LDL to HDL, isn't that about a 2:1 ratio? Though the numbers them selves are high using the US unit of measurement, the ratio is nearly ideal. I'd be more concerned about the low (again, the US measurement) triglycerides. I'll assume you don't use the US measurements and I don't know about those so we'll have to wait for someone to speak up but what I do see is the 2:1 ratio which is very good.
I would still be concerned about an LDL of 147, even with an HDL level in the normal to high range. Much depends on the type of HDL particles that make up your HDL number. These can range from small to large with small being the most desirable. Studies have found that larger "fluffy" HDL particles are not as effective as smaller particles when it comes to binding with LDL to remove it from your system. There are other cholesterol tests that determine the breakdown of particle size in your cholesterol if you want to go there, many are starting to look at those numbers as part of an overall lipid profile.
In your case, most doctors would recommend treating the LDL level with either lifestyle changes or statin therapy, you should discuss your options with your doctor.
Also, I wouldn't worry about you TGLs being low, 70 is a great number.
Yes, that's what HDL does, however, I'm glad you questioned this as in re-reading my post I realized I had it backwards, I need to slow down sometimes:)
From the NCBI;
"Participants with the smallest HDL particles had the most unfavourable cardiometabolic risk profile whereas those with the largest HDL particles had the most favourable risk profile."
This is due to the smallest particles of HDL's inability to bind with LDL. This is why a high HDL number can be misleading, not all HDL is equal. If one's HDL is made up primarily of the smallest particles, they do no benefit from the preventative nature of HDL, instead it puts them at more of a risk.
You know, ideas are always changing about how cholesterol lipids are managed in the body, but there is one thing for sure, cholesterol is very important or we die. Anyway, lets look at your scenario from the NCBI for one moment.....
What they are saying is, bind/remove from body. This is impossible. Look at it this way....
A person with a ratio of 2:1 or 3:1 would be producing LDL 2x or 3x faster than HDL. As soon as an HDL protein is released from the Liver, it would immediately bind with an LDL, and be removed from the body. The balance? We would have ZERO HDL and lots of LDL. See the problem?
Lipids are complex protein molecules, and all protein molecules are identifiied in the body the same way, they have markers. A HDL is identical to a LDL, the only difference is the marker. Both HDL and LDL have fat in them, and HDL could be converted into a LDL by changing its marker. This is the beauty of lipids. Even sex hormones are in proteins and have markers, it's a highly used system. A HDL molecule simply has the right shape/key to chemically lock on to an LDL and chemically alter the marker on the LDL, then they seperate. The new marker on the LDL is the right key to lock into the recycle area of the Liver, it isn't thrown away, it's reused. This way we keep HDL in the blood. It was thought a while ago that synthesising HDL and basically injecting millions of them into a blood stream might be a good clean up exercise. However, it was soon realised through findings that it wouldn't work. Trapped lipids are trapped and will not return to the Liver. They are also very quickly broken down by the immune system trying to catalyse repairs in the area.
You are correct about Lipid sizes though, which is a fairly recent discovery. This, according to latest findings, is greatly affected by diet. Large LDL tend not to become trapped in damaged/inflamed vessels. The other problem caused by diet of course is oxidation, which damages the protein on the lipid. A lot is still to be learned but research is continually uncovering more mysteries.
Your view is a little simplistic. The missing piece is the lipid recycling done by our bodies .HDL particles take up cholesterol, transferring some of it to other plasma lipoproteins, or HDL can deliver cholesterol directly back to the liver via specialized receptors that take it up for processing and/or elimination. Once the cholesterol has been delivered to the liver, it is converted into bile acids which are then secreted into the small intestines. Most bile acids (produced in the liver by conversion of cholesterol) are recycled to the liver, but some are eliminated by fecal excretion, which represents a source of cholesterol loss from the body. It is believed that 95% of the cholesterol returned to the liver and converted into bile acids is recycled by the liver back into the bloodstream as lipids. That is how fenofibrates work, they inhibit the "recycling" process of cholesterol in the intestines by limiting the uptake of bile acids from the liver. Statins work by reducing the amount of LDL created by the liver initially.
The process is called return cholesterol transport.
So with HDL being a major contributor to atheroscerosis, why do you believe people are continually being told to increase their hdl?
It has been known for some time that HDL in people with heart disease have 5 of the 48 proteins enriched. These 'enriched' proteins do not exist in healthy people. It is known that these enrichments come from macrophages and the transfer of the proteins from the macrophage turns on a blocking mechanism, meaning no HDL can remove the fat, allowing it to turn into a foam cell, the start of atheroscerosis. It is known that HDL is a major control mechanism in the fight against infections, with its complex structure of 48 proteins. When an artery becomes inflamed, HDL goes to the rescue and actually signals monocytes to the area, which HDL programs. LDL feed cholesterol into the macrophages but HDL seem to block themselves the ability to remove it, by stealing proteins. The macrophages emit a bleach, containing a form of chlorine, which not only fights infection, but damages lipids. It realigns the proteins making them harmful. This has all been reproduced in labs and papers on it have existed for years. They have even developed cures for parasitic infections in Africa by taking some of the proteins that exist on HDL. So, HDL still has a lot to be discovered, but it appears it plays a much bigger role than removing cholesterol from cells. It appears it contributes to atheroscerosis by controlling the macrophages and becoming oxidised, and it plays a huge role in the immune system as a whole. When mice were deprived of HDL, their arteries infamed, causing death. Re-introduction quickly into deprived mice showed a recovery but atherosclerosis as a result. Now the proteins of HDL are fully mapped and more is understood, maybe they will be able to re-engineer the lipids for CAD sufferers and treat the disease in the artery walls.
I think the university of Washington are looking into statistics again, wondering if LDL is the real problem and not HDL. Graphs show that high levels of LDL seem to comply with heart disease, but it's also the same with HDL. Has everyone been concentrating on the wrong lipid?
Sorry Ed, I don't follow you at all, I think you've strayed a little off topic. I never said HDL contributed to CAD, my point is only that a high level of HDL can be misleading as not all HDL is created equal. Smaller particles are not as effective as larger particles when binding to LDL so if you have a high LDL and a high HDL, the two don't necessarily cancel each other out which is why doctors almost always treat high levels of LDL first.
Here, the OP has a high LDL of 147 and an equally high HDL of 68 and he is asking if he should worry about his LDL. If it were me, I would treat the high LDL, that's all I'm saying. I then explained why I would treat the LDL and not depend on my HDL keeping things in check. I guess I just don't understand what the rest of this has to do with the OP's question, but it is interesting information, most of which I have read.
No, I'm saying HDL is now believed to contribute to artery disease. Latest findings with experiments on mice in Washington University have found HDL has a lot of functions, not just retrieving cholesterol from cells. Anyway, you read the rest.
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