People are free to believe what they want to believe. Unfortunately, the burden of proof is those that are contradicting the consensus within the field of cardiology. If you want to bet your life on quack doctors trying to sell you a Keto diet, good for you.
Correct! And it's being proven in RCTs on a frequent basis now only to be "unscientifically" explained away like you do below reference the UCLA study. If these studies disagree with your world view and you don't have data to refute them, than just make personal attacks on the doctors and researchers.
Wrong on the data and wrong on the interpretations. I outlined this clearly in my posts.
Low-density lipoproteins cause CVD
No, it's still right no matter how many studies you choose to ignore. I'll produce more studies for you to ignore or explain away but there is no need to. Instead, everyone read the study that EyeBRollin links above to prove his point. Is this all it takes to convince you that your right? Other researchers decided to look deeper into this study to find this compelling evidence leading to this scientific "consensus". Among the many issues they found was that there were many cohort studies finding very little if any connection between LDL and cardiovascular disease. Well you can't have a consensus with those pesky studies included.
https://pubmed.ncbi.nlm.nih.gov/29353277/
Total cholesterol is not the main number looked for on a lipid panel. It's LDL cholesterol and non-HDL cholesterol. HDL cholesterol and triglycerides are
markers, not makers. If you have a fvcked up HDL / Triglyceride ratio you have insulin resistance / T2D and are at increased risk.
If you have high LDL and a perfect HDL / Triglyceride ratio, you will still get atheroscolersis. LDL usually correlates with Apo-B, but not always. Apo-B is on all atherosclerotic particles.
ApoB is causal in atherosclerosis.
Blood test can measure your HDL and Triglycerides. We can't measure LDL we can only estimate. This is one reason APO-B is important coupled with, as you state above, it's affinity to atherosclerotic particles. However, you're going to have to provide receipts for your statement above that high LDL and perfect HDL/ Triglyceride ratio will produce atherosclerosis. And please no more observational studies such as the one above. I'm not so sure that even the other Lipid hypothesis apologists would agree. But hey, I'm open minded. Change my mind.
Which guidelines? The current guidelines are that LDL should be under 100 mg/DL for people with no other risk factors. For people with risk factors, or who already have plaque, diabetes, or heart disease, it needs to be under 70 mg / Dl. Not only does the level need to be below those values,
you need to keep it there for as long as possible. If your LDL has been high for 30 years and you lower it to a healthy level, it does not undo what happened the past 30 years. Measuring someone's lipids at the time of heart attack tells
nothing about what their lipids have been the previous 50 years of their lives.
Besides, "see my above answers" I'll add this. The lipid hypothesis crowd has so bought into the cholesterol causes heart disease idea and it just doesn't pan out. Besides the some of the other studies that you didn't bother reading, there are many studies that show a U shaped pattern with cholesterol. However, LDL lower than 70 as you so excitedly espouse above has shown to increase all cause morbidity slightly more than too high LDL. LDL is protective and is an important component to our immune system. That's why you are susceptible to die from many things with low LDL including heart disease. Have we already forgotten about Co%$d? If one is on the other end of the U it's a higher probability it's from heart disease. But since I'm on the Thrombogenic theory side and not the LDL/ Cholesterol hypothesis I say the LDL is high because of the much damaged endothelium needs repaired. LDL increases when you cut yourself or break a leg. It helps fight bacteria. If you get heart disease when its low and you get it when it's high how is LDL causal?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6832139/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934492/
Of course. That does not mean they are
causal. IR/ T2D also strongly correlates with obesity, which has deleterious effects on blood pressure, lipids, and pretty much every biomarker you can think of. In other words, a diabetic is usually overweight and has terrible lipids across the board.
Please tell these rogue researchers with their ridiculous 121 citations EyeBRollin's endothelium dysfunction/ injury hypothesis before they waste anymore of our time.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3831119/
Does not make saturated fat healthy. Saturated fat downregulates the LDL receptors on the liver. In laymen's terms, that means it reduces the body's ability to clear those LDL particles out of the blood. Guess where those particles end up?
I am not pro-sugar. Replacing sugar with saturated fat may be an improvement for most people. It does not make saturated fat a good choice. It simply means it is better than sugar. We are better off replacing saturated fat for
unsaturated fat and complex carbohydrates that have their natural fiber content in-tact.
1) Dietary carbohydrates increase levels of highly atherogenic small, dense LDL cholesterol (sdLDL-C).
2) Dietary saturated fat increases levels of both HDL cholesterol (which is inversely correlated with cardiovascular disease) and large buoyant LDL cholesterol (which is not known to be atherogenic).
You will get improvement on
any diet that dumps white sugar and ultra processed junk food. The Mediterranean diet
is a low saturated fat diet!
Thank you for proving my point before needlessly pointing out that one of the 3 is low in saturated fat. The other two likely are not. Like you said though, they dump the sugar and processed foods.
LDL particle size does not matter. People with FH (familial hypercholesterolemia) have mostly large-buoyant LDL particles. They also are dead by 40 if they don't get aggressive lipid lowering treatment. All LDL particles can invade the artery wall. There can be some discordance between LDL and Apo-B if your LDL is at a borderline healthy level (100-120) and you have mostly large particles. Beyond that, you won't find a cardiologist or lipidologist that thinks an LDL of >130 will be healthy even if it is mostly large fluffy LDL.
Your FH example accounts for less than 1/2 of a percent of the population. That said, thank you for bringing them up again. People with FH live as long as everyone else. There are people with FH in their 80s. And yes there are some in their 20s that have heart attacks. So why do some live into their 80s with sky high LDL and no heart disease and others with sky high LDL have heart attacks in their 20s? Luckily some researchers thought this to be a logical question. Well these quack doctors found that there was another gene involved that people with FH are more likely to have. But not all. Again, if LDL causes heart disease then why do most with FH live as long or longer then rest of the population regardless of LDL levels. Hold on tight to your, LDL causes heart disease" idea and read yet another pesky study.
https://www.mdpi.com/1422-0067/23/16/9146 . By the way, again. Particle size matters. Please don't make me produce all the evidence.
It becomes damaged due to LDL particles invading the artery wall.
As soon as I receive your study (RCTs please) showing non-oxidized LDL A can invade the artery walls I will send it off to the leading researchers on both sides of the discussion. They're all in for a big surprise. You may get a Noble Prize for this discovery.
High blood pressure, high blood sugar, and inflammation are all factors that exacerbate the process. However, if your LDL is only 40, you still aren't going to be laying plaques. Atherosclerosis does not happen at an LDL level <70. Hence, why it is the target level for diabetics.
As I've laid out and provided receipts above, if your LDL is 40 you are correct, you won't get heart disease. That's because the cancer or some other all cause morbidity will likely kill you first.
Correct. That is why it is carried via lipoproteins.
This is where your explanation falls apart. All LDL particles are small enough to invade the endothelium. And when those larger particles do get into the wall, they contain more cholesterol. Particle size is largely a distraction.
The number of LDL particles, which is reflected by Apo-B (all atherosclerotic particles contain Apo-B), is what to focus on.
Again, I'm going to ignore your "All LDL" comment and refer you to the above. Lol! Ok, my explanation falls apart as you then proceed to back in to the right answer while meaning to tear my argument apart. Below is from Journal of Clinical Lipidology 2011.
Patients may have relatively low “bad” LDL chol but a high LDL-P. Meaning lots of boats on the river but not much chol payload. This could result in the patient being told they are low risk when in fact, their CVD risk is quite high.
Patients may have high LDL but a low LDL-P. Meaning lots of payload but not many boats on the river. This could result in needless chol medication being prescribed.
They found that the highest incidence of CVD was in patients with the highest LDL-P and the lowest LDL. This is not a typo.
I guarantee most cardiologists are not trying to kill you.
I agree! Most are just lacking the intestinal fortitude to question a failing hypothesis.
