bulkbiker
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More up to date?
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8586008/
Looks like low LDL might not be so good..
Please educate me on fats!
- Thread starter MoorT2
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More up to date?
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8586008/
Looks like low LDL might not be so good..
Oldvatr
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I think of it like this. The chylomicrons are the ocean supertankers transporting crude oil to the refinery (i.e. from gut to liver) There it is refracted / cracked, and in humans the fatty acids are stripped out, reassembled into trigs and packed into the VLDL road tankers. These carry useful amino acids, minerals etc to places that need it. As they go they fill up the LDl mini tankers that feed our tissues. When the LDL is finished it waits for the HDL recycling squad, who return it to the liver to be replenished for the next run.
We need LDL. We stop working if it gets too low. Our body manufactures LDL as required to move fat to and from the adipose tissue and stores. It is essential. But it can become damaged and lose its ability to replenish. The HDL cannot always pick it up for recycling, and it hangs arund in the blood as the Trigs otherwise known as sdldl small dense LDL , and it is this that gets measured in the blood test as the Trigs, and which is suspected of being the real bad guys in the plaque business. So LDL is not dietary fat at all. It is fat from the liver and adipocytes. The LDL has no concept of SFA/ PUFA/ MUFA but is interested in chain length instead. If we are losing weight, then the LDL rate increases to carry the lipids to be burnt. if we exercise - ditto. If we eat it is the chylomicrons that fill our blood not LDL. That (LDL) increases after a meal to refill the stores that were used up since the previous meal. These are all natural processes that we are designed to have happen. But sometimes things go wrong i.e. dyslipedemia. insulin Resistance, insulin insufficiency. But LDL is not a constant. It shifts when you eat, when you don't eat morning evening fasting. That is why it makes such a lousy marker for CVD.
We need LDL. We stop working if it gets too low. Our body manufactures LDL as required to move fat to and from the adipose tissue and stores. It is essential. But it can become damaged and lose its ability to replenish. The HDL cannot always pick it up for recycling, and it hangs arund in the blood as the Trigs otherwise known as sdldl small dense LDL , and it is this that gets measured in the blood test as the Trigs, and which is suspected of being the real bad guys in the plaque business. So LDL is not dietary fat at all. It is fat from the liver and adipocytes. The LDL has no concept of SFA/ PUFA/ MUFA but is interested in chain length instead. If we are losing weight, then the LDL rate increases to carry the lipids to be burnt. if we exercise - ditto. If we eat it is the chylomicrons that fill our blood not LDL. That (LDL) increases after a meal to refill the stores that were used up since the previous meal. These are all natural processes that we are designed to have happen. But sometimes things go wrong i.e. dyslipedemia. insulin Resistance, insulin insufficiency. But LDL is not a constant. It shifts when you eat, when you don't eat morning evening fasting. That is why it makes such a lousy marker for CVD.
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