Discussion of dietary cholesterol and cardiovascular disease

(B Creighton) #1

I would say definitely. I am 60 and got down to 175 doing keto in the winter time. I allowed the house to be in the 60s to encourage conversion to more brown fat. I did strength training, but not to lose weight, although a gain in muscle may have contributed. One year later I weighed in this morning at 177. At my peak some 5 years ago I was 218. I have changed my breakfast some, and eat higher quality meats for dinner. I love eating cruciferous and green vegetables. Now I eat a lot less root vegetables to stay lower carb. I have never counted my total calories for the day, and actually tried not to cut my total caloric input for any length of time, as I didn’t want to slow my metabolism. Yesterday, I went to a buffet restaurant with my wife to celebrate our 28th, and although I really liked the shrimp rice, I didn’t eat too much of it or the lasagna - I really don’t eat pasta anymore, unless going out. I did have a large plate from the salad bar with kale salad, carrot salad, potato salad, broccoli, sunflower seeds, eggs, etc. With these ingredients I enjoy it without any other salad dressing. This morning I am fasting til dinner, and I know I had excess carbs yesterday. Back to lower carb again. This winter I will probably do stricter keto again, but I always eat some fruit in the form of berries and some greens and cruciferous veggies. That is when I seem to enjoy my food the most and seem to be at my best.

Incidentally, Ancel Keyes lived to be a hundred I believe, but not on his polyunsaturated oil diet ideas. Maybe his Minnesota experiments with corn oil disuaded him from that. He retired to Italy where he used lots of olive oil. I am not so sure that the high cholesterol in eggs is not a concern. I do not worry about it if I cook the eggs fresh out of the shell, but I try to avoid any processed foods containing eggs. Foods like cheap mayonnaise with soybean oil have high levels of very oxidized cholesterol. No cheap powdered eggs for me, etc.

(Bacon enough and time) #2

A number of studies have been done on the effect of dietary cholesterol on serum cholesterol. All of them confirmed Keys’s original work: serum cholesterol is not affected by cholesterol in the diet. If we eat cholesterol, the body uses it and doesn’t make as much. If we avoid eating cholesterol, the body makes more to compensate. This is why (according to Nina Teicholz) the AHA quietly dropped restricting dietary cholesterol from its recommendations.

Now, whether or not we should worry about our serum cholesterol is a different question, although the evidence is pretty conclusive that a low ratio of triglycerides to HDL means low cardiovascular risk, regardless of what LDL is doing. But at least we can eat our eggs, knowing that the amount of cholesterol in them is irrelevant to our lipid numbers.

(Chuck) #3

That is why i have said real food only, no fast food, no highly processed food or highly refined foods, no artificial sweeteners. I love my eggs a few times a week, and I love my red meat too.

(B Creighton) #4

I basically agree with this, but this is the problem imho. If you are eating damaged ie oxidized cholesterol, your body is going to use it… I believe that is half of the problem with processed foods. Their cholesterol is more oxidized. I further believe that LDL our bodies make can be damaged by what we eat, which is a slightly different problem. Either way I believe we can end up with more damaged ie oxidized or glycated LDL. The total cholesterol number may not change much - but that has never been the true issue. It is an erroneous metric. There are plenty of people with “normal”: LDL levels which end up on the operating table for CVD reasons. That is why the AHA gave up on this metric. So what causes them to end up with CVD if it is not the amount of LDL in their bodies? It is the CHARACTER of their LDL that can cause it to get caught in the artery walls. The fact that LDL starting the atherosclerotic process is not really an issue in the science anymore. That is what causes the macrophages to end up there and become foam cells, and begin the inflammation process. Healthy LDL made by the liver is not an issue. It is what happens to it later that is the problem, and that depends on what we eat. LDL is NOT the “bad cholesterol,” but it is the particle that can become abnormal on a diet with lots of processed foods including refined vegetable oils - something I feel most vegans have failed to learn because of the current biases which have existed for decades… I still hear it from vegans like Mic the Vegan. I believe it is a huge problem for aspiring vegans like my wife - who only realize after they bought all those veggie burgers that they are full of gmo soybean oil, and the implications that can mean for their cardiovascular health.

(B Creighton) #5

xactly :slight_smile:

(Bacon enough and time) #6

I’m not sure how that makes sense. Why would our body want to absorb damaged cholesterol? Unless you can quote a couple of studies showing that the body does this, and elucidating the mechanism by which it works, I’m not going to join you in this particular worry.

Also: what on earth are you eating, that damaged cholesterol is part of your diet? A far bigger worry, according to Paul Mason, is plant sterols, which do get absorbed by the body and which replace its own natural cholesterol in cell walls etc., thereby causing problems. (He hypothesises that the “cholesterol” found in arterial plaques may very well be plant sterols, instead of actual cholesterol.)

This is perfectly true. Something like 75% of people presenting in the emergency room with their first heart attack have low or normal cholesterol levels. A dispassionate observer might actually conclude that LDL levels therefore have nothing to do with cardiovascular disease. So you have a choice: either you can swallow the argument of the statin industry, which says, “See! It’s even deadlier than we thought!” or else you can entertain the possibility that perhaps cardiovascular disease might actually be caused by something else.

Let’s think about this: If I told you that eating grapes causes cardiovascular disease, but you observed people who ate plenty of grapes but did not develop cardiovascular disease and plenty of others who developed cardiovascular disease while eating few or no grapes, would you still believe my hypothesis?

Studies such as Ancel Keys’s own Minnesota Coronary Study actually showed a correlation between lower cholesterol and higher cardiovascular disease. Statisticians all agree that such a negative correlation can be taken as proof that A does not cause B (or vice versa). Yet instead of revising their hypothesis, Keys had his name removed from the study, and the other principal investigator withheld publication for almost two decades. The Sydney Heart Study has a similar story.

Research on families with familial hypercholesterolaemia–some of it dating back to the 1960’s–consistently shows that elevated LDL does not correlate with the development of cardiovascular disease. In other words, a little over half the people studied live perfectly normal lives and die at advanced ages of other causes, despite (or possibly even because of) their elevated LDL Their relatives who do develop cardiovascular disease all happen to be the ones who also have genetic variations that make their blood clot more readily. Ravnskov and Diamond have written papers to suggest that hypercoagulability is the root cause behind all cardiovascular disease, and our government-recommended high-carbohydrate diet works very well to increase the coagulability of our blood (glycated haemoglobin, for example, makes red blood corpuscles “stickier”).

I remember well how the first dietary warning was saturated fat. Then it became elevated total cholesterol, then LDL, then there was “good” cholesterol and “bad” cholesterol, and now it’s particle sizes and numbers. But wait! We were wrong–it’s oxidised particles that are the problem. This has all the hallmarks of a failed hypothesis being tinkered with to keep it alive.

The most robust correlation between lipid numbers and cardiovascular disease is the ratio of triglycerides to HDL. A high ratio associates with high risk of CVD, a low ratio associates with minimal risk. This goes hand in hand with the NMR analysis of the particle sizes; a low ratio of triglycerides to HDL guarantees a healthy Pattern A. Another great assessment of CVD risk is the amount of calcified arterial plaque: a low or non-existent Agatston score indicates minimal risk.

I’m sorry to be so long-winded, but I hope some of these thoughts can allay your fears.

(Bob M) #7

This is Malcolm Kendrick’s argument, too: they keep moving goalposts so you can’t ever attack the hypothesis.

(B Creighton) #8

That is of course your prerogative. The science is newer, but relatively unknown. I believe because big food doesn’t want it known and they control a large percentage of the advertising dollars in the MSM. But to try to answer your question, I think science has not shown the why’s yet. My guess is the body absorbs it because we were not designed with eating processed foods in mind. Our bodies just don’t have a mechanism to filter out oxidized or damaged cholesterol. Because you asked, here are some studies on oxidized LDL and atherosclerosis.

and some on omega 6 oils and CVD
Of course processed foods are full of this stuff, so of course, big food is not interested in this science.

You asked me to show the science. Here is mine:
I call poo on Mason’s hypothesis. The science does not support it, but isn’t there to show a particular benefit in regards to LDL yet. However, there is plenty of science out there linking polyphenols to longevity and lower cases of CVD. Yeah, they are the old type correlation studies, but what have you got?
As to “what on earth are you eating, that damaged cholesterol is part of your diet?” Hopefully, a shrinking list of foods. When eating animal products, it simply is not really possible to get away from all oxidation of LDL, but for instance I have stopped eating canned tuna. It is a very highly oxidized food because the tuna is broken up into small chuinks exposed to the air and cooked. Now I eat canned sardines. I prefer Wild Planet, because the sardines are whole with their protective skin on and the ones I buy are packed in extra virgin olive oil. They are quite good, and although I am not aware of testing for oxidized LDL levels, logic dictates their method of preparation is far superior to protect the product from oxidation. Most of the seafood I buy is or was frozen. I prefer to buy it virtually vacuum packed or in the case of shrimp still in the shell and raw. I am positive these shrimp are going to have far less oxidized cholesterol than the open air, pre-shelled, pre-cooked and farmed shrimp commonly sold now. I am not going to belabor the point further. Until this last century man was eating fresh wild seafood, and fresh grass-fed beef, etc, and heart disease was little known. However, they did eat dried meats. I no longer do.

I should add that I am not that convinced that we absorb very much dietary cholesterol. There seems to be evidence that we poop most of it out. Assuming this to be so, probably most of the problem occurs from what we eat, which oxidizes and glycates the LDL after our bodies make it.

(Bacon enough and time) #9

That LDL particles in the body can become oxidised is well-known. It is believed to be a function of “dwell time” in the blood stream. And a ketogenic way of eating can reduce the dwell time and shift the particle count and size pattern in a healthier direction.

But I’m not familiar with how cholesterol itself becomes oxidised, and the references you provided don’t address the matter of cholesterol oxidised before ingestion. So I was curious.

You are of course free to believe Dr. Mason or not. I just found it an interesting alternative. Plant sterols are known to be used in cell walls in place of cholesterol, and they are known to cause problems. Dr. Mason’s hypothesis that industrial seed oils reduce serum cholesterol by replacing it with phytosterols is definitely plausible, though I haven’t seen any research to confirm or deny it. Likewise with his point that what appears to be cholesterol in arterial plaque could easily be phytosterols. But if I were going to worry about any of this, Dr. Mason’s concerns seem more worthy of my time and energy.

The whole notion of LDL and cholesterol being somehow implicated in cardiovascular disease is based on flawed science, and there is too much contrary data to ignore. My take is that this is a particularly hard hypothesis for people to give up, so they keep refining it. In my lifetime we have gone from “meat is good for you” to “saturated fat will kill you” to “no, actually, it’s cholesterol that kills you” to “did we say cholesterol? we meant LDL” and lately “no, it’s the LDL particle count that matters” and now “sorry, it’s oxidised LDL that’s the problem.” So you’ll forgive me if I don’t share your anxieties about cholesterol. It’s just too important to the body, and there is just too much evidence associating higher LDL with a stronger immune system and greater longevity.

Please note that I am not claiming LDL is not important, but rather that the notion that it causes cardiovascular disease is mistaken, if not an outright lie.

(B Creighton) #10

Yes, that is at least partially true. As you say “believed.” I will admit the process is not fully understood yet, and that is partially why many are still calling LDL “bad.”

The old data is just badly flawed and outdated. The new data doesn’t leave a lot of wiggle room. Oxidized and glycated LDL is at the root.

I have no problem giving up the notion that LDL is “bad.” My sole interest in researching the issue was to get to the root of the causes of CVD. My conclusion is that there are several causes, but I now believe oxLDL to be the primary driving force for CVD. I find the newest science just too compelling, and it makes sense to me, whereas the old “science” is the poor correlation studies. The newest science shows the actual substances involved in the start of the plaque process, and oxLDL is there.

LDL is most definitely important. The cholesterol it carries are essentially a 4rth macronutrient. It is kind of like glucose and ketones in that it is so important that our livers make it. I believe it is too bad that it has become known as “the bad” cholesterol. It is used by every cell of the body. I agree with you that the notion high LDL counts are “the risk” for CVD is a lie, but we will just have to disagree about the other science I have brought up I guess. The science is virtually conclusive that LDL particles which get trapped in the cardiovascular walls are the beginning of CVD. Rather than turning a blind eye to it, I am focused on finding out why and how that happens. Also, science has found that oxidized LDL particles are found in the foam cells. The macrophage cells show up to get rid of the abnormal LDL particle. That seems to be the only known response or defense of the body to these abnormal particles. The start of disease seems to be that there are just too many of these particles for the macrophage to handle, and it becomes a “foam cell.” One or two of them obviously is not going to overwhelm the macrophage. But, people with an oxLDL count in the 200s are basically always in the stages of CVD. I am not going to reiterate what I believe about the process, but you are right that part of the issue is “dwell time” of the LDL particles. I believe the science will eventually show that heavily oxidized and glycated LDL particles no longer “fit” in the LDL receptors of the liver, and so end up circulated round and round while becoming more and more oxidized and shrinking in size as the fats and cholesterol continue to slowly leak out. Because these particles are abnormal, they don’t get recycled by the liver. They essntially become abnormally small and that is the danger. When they are filled by the liver with fats and cholesterol, they are called VLDL, and do not pose a risk, as they are just too large to get stuck in the endothelium.

(Bacon enough and time) #11

What do you think of the proposition put forth by Ravnskov, Kendrick, and Diamond, among others, who hypothesis that it is hypercoagulability and not LDL that is the real cause of arterial damage, and hence of atherosclerosis? This certainly seems to be the case in people with familial hypercholesterolaemia, slightly more than half of whom never develop cardiovascular disease and die at perfectly normal ages. Their relatives who do develop cardiovascular disease and die earlier all share variants of fibrinogen and clotting factor VIII that make their blood coagulate more easily. This was observed in the 1960s, and has been seen in studies ever since.

So it would appear that LDL has a much smaller role in the development of cardiovascular disease than has hitherto been hypothesised. In fact, all of the large government-funded studies intended to support the diet-heart hypothesis have show either inconclusive results or negative correlations between LDL levels and cardiovascular disease. One such study was designed by Ancel Keys himself. He was so annoyed with the results that he had his name removed from the study. The other researcher withheld publication for two decades, then place the study in a journal not read by anyone in the field.

(Bacon enough and time) #12

So far as I know, cholesterol is not a nutrient. It is not metabolised, but rather used to build cell walls, conduct neural signals, build myelar sheaths, form Vitamin D, progesterone, and testosterone, fight bacterial infections, and so forth. It is glucose and fatty acids that the body metabolises into ATP, carbon dioxide, and water. And not only does the liver make cholesterol, every other cell in the body synthesises it as well, if necessary, or borrows it from the lipoproteins (which is why they carry it). While a significant percentage of the brain is made of cholesterol, it all has to be made in the brain, because it is too large to cross the blood-brain barrier. It’s a fascinating molecule.

The purpose of the lipoproteins is to provide a water-soluble carrier for fatty-acids, cholesterol, and, I believe certain other nutrients that are not water-soluble. VLDL leaves the liver packed with triglycerides and slowly shrinks as it delivers them to cells that need energy, thus turning into IDL, and then into LDL. And, if things go wrong, eventually into small, dense LDL.

I fear it’s not as close to conclusive as you may think. Many researchers believe that the purpose of arterial plaque is very much like that of any other scab in the body: to hold a wound closed. The scab is by no means the beginning of the damage, it is part of the process by which the body deals with damage. In this light, the presence of cholesterol can be seen as part of the repair process. In my book, to say that cholesterol, because it is present in plaque, must have caused the plaque, is very much akin to saying that because fire trucks are present at fires, they must be causing the fires.

Ravnskov and Diamond have suggested that the reason atherosclerosis is not seen in healthy people is that their bodies can repair arterial damage as fast as it occurs. It is only when the rate of damage is accelerated beyond the normal rate of repair that the body is forced to resort to plaque formation to keep things together. I believe that the main reason people can’t let go of cholesterol and lipoproteins as causal factors is simply that letting go would mean admitting that our dietary advice given out officially for the past 50-60 years has been completely wrong. And the authorities are not about to admit that. The result is that our efforts to prevent and heal cardiovascular disease are unsuccessful, because we cannot acknowledge the true cause. Well, the world is as it is, not as we would have it be.

(B Creighton) #13

Coagulability is an aggravating factor in the end stages of the disease. It perhaps may lend to the cause. While I strongly suspect oxLDL is much more prone to becoming stuck in the endothelium, I am not a biomedical researcher, and this process is I admit not fully understood. I am just pointing to the studies which show oxLDL is present in the foam cells. That is a very strong inference that it is involved in the beginning of the plaque formation. Does coagulability lend to that? I have to concede I do not know. It is certainly conceivable. Once the plaque ruptures coabulability is definitely involved in the resulting strokes, and heart attacks. Despite my harping on oxLDL, glycatedLDL is probably just as bad. I believe there are other causes of CVD as well.

It is not a nutrient for energy. That is true, but perhaps about 5% of our cholesterol is dietary cholesterol, which is absorbed and used in all those functions you mention. That makes it a nutrient as far as I am concerned.

Exactly. Lp(a) is also known to be risk factor for CVD. About 8-12% of the population will genetically make abnormal Lp(a) particles. This segment of the population is def at greater risk of CVD. Why? Because these extra small particles tend to get stuck in the endothelium which starts the process I have been discussing. Hence oxLDL is definitely NOT the only cause of CVD, but these abnormally small, dense LDL particles are definitely a risk factor - for the same reasons Lp(a) is.

Yep again. The body even calcifies it to try to keep it sealed, because if it ruptures, it is going to form a blood clot in the artery which is very dangerous for everything down stream, and is what ends up killing people.

I can’t disagree with this, because I have already said the macrophages can control small amounts of oxLDL effectively. It is when they are overwhelmed that the atherosclerotic process progresses. This process may vary significantly between various people. I don’t think we know.

oxLDL ends up in the macrophage because it doesn’t belong in the endothelium. It is not part of the repair process. The macrophages end up gorging on oxLDL until they rupture and die as a foam cell.

(Bob M) #14

Don’t get too excited. I have extremely high Lp(a), top x% (5%? 2%?) of Lp(a), yet got a zero score on a CAC scan. My Lp(a) is so high, and my LDL “low”, that I once calculated that some insane amount of my LDL (80%? 70%) was Lp(a).

Here’s one example:


My Lp(a) varies typically from the mid 200s to greater than 300 nmol/l. I’m in the tiny red part of the left curve.

Edit: In fact, if you go by mg/dL, my Lp(a) (about 150mg/dL) is HIGHER than my LDL (usually less than 100mg/dL). That’s weight, not number, though.

(Jenna Ericson) #15

I had made a note a while ago that lp(a) picks up oxidative phospholipids. Phospholipids are an essential part of biological membranes. Maybe, like with other lipid biomarkers, lp(a) might be higher in the context of a high fat diet, but if the diet is ketogenic it’s probably not problematic.


I’m still not convinced in the key role of cholesterol in CVD.

However that’s easy for me to say…my lipids, tryglycerides, cholesterol markers are all within the healthy range, and I’m no longer type 2.

My rhetorical question is…why am I still being prescribed a daily statin when my cholesterol was never high but the NHS GPs prescribe it automatically if you go type 2. (?) And it isn’t withdrawn when you are no longer type 2.


(Chuck) #17

I was taken off my cholesterol medication a little over a week ago as well as my diuretic. I never understood why I was on the cholesterol medication in the first place. I am still taking a small dose of calcium blockers and I am hoping I can get off of it soon. I am not a diabetic but it does run in my family. Even when I was eating a very high carb diet my blood sugar was always on the low side of normal. Now I am fasting an average of 19.5 hours per day and eating a moderately low carb diet all real food only. My blood sugar is still low normal. I only at eggs 2 or 3 times a week, but I eat plenty of red meat as well as pork, chicken, lamb, and seafood. The only issues I had with my latest lab results was my potassium was a point low and my zinc was a point high. I believe my potassium level will increase now that I am not on diuretics, my zinc issues is due to supplements I have to take for macular degeneration. My HDL was close to max for a man and my triglycerides was about 50. So my ratio was damn near perfect.

(Bacon enough and time) #18

That’s a good question to pose to NICE, but you probably won’t get any answer from them.

The logic is tediously convoluted, but I think that (facetiously put, but seriously meant) it boils down to “because Professor Sir Rory Collins says so.”

Remember that some of the knightly professor’s colleagues are so enthusiastic about statins that they believe statins should be added to the public water supply. And they have data on their side; studies do show that this would seriously enhance the annual bonuses of pharmaceutical company executives.


I just quit taking the cholesterol meds after a while. I am still alive and kicking.

(B Creighton) #20

Doctors have been convinced by the drug companies that statins are great, and should be prescribed to everyone - what a surprise… They made my dad believe that too. He told me everyone should be on a statin. I don’t plan to get on any drugs on a chronic basis, which is one reason why I started researching health issues, to turn my health around. I feel like real science is actually starting to get somewhere with the real causes of CVD, but it is getting ignored. The drug companies who make billions off statins certainly aren’t interested in the public learning they don’t really need them… or of learning their risks.