Posted on 11/27/2025 4:14:18 PM PST by SeekAndFind
Once upon a time, cholesterol was simple. This molecule, it was proclaimed, came in two varieties: an artery-clogging “bad” sort and an artery-clearing “good” one. The difference was not in the cholesterol molecules themselves, but rather in the way they are packaged up for transport in the bloodstream as nanoparticles called low-density lipoproteins (LDLs) and high-density lipoproteins (HDLs).
The public-health message was clear: minimise the bad LDL-cholesterol by cutting down on fatty foods, red meat and dairy products. Increase the good HDL type by doing more exercise and eating more fruits and vegetables. Since a third of heart attacks and a fifth of strokes are blamed on too much of the former or too little of the latter—or both—this message is important. Helpful drugs have also been widely available since the 1990s. Statins, for example, boost clearance of LDL by the liver.
A new picture of cholesterol has been emerging in recent years, however, thanks to several strands of research over the past two decades. Medical guidelines are now being rewritten to better reflect who is at most risk of heart disease. The standard measure of “bad” cholesterol, it turns out, fails to account for the riskiest form of it. This extra-bad cholesterol is also resistant to the usual countermeasures.
Scientists are also trying to solve a mystery: why is it that “good” cholesterol appears, in many cases, to end up being bad news? At very high levels, HDL-cholesterol has recently been linked with higher mortality and a wide range of health problems, including heart disease and cancer.
These discoveries come from a better scientific understanding of the lipoprotein particles themselves, which turn out to come in more varieties than just LDLs and HDLs. It appears that there is a whole lipoprotein ecosystem. And, as in a real ecosystem, the denizens have different roles. Some are more dangerous than others.
It becomes troublesome, though, when it accumulates in the walls of arteries, where it provokes the formation of structures called plaques. They may rupture and create blood clots that block arteries, leading to heart attacks and strokes.
Besides cholesterol, lipoprotein particles comprise various fats, proteins and other molecules. Acting in concert they shuttle cholesterol between the cells that use it and the liver, where it is made.
Some lipoproteins—most notably, LDLs—deliver their cargo to cells in need of a supply. Once they have dropped it they return to the liver for disposal. Others, particularly HDLs, collect cholesterol that is surplus to requirement (mopping up the cholesterol from dead cells, for example) and carry it back to the liver. Together, LDLs and HDLs account for 80-90% of the cholesterol in circulation.
Plaque formation happens when this system gets out of whack. Too much LDL cholesterol, the theory goes, results in the stuff being deposited in arterial walls faster than HDLs can clear it away. And that, particularly if exacerbated by high blood pressure or chronic inflammation, means trouble.
But LDL is not the only bad particle in town. Around a fifth of people have a genetic variant that causes their bodies to make a troublesome protein called apolipoprotein(a), which then attaches itself to standard LDLs to create novel lipoprotein(a), or Lp(a) particles. People with high levels of such particles are several times more likely to develop premature heart disease than those with little or none of them.
Worryingly, these high-risk patients often pass standard cholesterol checkups—which do not look for Lp(a)—with flying colours. Lp(a) levels are impervious to changes in diet or lifestyle, although drugs from Amgen, Eli Lily and Novartis are on the horizon.
Yet another troublesome LDL-like particle, again not measured in standard medical tests, is called a remnant. These are leftovers of large lipoproteins such as chylomicrons (which carry fats from food) that have delivered their cargo of other molecules, and typically carry several times more cholesterol than an ordinary LDL particle.
In theory, because remnants are larger than LDLs, it is harder for them to cause trouble by penetrating the protective lining of the arterial wall. But the proteins and fats on their surfaces can do serious damage. On a per-particle basis, remnants are up to four times more likely to cause heart disease than LDLs.
The revelations about remnants are among those that have led scientists to think that the problem could be too many LDL particles themselves, rather than too much of their cargo, the so-called bad cholesterol. As it happens, lipoproteins that are liable to get stuck and spill their cholesterol into the artery wall do so thanks to a protein on their surface called apolipoprotein-B (ApoB). Conveniently, each particle is wrapped in a single strand of it. It thus follows that an easy way to measure the number of such potentially problematic particles is simply to count ApoB.
The European Society of Cardiology now endorses this method as a better way to measure risk to the heart, but this has not yet trickled into the calculators used by most doctors in Europe and America. Yet it completely changes the results. Some 20-30% of people have high ApoB and low LDL-cholesterol—a group falsely reassured by typical checkups.
Relatively low HDL-cholesterol could be a reflection of metabolic conditions such as diabetes, which come with high numbers of remnants—and the risks associated with them. Drinking alcohol raises HDL-cholesterol, so the health problems linked with very high levels could be caused in some cases by heavy drinking (which people tend to lie about in studies).
But there seems to be more going on than what alcohol could explain. HDL’s jobs in the body are many and varied; it picks up some bacterial toxins, for example. One guess is that HDL particles which are stuffed full of cholesterol are dysfunctional in some way, resulting in all sorts of problems.
Observational evidence has implicated very high HDL-cholesterol (at the levels found in 3-10% of people) in conditions as varied as diabetes, non-alcoholic fatty-liver disease, chronic kidney disease, age-related macular degeneration, Alzheimer’s and cancer. Some scientists now think that dysfunctional HDL may be as bad as LDL.
Scientists reckon HDLs may also protect blood vessels by fighting inflammation, preventing artery damage, supporting tissue repair, reducing blood clots, and helping control immune responses and metabolism. None of this has much to do with how much cholesterol they carry.
All told, some 280 proteins and counting are thought to be part of HDLs. But working out which proteins may sit on the more dangerous HDL particles is tricky because each particle carries only a subset of two or three of these proteins. So far, six Nobel prizes have marked the emerging understanding of the science of cholesterol.
Untangling the increasingly knotty mystery of the lipoprotein ecosystem will probably be rewarded with a few more gongs. ■
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I was put on Lipitor for high cholesterol... Then I went for a dye test on my heart. The young fellow who did that dye test was a cardiologist who looked like he was just out of high school... Several other people were undergoing the same test on the day that I had mine... They were being told that they would need bypasses and that they were given stints etc., to ensure that they would continue living... My young doctor told me that my arteries were so clean that I didn’t even need to be on a statin and that I could discontinue the Lipitor prescription... I did discontinue it for about a year or so... But my cholesterol remained very high, so my regular doctor put me back on it.
Thankfully I’ve never had any side effects from taking Lipitor and I’ve never had any cardiac problems... But every now and then I wonder... Isn’t it possible that having high cholesterol isn’t exactly a guarantee that you’ll have a heart attack? Nobody in my family has ever had or died from a heart attack... Maybe your genetics have more to do with it than your cholesterol.
If Jim Fixx were alive, I guess we could ask him... His father died of a heart attach and he thought running and exercise would help him prevent one... It didn’t.
The human brain is basically made out of fat and cholesterol. Your brain uses cholesterol on its own”wiring” like insulation. No wonder fat and cholesterol are considered horrible and something to be regulated and strangled out. Of course the elite want us to be dwarfed
There is a simple NO COST method to prevent coronary occlusion which brings on heart attacks. It is daily brisk walk for 30 minutes. I am 85 y.o. and EKG just 2 weeks indicated normal heart function, never had a heart attack. During my late 50’s I had bad a missing heart beat after every 10 beats or so. Also had chest pain after eating a meal with meat. And blood pressure was on high side with border line diabetic condition. I quit my job and took up golf to kill time. Gradually increased my play to 5 rounds of 18 holes every week. That adds up to 30 miles of walking every week. To my surprise all my health issues disappeared after a year. No doctor ever told me walking 30 miles/week cures heart issues.
Results all seem in normal range
But something going on with my liver.
Follow up with Dr. next week
And a happy Thanksgiving to one and all
Exercise in moderation is good for you.
It does not guarantee no heart problems. Many people who consistently exercise have had hear problems and hear attacks.
My brother is one such.
Depends on type of exercise. Worst exercise for heart is lifting weights or using weight machines. Only thing I ever do in the gym is use treadmill to walk briskly.
My brother had been an avid runner.
However, he ate a lot of Wisconsin Farm (German heritage) food throughout his life. His wife is a good cook.
Now he regularly walks several miles a day.
My cholesterol is 314...but I am not worried...my CRP is .71
Insulin resistance and inflammation are big factors, I believe.
Bookmark
Although you didn’t say specifically that you have a fatty liver, some meds will help with that, such as GLP-1s.
Plaque in the arteries is more a concern than LDLs. You need both cholesterol to build and restore cells.
I was a runner, down hill ski racer won 3 medals in skiing.
But what saved me was walking 30 miles every week all year playing golf. It is the least boring exercise ever.
Mark Twain often was right, but he got golf wrong, calling it “a good walk, spoiled.”
What was your cholesterol reading??
Being Canadian our readings are different... 5.5 is considered a good reading in Canada... Mine was 10+ and even with a steady prescription of Lipitor it hovers around 7.5
When I was 60 - a doctor told me I had to go o statins for cholesterol.
I told him I thought my cholesterol was in good shape and he said that it was, but the heart association recommended the statins to males over 55 because they were the higher risk group. I told him I needed a more compelling reason to put that poison in my system - and reminded him that those on statins did not tend to live better/longer lives.
I’m now in my 70s - had an echocardiogram before starting radiation and chemo for esophageal cancer a few years ago and it showed “minimal plaque”. Talked with doctors about the earlier deal and they said that the statins were no longer being universally recommended for males over 55 because there was no evidence they did any real good except in the most severe cases....and even that was as much theory as fact.
After playing golf for 50+ years, this is what I discovered.
If can’t break 55 on 9 holes, golf is terrible game. Ball does not go in the direction desired and lose many balls
If can’t break 50, golf is still annoying. You are a drag on your fellow golfers in your foursome.
If can break 50 consistently, golf suddenly becomes interesting.
If can break 45 consistently, you can’t get enough golf! You live the game and become obsessed with breaking 40 occasionally.
About thirty years ago, when I was 45, I began having frequent and increasingly severe chest pains. That seemed ominous enough to send me to my doctor. In turn, my doctor sent me for an angiogram, but the cardiologist pronounced, "Your arteries look pretty good!"
My doctor's verdict was simply that I was working too hard and that, to my wife's chagrin, I needed to play more golf! And sure enough, no more chest pains....
Haha a story with happy ending!
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