First, I would like to apologize to followers of this thread. I’ve been at a conference a didn’t realize EyeBRollin’s misinformation, in response to my thread, has stayed here for this long with no rebuttal. I’ll do my best to keep it short. If anyone needs me to produce any research to back up my assertions just let me know.
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.
Cholesterol is a poor predictor for heart disease. Your LDL number even more so. HDL to triglyceride ratio is a better indicator but still incomplete. APO B a little better.
Wrong on the data and wrong on the interpretations. I outlined this clearly in my posts.
Low-density lipoproteins cause CVD
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.
One study showed that of the over 130,000 patients admitted to the hospital for heart attacks, 75% had normal Cholesterol levels based on todays guidelines. And almost 50% of those had what was considered optimal LDL levels, like less than 100 mg/ Dl.
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.
Insulin resistance and diabetes markers are proving to be a much more reliable window into whether someone is at risk of a cardiac event.
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.
Sugar intake does much more damage to the heart than saturated fat.
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.
That’s a fact. This is why some are getting improvement with a lower carb, keto, or Mediterranean diet. Cholesterol does not cause heart disease!
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!
I’m surprised that a person who touts the superiority of measuring APO B can then turn around a say LDL particle size doesn’t matter. The reason APO B is better is the same reason LDL was a poor indicator for predicting heart disease. Not only does APO B become oxidized and attach itself to small dense and sticky LDL, it attaches itself to IDL and VLDL.
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.
Studies of the last 20 years and longer say this. The lining of the heart arteries (The endothelium) becomes damaged.
It becomes damaged due to LDL particles invading the artery wall.
The endothelium is much like an accordion with a nonstick surface) It can become damaged by things like chronic high blood pressure, free radicals, and wait for it……..glycation. (That’s glucose, same as sugar) As sugar rots your teeth it's just as hard on your heart. The damage itself becomes inflamed and oxidated. Now things begin to stick to the walls of the artery in the spot of the damaged nonstick surface. The collecting plaque is made of several things not just cholesterol. In order for LDL to stick and also get under the damaged endothelium in the artery, it must be oxidized. Oxidized LDL (small dense, and sticky is most susceptible to oxidation) often becomes oxidized through glycation. (There’s that stubborn sugar again. This small, dense, and sticky oxidized LDL then gathers with the other substances like rogue calcium to begin forming plaque. Non oxidized LDL (LDL A) does not contribute in any significant way to arterial plaque. Backinthegame78’s recommendation on K2 helps mitigate this rogue calcium. By the way, arterial plaque is made of way more calcium compared to cholesterol. Does that mean we need to lower calcium too.
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.
Understand that cholesterol is hydrophobic. It can’t travel in the blood without a buoyant vessel. HDL, LDL, and triglycerides help transport cholesterol to where it is needed. These are kind of like balloons with a bit of helium.
Correct. That is why it is carried via lipoproteins.
A healthy LDL, LDL A, has a very very difficult time becoming plaque. It’s too buoyant and too big. LDL B acts nothing like a balloon but more like a heavy sticky ball. LDL A would also have a very difficult time getting into and under the endothelium tissue.
Bottom line, LDL particle size matters. Especially to those with metabolic syndrome and insulin resistance. If it doesn't matter please provide the research, preferably from the last 20 years.
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.
If anyone requests, I have a cloud folder full of articles and studies. I don't claim to know or understand all. But I do recognize that the doctors and experts are clinging to a busted hypothesis that their egos and wallets refuse to let go of. And it's killing us.
I guarantee most cardiologists are not trying to kill you.
www.nbcnews.com
