LDLs play Little to NO Role in Mortality

LDLs Play Little to NO ROLE in Heart Disease

Half of us are dying of heart disease so this is no trivial matter. Our obsession with cholesterol started with President Eisenhower who had multiple heart attacks while in the White House, with a stroke thrown in for good measure. He finally died of congestive heart failure in 1969 at age 78. He went on a low cholesterol diet and his blood cholesterol went up. He was miserable. Lesions in the heart that plug up the heart are filled with cholesterol so it was just assumed you had to eat less cholesterol. It was there, it must be the cause. That started the obsession with cholesterol. It's been misplaced.

To fix a disease, you have to understand what is causing it. We have had multiple studies in the last few years that reflect an alternative reality. Bathum's study in Scand Jr Pri Health Care is one of the best, among many. In that study, over 118,000 adults, over age 50 were followed for LDLs, Triglycerides, HDLs, statin use, and mortality. With over a million human years of data, their data showed what many other studies have shown: LDL cholesterol has no impact on mortality. In fact, low cholesterol (< 190) has higher mortality than a total cholesterol of 270. For example, for ages 60-70, total cholesterol of 193-232 has 0.68 of the mortality of cholesterol below 193. And 0.67 of the mortality if their cholesterol was between 230 and 270. That's a 32% reduction in mortality, having a cholesterol way above what we consider normal in America, being < 200. We are advising people to lower their cholesterol into a range that is associated with a higher mortality.

Now, confounding all that is that folks on statins had lower mortality as well, somewhat in the same range, some 30%. That confirms the irrefutable benefit statins provide to heart disease once one has had a heart attack. Hmmm. But is the cholesterol lowering effect what actually makes the benefit. That hasn't been proven. And the people who were started on statins were all those with higher cholesterol and therefore lower mortality to start with. So, maybe, just maybe, there is NO BENEFIT.

The authors concluded that only high triglycerides were associated with higher mortality, at least in women. HDLs are protective, yes. But LDLs appear not to be the main problem if any problem at all.

Are we barking up the wrong tree? It is unequivocal that cholesterol accumulates in artery walls. That is proven and clearly apparent. But what is making the cholesterol accumulate?

Ah! There is research to show just that. If you do metabolomic studies of the lipids that predict future heart attacks and strokes, it's not cholesterol that comes out on top, it's plasmalogens, at low levels. Remember, metabolomic studies measure everything, without bias, and then observe what statistically holds up to benefit. That study called the SCORE Study, followed 1852 adults for 16 years and obtained blood levels on 1,228 metabolites every year. They then did the number crunching for statistical validity of what predicted future trouble.

Yes, cholesterol was in the mix but it was low plasmalogens that emerged as most predictive of future unstable angina and heart attack. Whoa! Once again, high cholesterol didn't predict future trouble. Low plasmalogens did.

Here is the probable sequence. Oxidative stress releases a flood of peroxide and the -OH ion. Plasmalogen lipids, present in the endothelial cells of arteries, are the only lipids to contain a vinyl-ether bond that soaks up those peroxide and -OH ions, neutralizing them. That depletes the plasmalogen molecules which are critical for playing a key role in membrane function. Without plasmalogens, membranes get stiffer and have a hard time secreting cholesterol, so HDL levels fall. Endothelial cells shrink their footprint, exposing the basement membrane for LDL particles to stick to. Without that loss of plasmalogens, the endothelial cells would maintain their coating of the artery, protecting them. So LDLs are at the party. They play a huge role in making trouble with accumulations of cholesterol, but they aren't the core root cause. It's fixing the root cause that will prevent the disease.

It's the oxidative stress, probably most prominently driven by the sugar and white flour we eat, and the visceral fat we then develop. That depletes plasmalogens and cells start to separate with membranes that get stiffer and less functional. THEN, and only then, do LDLs start to accumulate.

Got it? It's not the cholesterol that is the root cause. It's that tummy fat, that sugar, that ice cream that starts the ball rolling. We lose plasmalogens. We can measure that. And their loss is the single best predictor of future heart disease. If you want to see into the future for your #1 risk, measure your plasmalogens.

Then, there is the inexorable loss of Nitric Oxide with aging. That is the other prominent wild card in the mix. Eat all the vegetables you can.

www.What will Work for me? Now, here there is some hope. We can now measure and replace missing plasmalogens. I have personally been tormented for years with lousy HDLs and I have done everything but stand on my head to get my HDLs up. I have never been successful, until this last year when I started taking plasmalogen replacements. From an HDL of 28, I am now up to 58. I'm thrilled. Combine plasmalogen replacement with Nitric Oxide replacement as the means of regrowing your glycocalyx and giving your arteries their natural coating, and we can really get to the heart of your heart. How interested is BIG Pharma and BIG Health Care in cutting your risk of heart disease, the #1 health-spend in America? You are interested. But you may not get help. Should you be on a statin? They do reduce mortality, but not for the reason you think. The cholesterol effect is irrelevant. They likely are playing a role as antiinflammatory, reducing the oxidative stress, and reducing the loss of plasmalogens. That research is waiting to be done.

References: Scan Jr Pri Health Care - Bathum, Heart Attack and Stroke, JCI Insight, MedRXIV,

Pop Quiz

1. If I measure everything in my blood, every year, for over a decade, what compound will jump out as being the best predictor of future heart attacks?                                     Answer: Plasmalogens

2. What role do plasmalogens play in the wall of the artery?                             Answer: No fair. Diidn't fully discuss this. But here it is. They are the most fluid of membrane lipids because they are where DHA, fish oil, ends up. That fluidity and the ability to shape shift allows some unique properties. The membrane can stretch and bend. That's very useful for an artery with a pulse going through it. It's also important to allow the endothelial cell of the artery membrayes to be very thin and connect to all their partner cells. Finally, the proteins embedded in the wall of the endothelial cell can shape shift because of that fluidity. All that is degraded as plasmogens are lost. Their achilles heel is the vinyl-ether bond they possess that is the anti-oxidant of FIRST resort, That protection is nice, for a short term event. It becomes a liability with persistent oxidative stress.

3. Who has a lower life expectancy, someone with a cholesterol of 150 or someone with 250?                     Answer: I'll take the 250 any day of the week.

4. What is the best marker of my artery cells being healthy?                                  Answer: Lower triglycerides and higher HDL. They indicate properly function cholesterol transport.

5. How can I naturally raise my own plasmalogens?                          Answer: First, stop the burning. This is why you need to cut down on sugar and white flour. Lose the tummy fat. Intermittent fasting and compressing calories into 8 hours turn on peroxisomes to make more plasmalogens. Exercise also deplete glucose stores and switches you to fat burning, stimulating the peroxisome to make more plasmalogens. So, the simplistic phrase "Eat right and exercise more!" holds water. Do it.