Cholesterol and Heart Disease - what you've been led to believe is all wrong

[RAE]

Dr. Zoe Harcombe, who has a pHD in Public Health Nutrition, has studied and written extensively about nutrition, especially dietary fat and its role in the human diet. I thought this article that she wrote a few years back, about cholesterol and heart disease, would be of interest to some on the forum. The article is a bit lengthy, but not hard to get through, as her writing style is easy to read. The article may change what you believe about cholesterol and heart disease - she makes a pretty compelling case that what we have been led to believe for years is all wrong.

This is a little bit about Dr. Harcombe:
Zoë Harcombe – Zoë Harcombe

This is the article mentioned above:
Cholesterol & heart disease – there is a relationship, but it’s not what you think – Zoë Harcombe

 

[street]

Very interesting article and thank you for posting it.

 

[Teacher Terry]

We have never bought into needing cholesterol medication and would never take it. It also negatively affects memory. You couldn’t pay me to take it.

 

[ProspectiveBum]

I took a statin for about a year. It did an amazing job of lowering my cholesterol, but also gave me muscle soreness. I've since moved to a low-carb diet and have stopped taking all meds. My cholesterol numbers are higher (on the high side of normal), but I don't care. I feel great.

I think our understanding of nutrition is mostly wrong. Very frustrating, as I've watched relatives who struggle to follow doctor's advice and continue to suffer from diabetes and heart issues. I feel better now, doing low-carb and intermittent fasting, than I have for most of my adult life.

 

[Katsmeow]

FWIW, this is a controversial person and her views are not really supported by more mainstream experts. People who give these kinds of different views often get a lot of press. That doesn't make them right.

Arguing nutrition is starting to be a lot like arguing religion or politics so I am not going to say more. I would suggest that people who are interested in her views also look at the writings and research of people on the other side of the debate...

 

[braumeister]

Arguing nutrition is starting to be a lot like arguing religion or politics.

That is so true.
There is one difference, in that this debate has a lot of science that each side can point to. We can look at the science and decide for ourselves what is more likely to be valid.

 

[Montecfo]

I found the article interesting. I continue to puzzle about why I needed a 2nd stent this year, adjacent to my first one which is 12 years old. In the interim, I took a statin religiously, continued to exercise (never an issue), had my lipid panels done every 6 months to a year and saw my cardiologist as directed. I also cleared a nuclear stress test in February. But I still needed that 2nd stent in June. My doctors were very surprised at this.

I have quizzed my cardiologist extensively about this. He says I'm "doing everything right".

It isn't very reassuring.

 

[donheff]

I am very skeptical about the dangers of high cholesterol and the use of statins. After years of controversy, including a skeptical Australian Science program being taken off TV, I ultimately concluded that the science probably supports use of statins after a coronary event and to a much lesser extent in other individuals with high cholesterol without other risk factors. But I also think the side effects are far more common than the drug sheets attest. I quit taking statins yeasr ago and I am still in the upper 2% of metabolic health. The charts would indicate that I should be on a statin (slightly high LDLC, but my GP agrees that I can safely skip it.

 

[Amethyst]

High cholesterol and arterial disease (cardiac and stroke) run in my family, and my LDL started trending high several years ago. My total cholesterol has been as high as 233. However, my HDL is usually between 70 and 80 due to exercise, and my Dr. has not yet seen fit to prescribe a statin.

I am trying to lower my LDL by taking plant sterols (Cholestoff), but haven't been tested recently enough to say whether this rather costly supplement is doing any good.

OTOH my much older brother (75) has had several heart attacks and a bypass operation; his total Cholesterol was over 300 when he was only in his 30's. It would appear that he is alive and kicking b/c of statins, since he is overweight, in that peculiarly heart-attacky way (barrel-shaped build with a gut).

I am very skeptical about the dangers of high cholesterol and the use of statins. After years of controversy, including a skeptical Australian Science program being taken off TV, I ultimately concluded that the science probably supports use of statins after a coronary event and to a much lesser extent in other individuals with high cholesterol without other risk factors. But I also think the side effects are far more common than the drug sheets attest. I quit taking statins yeasr ago and I am still in the upper 2% of metabolic health. The charts would indicate that I should be on a statin (slightly high LDLC, but my GP agrees that I can safely skip it.

 

[donheff]

High cholesterol and arterial disease (cardiac and stroke) run in my family, and my LDL started trending high several years ago. My total cholesterol has been as high as 233. However, my HDL is usually between 70 and 80 due to exercise, and my Dr. has not yet seen fit to prescribe a statin.

I am trying to lower my LDL by taking plant sterols (Cholestoff), but haven't been tested recently enough to say whether this rather costly supplement is doing any good.

OTOH my much older brother (75) has had several heart attacks and a bypass operation; his total Cholesterol was over 300 when he was only in his 30's. It would appear that he is alive and kicking b/c of statins, since he is overweight, in that peculiarly heart-attacky way (barrel-shaped build with a gut).

No famillial high cholesterol in my family but my numbers are the same as yours and I have no interest in statins or in lowering cholesterol. In fact the stats say that highish cholesterol is a good thing in the over 70 cohort which I entered this year. But to be fair, I do have excellent numbers elsewhere (BP, sugar, weight, triglycerides).

 

[braumeister]

High cholesterol and arterial disease (cardiac and stroke) run in my family …

OTOH my much older brother (75) has had several heart attacks and a bypass operation; his total Cholesterol was over 300 when he was only in his 30's. It would appear that he is alive and kicking b/c of statins.

For every anecdote that makes a point, there is another that refutes it.

My total cholesterol has been high (usually close to 300, sometimes above) all my life. But HDL is high and triglycerides are low, so I'm fine with that. My last doctor constantly tried to put me on statins, and I actually tried it for a few years a long time ago. The side effect of muscle weakness made me stop.

My new doctor wasn't so pushy about it, but he talked me into a stress echocardiogram last month to see if there was any blockage. There wasn't. Completely normal result.

So anecdotes like yours and mine contradict each other and shouldn't really count when someone is looking at the science.

 

[ER Eddie]

There's a ton of research and good literature out there, debunking what "experts" have told us for 30+ years about the dangers of cholesterol and fat more generally. It was based on bad science to begin with, abetted by governmental expediency, then supported mightily by the food industry.

The story is out there for anyone who's at all curious, and there is really no question but that the fundamental assumptions of the "cholesterol is bad" model collapsed a long time ago -- although it takes a long time for the news to overcome dogma and groupthink and filter out to physicians, dieticians, etc., many of whom have still not gotten the word.

 

[Rianne]

Science can be:
1. Science paid for by the pharma companies, food co., ingredients co., or any other co. to benefit the science results. This is not new. As consumers we should look for the source of the scientific data.

2. There are many ways to conclude a "study." And many ways to conduct a "study."

"A double-blind study is one in which neither the participants nor the experimenters know who is receiving a particular treatment. This procedure is utilized to prevent bias in research results. Double-blind studies are particularly useful for preventing bias due to demand characteristics or the placebo effect."
Who benefits from the results of the study is the big question that is rarely answered in news reports.

 

[braumeister]

There are many ways to conclude a "study."

That's not true at all.

The only acceptable way to conclude a study is with the sentence "More research is needed."

 

[CaptTom]

Science exists at the frontiers of knowledge.

To say it's "wrong" is to misunderstand. New ideas come up, and are tested. A partial understanding emerges. Cholesterol appears to be associated with bad medical outcomes. That drives more research, and it turns out there are different kinds of cholesterol, HDL and LDL. More research further narrows how these things can interact with various other factors. We learn to better refine who should and should not be concerned, and with what.

The research continues. Blanket statements about what's "good" and "bad" become more nuanced and individualized over time.

But to dismiss all research because we don't yet know all the details affecting every individual is like throwing out the baby with the bath water. Far better to use the best and most current information, and stay alert for updates which may affect us personally.

 

[footenote]

If your doctor pushes statins, ask him about Number Needed to Treat (NNT) statistics.

If 104 people with no history of heart disease take statins, one person will benefit (not have a heart attack). Of 50 people taking statins, one will develop diabetes and 10% will experience muscle damage.

In a population with history of heart disease, 83 people will take statins for one of them to prevent one additional death. Harms are identical to those above.

A large, randomized, 5-year trial of the Mediterranean diet showed 61 people on the diet prevented heart attack, stroke or death for one person.

There is plenty of hard science showing statins have high NNT and serious, common side effects. There is also hard science showing Mediterranean (or similar low carb) diets have the same or better outcomes with no side effects.

(My "N of 1" story: LCHF helped me lose 50 lbs and my cholesterol numbers are ideal. And DH is no longer pre-diabetic. I don't claim this diet works for everyone. But for many of us, it is a life-saver.)

 

[rgarling]

"If 104 people with no history of heart disease take statins, one person will benefit (not have a heart attack). Of 50 people taking statins, one will develop diabetes and 10% will experience muscle damage. "

Statistics vary! Recent studies show NO BENEFIT for statins in primary prevention.

 

[flintnational]

My N=1. My cholesterol was 280 untreated and around 200 with statins. About 8 years ago, I went on a low carb diet and lost 30 lbs (still on it - its just how we eat). My HDL went up and my trigs, glucose and BP all went down. Today my cholesterol runs around 260 without statins.

With my diet changes, weight loss and no family history of heart disease, my GP was fine with dropping the statin. Based on my study of the data, I was coming off anyway. He just happened to agree with me.

 

[RAE]

High cholesterol and arterial disease (cardiac and stroke) run in my family, and my LDL started trending high several years ago. My total cholesterol has been as high as 233. However, my HDL is usually between 70 and 80 due to exercise, and my Dr. has not yet seen fit to prescribe a statin.

I am trying to lower my LDL by taking plant sterols (Cholestoff), but haven't been tested recently enough to say whether this rather costly supplement is doing any good.

OTOH my much older brother (75) has had several heart attacks and a bypass operation; his total Cholesterol was over 300 when he was only in his 30's. It would appear that he is alive and kicking b/c of statins, since he is overweight, in that peculiarly heart-attacky way (barrel-shaped build with a gut).

LDL will often rise along with total cholesterol, but that's not necessarily a bad thing. If your triglycerides and HDL are fine, the chances are that your LDL is composed mostly of the large, fluffy particles, that pose no danger (and may actually be beneficial). Here is a published study that found that, in people over age 60, LDL actually had an inverse relationship with mortality.

https://bmjopen.bmj.com/content/bmjopen/6/6/e010401.full.pdf

There are also lots of studies that found the same inverse relationship between total cholesterol and longevity, particularly in those age 70 and over. Here is one paper that talks about some of those studies:

https://www.karger.com/Article/Pdf/381654

And here is an interesting quote from the authors of the above paper:

"High cholesterol levels are recognized as a major cause
of atherosclerosis. However, for more than half a century
some have challenged this notion. But which side is cor-
rect, and why can’t we come to a definitive conclusion
after all this time and with more and more scientific data
available? We believe the answer is very simple: for the
side defending this so-called cholesterol theory, the
amount of money at stake is too much to lose the fight."

 

[Chuckanut]

Earlier this year I took a deep dive into statins, cholesterol and diet.

It's not as simple as "take a statin and it will save you from a heart attack' or 'statins are evil things and should be avoided at all costs'.


Here's another source of information from a pretty smart guy. Lots of medical tech talk using big words.

https://peterattiamd.com/tag/statin/

Here's his quick refresher on the first 7 discussions of cholesterol. Yes, It's hard to follow if you're not a medical person.

(Not so) quick refresher on take-away points from previous posts, should you need it:

1. Cholesterol is “just” another fancy organic molecule in our body but with an interesting distinction: we eat it, we make it, we store it, and we excrete it – all in different amounts.
2. The pool of cholesterol in our body is essential for life. No cholesterol = no life.
3. Cholesterol exists in 2 forms – unesterified or “free” (UC) and esterified (CE) – and the form determines if we can absorb it or not, or store it or not (among other things).
4. Much of the cholesterol we eat is in the form of CE. It is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason this occurs is that CE not only has to be de-esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route.
5. Re-absorption of the cholesterol we synthesize in our body (i.e., endogenous produced cholesterol) is the dominant source of the cholesterol in our body. That is, most of the cholesterol in our body was made by our body.
6. The process of regulating cholesterol is very complex and multifaceted with multiple layers of control. I’ve only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated.
7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up. To see an important reference on this topic, please look here.
8. Cholesterol and triglycerides are not soluble in plasma (i.e., they can’t dissolve in water) and are therefore said to be hydrophobic.
9. To be carried anywhere in our body, say from your liver to your coronary artery, they need to be carried by a special protein-wrapped transport vessel called a lipoprotein.
10. As these “ships” called lipoproteins leave the liver they undergo a process of maturation where they shed much of their triglyceride “cargo” in the form of free fatty acid, and doing so makes them smaller and richer in cholesterol.
11. Special proteins, apoproteins, play an important role in moving lipoproteins around the body and facilitating their interactions with other cells. The most important of these are the apoB class, residing on VLDL, IDL, and LDL particles, and the apoA-I class, residing for the most part on the HDL particles.
12. Cholesterol transport in plasma occurs in both directions, from the liver and small intestine towards the periphery and back to the liver and small intestine (the “gut”).
13. The major function of the apoB-containing particles is to traffic energy (triglycerides) to muscles and phospholipids to all cells. Their cholesterol is trafficked back to the liver. The apoA-I containing particles traffic cholesterol to steroidogenic tissues, adipocytes (a storage organ for cholesterol ester) and ultimately back to the liver, gut, or steroidogenic tissue.
14. All lipoproteins are part of the human lipid transportation system and work harmoniously together to efficiently traffic lipids. As you are probably starting to appreciate, the trafficking pattern is highly complex and the lipoproteins constantly exchange their core and surface lipids.
15. The measurement of cholesterol has undergone a dramatic evolution over the past 70 years with technology at the heart of the advance.
16. Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C. LDL-C is measured or most often estimated.
17. More advanced cholesterol measuring tests do exist to directly measure LDL-C (though none are standardized), along with the cholesterol content of other lipoproteins (e.g., VLDL, IDL) or lipoprotein subparticles.
18. The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile. NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug naïve patients, before changes are noted in glucose or insulin levels.
19. The progression from a completely normal artery to a “clogged” or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues “fixing” the apoB containing particles in place AND making more space for more of them.
20. While inflammation plays a key role in this process, it’s the penetration of the endothelium and retention within the endothelium that drive the process.
21. The most common apoB containing lipoprotein in this process is certainly the LDL particle. However, Lp(a) and apoB containing lipoproteins play a role also, especially in the insulin resistant person.
22. If you want to stop atherosclerosis, you must lower the LDL particle number.
23. At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal.
24. “A particle is a particle is a particle.” If you don’t know the number, you don’t know the risk.
25. To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis (e.g., IMT) while holding LDL-P constant and then again holding LDL size constant. Only when you do this can you see that the relationship between size and event vanishes. The only thing that matters is the number of LDL particles – large, small, or mixed.

 

[Chuckanut]

Earlier this year I took a deep dive into statins, cholesterol and diet.

It's not as simple as "take a statin and it will save you from a heart attack' or 'statins are evil things and should be avoided at all costs'.

Here's another source of information from a pretty smart guy. Lots of medical tech talk using big words.

https://peterattiamd.com/tag/statin/

Here's his quick refresher on the first 9 discussions of cholesterol. Yes, It's hard to follow if you're not a medical person.

https://peterattiamd.com/the-straight-dope-on-cholesterol-part-ix/

What we’ve learned so far

1. Cholesterol is “just” another fancy organic molecule in our body but with an interesting distinction: we eat it, we make it, we store it, and we excrete it – all in different amounts.
2. The pool of cholesterol in our body is essential for life. No cholesterol = no life.
3. Cholesterol exists in 2 forms – unesterified or “free” (UC) and esterified (CE) – and the form determines if we can absorb it or not, or store it or not (among other things).
4. Much of the cholesterol we eat is in the form of CE. It is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason this occurs is that CE not only has to be de-esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route.
5. Re-absorption of the cholesterol we synthesize in our body (i.e., endogenous produced cholesterol) is the dominant source of the cholesterol in our body. That is, most of the cholesterol in our body was made by our body.
6. The process of regulating cholesterol is very complex and multifaceted with multiple layers of control. I’ve only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated.
7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up. To see an important reference on this topic, please look here.
8. Cholesterol and triglycerides are not soluble in plasma (i.e., they can’t dissolve in water) and are therefore said to be hydrophobic.
9. To be carried anywhere in our body, say from your liver to your coronary artery, they need to be carried by a special protein-wrapped transport vessel called a lipoprotein.
10. As these “ships” called lipoproteins leave the liver they undergo a process of maturation where they shed much of their triglyceride “cargo” in the form of free fatty acid, and doing so makes them smaller and richer in cholesterol.
11. Special proteins, apoproteins, play an important role in moving lipoproteins around the body and facilitating their interactions with other cells. The most important of these are the apoB class, residing on VLDL, IDL, and LDL particles, and the apoA-I class, residing for the most part on the HDL particles.
12. Cholesterol transport in plasma occurs in both directions, from the liver and small intestine towards the periphery and back to the liver and small intestine (the “gut”).
13. The major function of the apoB-containing particles is to traffic energy (triglycerides) to muscles and phospholipids to all cells. Their cholesterol is trafficked back to the liver. The apoA-I containing particles traffic cholesterol to steroidogenic tissues, adipocytes (a storage organ for cholesterol ester) and ultimately back to the liver, gut, or steroidogenic tissue.
14. All lipoproteins are part of the human lipid transportation system and work harmoniously together to efficiently traffic lipids. As you are probably starting to appreciate, the trafficking pattern is highly complex and the lipoproteins constantly exchange their core and surface lipids.
15. The measurement of cholesterol has undergone a dramatic evolution over the past 70 years with technology at the heart of the advance.
16. Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C. LDL-C is measured or most often estimated.
17. More advanced cholesterol measuring tests do exist to directly measure LDL-C (though none are standardized), along with the cholesterol content of other lipoproteins (e.g., VLDL, IDL) or lipoprotein subparticles.
18. The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile. NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug naïve patients, before changes are noted in glucose or insulin levels.
19. The progression from a completely normal artery to a “clogged” or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues “fixing” the apoB containing particles in place AND making more space for more of them.
20. While inflammation plays a key role in this process, it’s the penetration of the endothelium and retention within the endothelium that drive the process.
21. The most common apoB containing lipoprotein in this process is certainly the LDL particle. However, Lp(a) and apoB containing lipoproteins play a role also, especially in the insulin resistant person.
22. If you want to stop atherosclerosis, you must lower the LDL particle number. Period.
23. At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal.
24. “A particle is a particle is a particle.” If you don’t know the number, you don’t know the risk.
25. With respect to laboratory medicine, two markers that have a high correlation with a given outcome are concordant – they equally predict the same outcome. However, when the two tests do not correlate with each other they are said to be discordant.
26. LDL-P (or apoB) is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study.
27. LDL-C is only a good predictor of adverse cardiac events when it is concordant with LDL-P; otherwise it is a poor predictor of risk.
28. There is no way of determining which individual patient may have discordant LDL-C and LDL-P without measuring both markers.
29. Discordance between LDL-C and LDL-P is even greater in populations with metabolic syndrome, including patients with diabetes. Given the ubiquity of these conditions in the U.S. population, and the special risk such patients carry for cardiovascular disease, it is difficult to justify use of LDL-C, HDL-C, and TG alone for risk stratification in all but the most select patients.
30. To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis (e.g., IMT) while holding LDL-P constant and then again holding LDL size constant. Only when you do this can you see that the relationship between size and event vanishes. The only thing that matters is the number of LDL particles – large, small, or mixed.
31. HDL-C and HDL-P are not measuring the same thing, just as LDL-C and LDL-P are not.
32. Secondary to the total HDL-P, all things equal it seems smaller HDL particles are more protective than large ones.
33. As HDL-C levels rise, most often it is driven by a disproportionate rise in HDL size, not HDL-P.
34. In the trials which were designed to prove that a drug that raised HDL-C would provide a reduction in cardiovascular events, no benefit occurred: estrogen studies (HERS, WHI), fibrate studies (FIELD, ACCORD), niacin studies, and CETP inhibition studies (dalcetrapib and torcetrapib). But, this says nothing of what happens when you raise HDL-P.
35. Don’t believe the hype: HDL is important, and more HDL particles are better than few. But, raising HDL-C with a drug isn’t going to fix the problem. Making this even more complex is that HDL functionality is likely as important, or even more important, than HDL-P, but no such tests exist to “measure” this.

 

[street]

^ outstanding information and thank you.

 

[RAE]

Here's another source of information from a pretty smart guy. Lots of medical tech talk using big words.

https://peterattiamd.com/tag/statin/

I have read a lot of Attia's stuff and, although I'm sure he is a smart guy, I find his writing to be confusing (and VERY wordy), and not all that helpful (to me, anyway) in trying to understand this stuff - particularly LDL (LDL-P, LDL-C, etc) and how important it is in assessing one's risk for CVD.

The explanation below, from Axel F. Sigurdsson MD, Ph.D., FACC (a cardiologist in Iceland), is easier for me to understand, and is consistent with a lot of other stuff I have read about LDL.

LDL-C Does Not Reflect LDL Particle Size

It has been known for a couple of decades that the size of LDL particles may influence the risk of atherosclerosis. Studies suggest that small, dense LDL doesn’t travel alone, it typically comes along with low HDL-C and high triglycerides. This pattern has been called “lipoprotein pattern B”. Its opposite is “lipoprotein pattern A” where LDL particles are large, HDL-C often high and triglycerides low.
Interestingly, studies have shown that diets rich in saturated fat seem to increase LDL-particle size. Therefore, in theory, such diets could improve the lipid profile of individuals with small, dense LDL particles which is often associated with the metabolic syndrome. However, public health guidelines generally recommend avoidance of saturated fats as the may elevate LDL-C.


A Large Proportion of Patients with Coronary Artery Disease Don’t Have Elevated LDL-C

An often cited study published in 2009 reported lipid measurements among 232.000 patients with coronary artery disease admitted to hospitals in the U.S. between 2000 and 2006. Almost half of these individuals had LDL-C levels less than 100 mg/dl (2.6 mmol/l) which is relatively low. However, almost 55 percent of these patients had very low levels of HDL-C (less than 40 mg/dl or 1.0 mmol/l).
The study is a reminder that low LDL-C according to current definitions does not prevent coronary artery disease. Although some scientists claim that further lowering is needed, this has still not been proven.
The current evidence, therefore, indicates that when it comes to lipids and cardiovascular prevention, relying on LDL-C is an oversimplification and will not solve any problems in the long run. Many other factors have to be taken into account. Overemphasizing the role of LDL-C in order to increase the use of statin drugs is misleading and has to stop.
_______________________________________________________________


Probably the best predictor of CVD and heart attack risk (using the various lipid test results), according to numerous studies I've seen, is the Triglyceride/HDL ratio, as we have discussed before on the forum. Therefore, I can't get too concerned about LDL-C or total cholesterol, as I don't think either number tells us very much (except that you are likely to die early if you are over age 60-70, and your numbers for either one are too low).

 

[ER Eddie]

Science exists at the frontiers of knowledge.

To say it's "wrong" is to misunderstand. New ideas come up, and are tested. A partial understanding emerges. Cholesterol appears to be associated with bad medical outcomes. That drives more research, and it turns out there are different kinds of cholesterol, HDL and LDL.

It's not a simple story of science progressing incrementally, and "wrong" definitely applies. Ancel Keys and his cronies faked data to support a pet theory and willfully, knowingly ignored lots of evidence against it. It took decades before most understood he was wrong -- and not just wrong but criminally unethical. No telling how many millions of people suffered and/or died prematurely, because of it.

 

[Chuckanut]

The explanation below, from Axel F. Sigurdsson MD, Ph.D., FACC (a cardiologist in Iceland), is easier for me to understand, and is consistent with a lot of other stuff I have read about LDL.

I also like Sigurdsson. He writes more for the masses. Attia writes more for fellow professionals and the medical cognoscenti.

Alas, I have the high LDL Attia does not like, and the very good Trig/HDL ratio that Sigurdsson likes.
.