to make sound scientific inferences.”
I don't even understand how one can reach these conclusions. I've tried my absolute best to interpret what you've said generously, but there's only so much I can do given material like this.
This whole line of reasoning is also far closer to what you’re accusing me of - instead of discussing what the data show, we should just “trust the experts”. We can’t analyse Dr Davis’ data because he doesn’t even provide any, but we should just assume he’s telling the truth because he’s a cardiologist and therefore so well paid that he has no motivation to be wrong. We should ignore the evidence I’ve provided because it’s harder for laypeople to understand than this supposed expert just saying “trust me, I ran some CAC tests”.
> presumably somewhere is a researcher or practitioner who has done many CAC measurements and has studied whether cutting dietary fat changes the score or not, at this point I am not going to look for it.
I've already provided you even better evidence than that: a pooled analysis of studies where SFA is replaced with PUFA and cardiovascular events and coronary deaths are reduced. You don't need to go looking, I gave it to you: https://pubmed.ncbi.nlm.nih.gov/19211817/. If you want a more consumable version, here's an excellent podcast on it (all their stuff is good, you should see if there's anything else there of interest to you: https://sigmanutrition.com/episode481/).
It's a shame, but not entirely surprising that you no longer desire to continue the discussion. Fundamentally, I think you will always run into issues until you re-assess your underlying epistemic framework when it comes to assessing evidence. Until you do so, reading studies will be largely pointless as you have no reliable tools to interpret those studies. You're running before you can walk.
If you're interested, the Cut Through Nutrition podcast is quite a nice primer on how to think about nutrition science research, I'd highly recommend working through the episodes. Once you've internalised the concepts, it becomes a lot easier to see how quacks like Mason and Davis are operating, even without a great deal of domain-specific knowledge. Podcast is here: https://podcasts.apple.com/gb/podcast/cut-through-nutrition/...
Have a good week!
> "If there are any other causes of obstructive CAD other than fats getting into the artery walls, those cause would all have to be in that group as well (I don't know of any but I can speculate several)."
Here's one speculation of lay-person reasoning:
- Cosmetics people like Retinol skin creams because it makes skin look better. That's a fact that people recommend it.
- One way it does this by making it plumper, which smooths out wrinkles. I think that's a fact.
- It does this by increasing skin cell "turnover", i.e. what it does at the epithelial layer is trigger stem cells to split, making more skin cells, making thicker skin. That's a claim I've seen and am not sure if it's a fact, but it's a plausible mechanism of action.
- We eat retinol in our food, in the form of Vitamin A, that's a fact.
- Vitamin A gets through the guts into the body, that's a fact - it couldn't be a vitamin if it passed straight through us and out.
- Vitamin A gets into the blood stream; fact, there are lab tests of serum retinol levels.
- Vitamin A in the blood is supposed to be wrapped in Retinol Binding Protein to carry it through the blood, but it isn't always. It's normally captured by the liver, and released from the liver wrapped in RBP, but not all of it is captured by the liver and is free in the blood stream. The more of it in the diet, the more gets past the liver, the more of it is free in the blood stream. I've seen it claimed, have no sources to back it up.
- Blood vessels have an epithelial layer on the inside, an internal skin. Claim.
- Retinol in the diet -> retinol in the blood -> triggers stem cell split in the blood vessel walls -> thickening of the walls ("youthful!") -> narrowed blood vessels. Speculation.
(What do we have in this random link[1] I haven't read? "Until recently, it was thought that the sole important retinoid delivery pathway to tissues involved retinol bound to retinol-binding protein (RBP4). More recent findings, however, indicate that retinoids can be delivered to tissues through multiple overlapping delivery pathways, involving chylomicrons, very low density lipoprotein (VLDL) and low density lipoprotein (LDL)" - retinol is not only able to split stem cells, it's a pretty potent molecule in various forms; "Retinoids and immunotherapy may be used to treat high-risk or recurrent neuroblastoma" says Canadian Cancer Society; there's one bro-science connection for increased total LDL -> increased blood vessel damage which is nothing to do with the LDL per-se, but something it carries along with it. Something we eat a lot of as Vitamin A and carotenoids, something the US and Canada fortify flour and low-fat dairy and margarine with, which is another tie-in to both low-wheat and low-fat diet).
[Edit: it isn't relebant; thickened walls would be non-obstructive CAD].
Pregnant women have extremely high cholesterol (ridiculously high).
- There's a theory that if evolution designed pregnant women to have high cholesterol, then cholesterol cannot be the poison it's made out to be.
Cholesterol levels rise during second and third trimesters, but it’s not true at all to say that all pregnant women have “ridiculously high” cholesterol. Around 24% of women who have normal range cholesterol will go over the normal range for a few months, but it’s not accurate at all to say they all have “ridiculously high” cholesterol
Here is a good overview: https://pmc.ncbi.nlm.nih.gov/articles/PMC4989641/
Cholesterol metabolism is related to hormones that change during pregnancy, so downstream fluctuations in cholesterol aren’t surprising. Do not mistake this for intentional evolutionary pressure to increase cholesterol.
> if evolution designed pregnant women to have high cholesterol, then cholesterol cannot be the poison it's made out to be.
This is an incredibly pseudoscientific way of thinking. Pregnancy puts many pressures on the body, not all of which are good.
Did you know that blood coagulability also rises during pregnancy, which is clearly linked to cardiac events. There is an increased risk of cardiac events during pregnancy.
Saying “X happens during pregnancy therefore X must be good” is an extremely unscientific and uninformed take. I’m not surprised it’s being leveraged by the cholesterol truthers, but it’s wrong. This is the level of reasoning that seems to appeal to people on TikTok and Twitter who consume feel-good science in 15 second clips, but it makes anyone who has read any actual research on the subject depressed at how susceptible people have become to bad science that is dangerous to their health.
A few years ago, I have been diagnosed with incipient atherosclerosis. This was an unpleasant surprise for me, so I have immediately made serious changes in the food that I eat.
At that time, I was eating very high quantities of dairy, which has a high proportion of saturated fat.
Because I could not see any other factor that could cause the atherosclerosis, I have eliminated dairy from my food and I have changed completely the composition of the fats contained in my food.
I eat only food that I cook myself, so I know exactly which is the composition of the fat contained in it. Nowadays, at least 90% of my daily intake of fat comes from a combination of oils that I use when cooking food (typically 60 mL of extra virgin olive oil + 20 mL of cold-pressed sunflower oil + 10 mL of cod liver oil + 1 drop of an oil containing D3 and K2 vitamins).
Instead of any other kinds of dairy, now I use only a cheese substitute that looks and tastes like melted cheese, but it is made from whey protein concentrate (which has almost no fat) mixed with some vegetable oil and a few other ingredients for better flavor.
After changing completely the fatty acid profile of my fat consumption, after a year the symptoms of atherosclerosis have disappeared and there have been also other very noticeable signs of improved cardiovascular health. For instance, previously, I had cold feet and when sleeping I had to take care to keep them warm. Some months after changing the diet, they had become warm (presumably due to improved blood flow) and I have no longer needed any protection against lower temperatures.
So my diet change has very certainly improved a lot my health in a relatively short time of no more than a year, and that has persisted for the last three years. I cannot know if this is really caused by the change in the fatty acid profile, but I cannot see any other significant difference, except if the abundant dairy that I was eating before contained some other harmful substance or if the significant increase in the amount of eaten EV olive oil and cold-pressed sunflower oil has provided some benefits beyond the better fatty acid profile.
Logically, it is plausible that a reasonable amount of saturated fat, which is correlated with the amount of physical work, should not have any harmful effect.
As long as you burn enough calories daily to use all the fat intake for energy, it should not matter if that fat is saturated fat. However, when the fat is not completely used and some of it is deposited, then it is plausible that it is preferable if oleic acid (mono-unsaturated fatty acid) is the most abundant in food, because in normal conditions this is the most abundant fatty acid in the human reserve fat. When other fatty acids are much more abundant than oleic acid, they must be processed and converted before storage and the capacity for the conversion may be overwhelmed.
The negative connotations for "seed oils" are not applicable to all seed oils, but they refer only to the seed oils where linoleic acid is the most abundant acid.
Linoleic acid is an essential nutrient, but the need for it can be satisfied with 15 to 20 mL per day of a suitable seed oil, like sunflower oil. A greater daily intake than that can cause problems, because the excess linoleic acid must be converted into other fatty acids and also because some of its derivatives have physiological roles for which an excess quantity is not desirable.
Given these, it seems plausible that some fat composition is preferable to others. Like I said, I have acted on this assumption and it has worked very well for me, even if the real mechanism cannot be known, at least not yet.
Obviously the resulting obesity from consuming excess calories is a risk factor for CVD in itself, but the body of evidence would suggest that someone consuming >10% E from SFA, even if they’re in caloric equilibrium, will be at greater CVD risk than someone consuming less, all else held equal.
The main mechanism by which SFA is thought to increase CVD risk is by downregulation of LDL receptors, which occurs during the digestion/absorption of SFA, and is not a result of excess SFA hanging around in the body in some way. If you consume SFA, this pathway will be in play, regardless of how much is burned vs stored.
There’s no good evidence that seed oils/linoleic acid, refined or not, pose a risk for humans. There’s a lot of talk on the subject about on social media, but it’s almost entirely speculation based on animal studies.
I once bought the anti seed oil line, but on closer investigation of the evidence I changed my view and have replaced most of my SFA intake with MUFA/PUFA, mostly in the form of canola and olive oil.
However, it seems very implausible (or impossible) that humans evolved to need, or benefit from, industrially processed sunflower seeds and olive oil.
How has the total fat in your diet changed? I find it much more plausible that dramatically reducing cheese, cream, whole milk and full fat yoghurt has helped, than that replacing 20mL of cream with 20mL of sunflower oil has helped. It sounds like you have reduced fat overall - why then attribute the benefit to the vegetable oils / fat profile, specifically?
In general it matters what you replace the saturated fat with, though: you should replace it with unsaturated fat. Replacing it with carbs/simple sugars can apparently elevate LDL cholesterol and triglycerides: https://pmc.ncbi.nlm.nih.gov/articles/PMC2943062/
Olive oil is good, candy is bad. (News at 11.)
So if you’re, say, a vegan with very little cholesterol intake then adding some would result in significantly higher serum cholesterol. However, for most people in western populations, they’re already above the point where the effect tails off, which is why dietary guidelines generally don’t focus on dietary cholesterol anymore.
These aren’t alternative theories, they’re just reductive takes that try to ignore the big picture.
Reductive takes are really seductive for people who want to reduce everything into “good” or “bad” categories, but the body doesn’t work like that.
The part that confuses people is that the message has been simplified to “cholesterol bad” for so long that people are confused to discover that cholesterol is actually used by the body. Upon discovering these facts, reductive logic switches from “cholesterol bad” to “cholesterol good”, which is just as reductive.
The truth is that cholesterol is useful within the body, but that doesn’t mean that more of it is better. Despite all of the proponents of alternative theories trying to spin a different story, the bottom line is that cumulative lifetime LDL exposure is still correlated with heart disease.
That is the only thing you need to know about the debate if you want to reduce it to something simple. More LDL over time means more heart disease. A lot of people will try to “well actually…” various things around this, but it’s true.
Even the comments below are trying to tell you your own observation is impossible (that diet can’t affect cholesterol levels) when that’s clearly not true.
Cholesterol has become a hotbed of alternative medicine that doesn’t follow the science but sells well on social media. Don’t put too much confidence behind “alternative theories” when we have decades of evidence that 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.
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/
... in the Standard American Diet. Dr Paul Mason's video "The truth about high cholesterol"[1] at 9:40 he cites a study showing that increasing levels of "light buoyant undamaged LDL" do not correlate with increased heart disease risk over 15 years and 11,000 subjects. Then at 10:20 shows study results that increased levels of oxidised, damaged, small, dense LDL do correlate with increased heart disease. IIRC it's damaged by oxidation, glycation, plant phytosterol cholesterol-mimics (driven by increased seed oil consumption) and involved with disruption to lipid rafts which some medications cause, e.g. statins and anti-psychotics.
That talk is 1 of 3, they are here:
[1] The Truth about high cholesterol: https://www.youtube.com/watch?v=rdgS3PuSuyg "can we tell if we have normal or damaged LDL? Yes"
Part 2: The shady truth about statins: https://www.youtube.com/watch?v=I7r4j1u42V8& (studies showing they do lower cholesterol, and that doesn't lower the risk of heart disease).
Part 3: "Hard science on the real cause of heart disease - why you should avoid seed oils" - https://www.youtube.com/watch?v=-xCr3mvFCHM
[2] A comment I've made before about his views on saturated fats generally: https://news.ycombinator.com/item?id=32966148 linking to his talk "Saturated Fat is not dangerous" - https://www.youtube.com/watch?v=NUY_SDhxf4k
"Why your doctor thinks cholesterol is bad" - https://www.youtube.com/watch?v=j-nq60_oEIc
Paul Mason is a renowned spreader of misinformation on this topic (and many others). My favourite moment of his is when he tried to teach a clinical research scientist that the lipid hypothesis was false, and in doing so revealed that his entire argument against the lipid hypothesis was based on an undergraduate-level misreading of a study, after which he just ran away from the conversation instead of admitting he was wrong. Absolute chef’s kiss moment, enjoy: https://x.com/avibittmd/status/1335491375073271808?s=46
Since I don't have the knowledge to read this, why is this review better than the multiple review papers Dr Mason cites in the videos I linked?
> Absolute chef’s kiss moment, enjoy: https://x.com/avibittmd/status/1335491375073271808?s=46
This just says "it is so" and a page of numbers; X won't let me read the thread because I have no account, so... what is so? What intervention? What outcome is it showing? And how are they doing a six year study measuring people's daily energy intake down to 0.2 of a Calorie?
This is because a given individual with the same amount of lbLDL-c as someone else’s sdLDL-c (that is, mass of cholesterol in both), the person with the same mass of sdLDL-c will have more ApoB tagged lipoproteins and therefore more risk. But when we stop using LDL-c as the measure, and use ApoB, which is what lipidologists now recommend, then the risk from large and small LDL particles is more or less the same. That is, one particle of sdLDL carries about the same risk as one particle of lbLDL.
If you’d like something more consumable, lipidologist William Cromwell covers the topic very well in this video: https://youtu.be/kplh30RmYo8?si=WvDMwG-Z82voxDMp
It’s not hard to make an X account, but ok. I can link to the individual posts so you can have a laugh: Mason said the entirety of the lipid hypothesis was challenged by the fact that those randomised to reduced fat diets had a higher risk of dying in the 2006 WHI RCT: https://x.com/drpaulmason/status/1335411781557075968?s=46
It was pointed out to him that the lipid hypothesis is about P:S ratio, not total fat reduction: https://x.com/avibittmd/status/1335470882987323392?s=46 Avi explained the criteria a study would need to meet to challenge the LH: https://x.com/avibittmd/status/1335475024854192129?s=46 There’s some back and forth, eventually Mason says the rebuttal that WHI failed to significantly reduce serum cholesterol/was a failed intervention because it targeted total fat doesn’t make sense because the intervention arm of the WHI reduced their serum cholesterol by 30%,so clearly the intervention was significant according to the LH: https://x.com/drpaulmason/status/1335488114534481920?s=46 Avi asks him what he’s talking about, the serum cholesterol between intervention and control was basically the same, showing the table in the study: https://x.com/avibittmd/status/1335488453417562112?s=46
Avi suggests he might have confused serum cholesterol with dietary cholesterol: https://x.com/avibittmd/status/1335489121486299138?s=46 They share the table from the study that confirms this: https://x.com/avibittmd/status/1335491375073271808?s=46
And then Paul, previously so headstrong and sure he was nailing everyone on this one, just peaces out from the conversation (or runs away, if you were to be less generous). His entire argument against the lipid argument was based on misreading dietary cholesterol as serum cholesterol. So good. No one should take him seriously, he’s either purposefully deceptive or completely incompetent at reading the evidence. Don’t see why anyone interested in reaching the truth should be interested in his arguments in either case.
That Twitter exchange; separate from the lipid hypothesis bit, are you saying in summary that Avi is not contesting the claim that the reduced fat group had a higher heart attack risk, only contesting which fat was reduced? They intervention group reduced dietary cholesterol by 30% and that didn't change their serum cholesterol at all and they had higher heart attack risk?? How does that track with your comments about you reducing your dietary fat, why are you if doing that doesn't change serum levels or death risk? That seems to track what Dr Davis says about CAC scores and reducing dietary fat not helping them.
From out here in layman's view, what people on many different sides are saying is about insulin resistance and metabolic syndrome being more important (and more modifiable). Say as a layman chain of reasoning: if most cholesterol in the blood is made by the liver rather than by diet, if one use for cholesterol is to shuttle repair materials to damaged sites around the body, if chronic inflammation is a sign of widespread low grade damage which needs lots of repair, if some of that damage is caused by glycation, if insulin resistance means more free blood glucose not being taken into cells so there's more in the blood to cause more damage, if damage is also caused by oxidised and rancid fats, if unsaturated fats oxidise more easily... then reducing (sugars, simple carbs, unsaturated fats) in the diet should result in reduced insulin resistance, in less damage, in lower levels of chronic inflammation, therefore in less cholesterol produced by the liver, in lower blood LDL of any size, in less cholesterol to be damaged and less free glucose to damage it, therefore in less plaque buildup, lower heart disease risk.
(At no point here am I saying "more fat is better" in absolute terms; I don't think that adding butter onto a takeaway makes it healthier).
Re: the twitter conversation: the diet heart hypothesis is specifically about replacing saturated fat with polyunsaturated fat. If you just reduce overall fat, you may even be making that P:S ratio worse. In the case of the WHI it means that the study is essentially null by default on that issue.
Dietary cholesterol is an interesting one - basically there is a significant effect of dietary cholesterol on serum cholesterol, but only when you go from very low to low levels. After that, the effect tails off dramatically. So in the general population you might not expect a 30% reduction to make a significant difference.
Additionally, you have to consider the overall picture. Maybe the reduction in dietary cholesterol did have a small beneficial effect, but the fact that the intervention group ended up with lower PUFA consumption than the control group meant this reduction was overshadowed by that effect.
There’s no evidence that oxidised fats in unsaturated fats are a cause for concern for health. Aside from that I don’t think stringing together a bunch of mechanisms and speculating about them is a particularly useful way to carry out science.
What we care about is actual outcomes from actual interventions. So yes, I agree that in those with metabolic disease and insulin resistance, we should address this issue. The evidence seems to suggest this is best done by losing weight. If there’s a certain dietary pattern that helps someone do that, great. If it’s a GLP-1 agonist, go for it. Whatever works.
But we also know that fat quality affects CVD risk too, and by a decent amount. So within whatever dietary pattern one settles on, replacing SFA with PUFA would also be a good idea. We can do both!
Ugh.
> "There’s no evidence that oxidised fats in unsaturated fats are a cause for concern for health."
https://openheart.bmj.com/content/5/2/e000898 says: "The low-density lipoprotein (LDL) oxidation hypothesis gained traction during the 1980s because it was noted that in general, native unoxidised LDL does not cause foam cell formation. In other words, LDL had to become oxidised first in order for atherosclerosis to develop [..] what causes LDL to become oxidised in the first place? It was later discovered that the oxidation of LDL was initiated by the oxidation of linoleic acid contained within the LDL particles [..] a more comprehensive theory, the ‘oxidised linoleic acid theory of coronary heart disease’, is as follows: dietary linoleic acid, especially when consumed from refined omega-6 vegetable oils, gets incorporated into all blood lipoproteins (such as LDL, VLDL and HDL) increasing the susceptibility of all lipoproteins to oxidise and hence increases cardiovascular risk [..] cholesterol was protected from oxidation if bound to saturated fat but susceptible to oxidation when bound to linoleic acid"
That is condeming oxidised serum fats, not oxidised dietary fats, but it appears to be condemning "omega-6-rich vegetable oils" in the diet because they are more likely to oxidise in the body(?). I'm guessing if they are already oxidised when eaten that matters, because the only way it couldn't matter is if we deconstructed fats we eat and rebuilt them completely from scratch and if we did that completely then none of any of this would matter. The link's Box 1 has 29 points criticising those fats, Box 2 has 1 point in their favour "reduces total cholesterol and LDL".
> "Aside from that I don’t think stringing together a bunch of mechanisms and speculating about them is a particularly useful way to carry out science."
Well I'm not gonna understand biology, chemistry, lipid science to the level of a PhD researcher, PhD statistician, medical doctor, or an interested smart amateur biologist/chemist, myself. If I also can't have a bro-science chain of layperson reasoning, then your position boils down to "Science is only for experts, and only the experts I choose, not those they believe the wrong things so they're quacks, trust me" which is .. disagreeable.
> "What we care about is actual outcomes from actual interventions."
We can't see those until people don't die of heart disease fourty years later. This is why I'm so on the side of Dr William Davis because the CAC score seems to be the only good non-invasive measure of plaque available, something which can show an almost direct outcome of intervention on plaque. Whereas "serum LDL went down" is easily measurable but doesn't show if plaque formation is slowed, stopped, reversed, or unchanged. I also think that if low-fat did avoid or reverse heart disease, the massive international push over the last 50 years for low-fat foods would have made it absolutely clear, and instead heart disease is up up up. Doubling down on "people simply didn't eat low-fat yoghurt hard enough, do that harder" is just so unconvincing.
> "But we also know that fat quality affects CVD risk too"
When you say fat quality, do you mean PUFA vs SFA? Or do you mean things like presense of Glyphosate, trans-fats, contaminations in the food chain, things ordinary people mean by quality?
> "and by a decent amount. So within whatever dietary pattern one settles on, replacing SFA with PUFA would also be a good idea. We can do both!"
You've made a strong case that reducing serum cholesterol would be a good idea. Not such a strong case that reducing dietary fat would be a good idea. And not much case at all that replacing SFA with PUFA is a good idea. Let's be clear that I'm lost in the details of SFA, PUFA, linoleics, Omegas, LDLs/HDLs, triglycerides, cholesterols, which ones are more important, which ones are a tiny effect but easier to study or more interesting to study. When someone is 150lbs overweight and insulin resistant and never does an exercise it can't possibly come down to wibbling over whether they ate two slices of bacon vs half an avocado, or whether they put butter or margarine on a scone that one time. On the other hand if someone is Mark Sisson[1] a lean former ironman runner and paleo/low-carb enthusiast who got famous for eating a "big-ass salad" everyday, who does intermittent fasting, eats salmon and leaves with avocado oil dressing for lunch, then a ribeye stake with asparagus and avocado for dinner, no snacks, no desert, who cares about health, is he at risk of heart disease because he put heavy cream in his one coffee of the day and has red meat on his plate instead of nutloaf?
I guess you're suggesting to remove a daily Starbucks coffee with whipped dairy cream and sugar, right? No-brainer, I would agree.
But telling Mark Sisson to replace that steak with tofu? He has solved or avoided so many other problems people have with food - no food cravings or hunger, he's not overweight, he's not fatigued or big swings of energy, he's unusually healthy for someone in a Western country at his age (50s IIRC) that he's gotta be doing a lot right, not a lot wrong. He's gotta be somewhere close to a good human diet even if that is too much meat to eat every day for other reasons.
> That is condeming oxidised serum fats, not oxidised dietary fats, but it appears to be condemning "omega-6-rich vegetable oils" in the diet because they are more likely to oxidise in the body(?)
We can just bypass that entire speculation, because to get there we've already made a logical leap, namely assuming that oxLDL is even something we should care about. All the evidence suggests that the oxidation of LDL almost entirely occurs within the arterial wall (https://pmc.ncbi.nlm.nih.gov/articles/PMC2924812/). When LDL is retained, oxidation is practically inevitable. The important thing is number of ApoB tagged particles.
So what would we expect to see in the real world if this hypothesis (that oxLDL is not an independent risk factor) was the case? Well, presumably if we adjusted oxLDL for ApoB, we would see the risk association disappear, since all oxLDL would be doing is just proxying for "amount of LDL", and the oxidation itself is not driving the risk. What do we actually see when we do this? When we perform a mutual adjustment of oxLDL and ApoB, and the association of risk from oxLDL disappears: https://pubmed.ncbi.nlm.nih.gov/16949489/ So even if the speculation that PUFAs increase oxLDL count were valid (and I'm not granting it is), it would appear to be irrelevant as far as risk of CVD goes.
> your position boils down to "Science is only for experts, and only the experts I choose, not those they believe the wrong things so they're quacks, trust me" which is .. disagreeable.
That's not my position at all. Please try to employ the principle of charity when interpreting my position, or this is going to be very slow going, and likely unproductive.
My point is that when you look at mechanisms, you're peering at one tiny part of a process of thousands (or more) moving parts. Just stringing together a bunch of those mechanisms into a narrative doesn't provide any kind of sound basis for making an inference about human health outcomes because it ignores every other mechanism at play. For example: mechanistically, exercise induces oxidative stress. I could do as you did above and string it together into a theory about how exercise is bad for your health, but I hope you'd agree that I'd be making a false inference.
My point is not that we then throw our hands up and say "I guess I'll leave science to the experts". I never said that. I said we have to base our inferences off the summation of all the mechanisms at play.
How do we do that? By looking at human outcome data (prospective cohort studies, mendelian randomisation, RCTs). Why don't we think exercise is unhealthy, despite the oxidative stress mechanism? Because we have human outcome data that shows the benefits of exercise. That is, we look at the exposure we're interested in (exercise) and the outcome we actually care about (say, mortality, or cardiovascular disease). Do people who exercise more have lower mortality rates when potential confounders are accounted for? If so, we have good reason to believe exercise is beneficial. This is how we should look at replacing SFA with PUFA. When we do that, what happens to the things we actually care about (heart disease, mortality etc)? Overwhelmingly, we improve outcomes. Why should we prize mechanisms above human health outcomes? It doesn't make sense to me.
> When you say fat quality, do you mean PUFA vs SFA?
Yes.
> Let's be clear that I'm lost in the details of SFA, PUFA, linoleics
The position I take is: - There seems to be a point, around 10% total energy from saturated fats, where risk increases significantly. Either side of that, changes to SFA still make a difference, but not to the same degree. - When it comes to reducing SFA, replacement is important. Replacing SFA with PUFA seems to be the most beneficial approach.
In prospective cohort studies, each 5%E from SFA replaced with PUFA resulted in a 13% lower risk of CVD events, and a 26% reduction in coronary deaths. In RCTs, we see a 21% reduction in CVD events when substituting PUFA in for SFA (https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD...). In general the reduction in risk seems to come out at about 20-30% depending on study characteristics. Considering CVD is one of the top killers in the Western world, I think that's something worth paying attention to.
I am so confused. What on earth is a " dense Low-Density-Lipid" ?
Please help me understand whether or not this is an oxymoron?
I tried to come up with a corollary but the best I have is “jumbo shrimp”. Sigh.
It's a term people use, e.g.
"Small Dense Low‐Density Lipoprotein Cholesterol Is the Most Atherogenic Lipoprotein Parameter in the Prospective Framingham Offspring Study" - Hiroaki Ikezaki MD, Elise Lim PhD, L. Adrienne Cupples PhD, Ching‐Ti Liu PhD, Bela F. Asztalos PhD, and Ernst J. Schaefer MD; Journal of the American Heart Association - https://www.ahajournals.org/doi/10.1161/JAHA.120.019140
do you know the parable of the drunk gentleman looking for his keys under a streetlamp at night? a policeman asked him where did he drop his keys, he pointed at a dark alleyway further away, so the policeman asked why he didn't look there instead, he replied "well there's no bloody light over there".
is it possible that you were deficient in some other nutrient, possibly even a trace one like some metal ion or maybe just some amino acid, and that's what caused the improvement in symptoms when you started eating flesh again? is it possible that you simply enjoyed the taste and then felt better about yourself? or any number of other changes in your life at the same time - taking more time cooking your meals, learning new recipes, trying new spices with it, etc?
LDL doesn't mean much, but rather the ratio of HDL:LDL. Low cholesterol is bad for the brain. Of course these are oversimplified statements.
There are known cases of older men with low testosterone level and high LDL, who after testosterone replacement therapy experienced a significant decrease in LDL. It's thought that the liver kept churning cholesterol in attempts to synthetize enough testosterone to no avail.
I believe that depression and cognitive dysfunction is a side-effect of too low cholesterol when people take statins, especially older folks, but excessive LDL also accumulates in arteries and lead to hypertension and/or diminished blood flow to organs, which itself leads to dementia, heart attacks, etc.
Some alternative theories I've come across:
- There's a theory that cholesterol is good for you. It's necessary for brain functioning. Low levels of "bad" cholesterol have been linked to depression.
- There's a theory that the high levels of cholesterol in blood clots found around ripped arteries may be due to the body trying to heal a rupture with cholesterol.
- There's a theory that seed oils and table sugar, which have only been mass consumed for the last 100 years or so, are what cause heart disease.
Personally, I have a very high level of both good and bad cholesterol. They shot up after I started eating a lot of non-veg food. And after they shot up, I stopped having depressive episodes.