MCTs are metabolized differently than LCTs. They are rapidly absorbed and go through the portal vein directly to the liver and then to mitochondria (energy). Coconut oil splits pathways; 65% (MCTs) 35% (LCT.) MCTs are purportedly not contributors to vascular lipid but do increase energy production in mitochondria.
There's a few peer reviewed published papers that suggest MCTs will have NO effect on LDL.
-Medium-chain triacylglycerols may not raise cholesterol
-Medium-chain triglycerides: an update
The general model for why E4 carriers have elevated blood lipid levels relates to the differential binding of different isoforms of APOE to lipoprotein particles. E2 and E3 preferentially bind triglyceride depleted lipoprotein particles, such as HDL, while E4 preferentially binds triglyceride rich lipoprotein particles, such as VLDL. The binding of APOE4 proteins to triglyceride rich particles is sufficient to slow activity of lipases on cell surfaces. Because the lipase activity is reduced, E4 carriers are slower in clearing VLDLs from circulation and therefore have elevated triglycerides in circulation (Dong et al 19994). I don't think it is accurate to say they hyperabsorb lipids.
Medium chain triglycerides (MCTs) are not processed the same way as LCT and do not end up in lipoprotein particles. Therefore, MCT metabolism should not be influenced by E4 carriage status. In support of this idea, we found no difference between levels of induced ketosis in E4+ and E4- subjects (Henderson et al 2009). Importantly, coconut oil contains mostly C12 and C14 fatty acids, which will be packaged into lipoprotein particles and their digestion, will be slowed by E4 carriage status, leading to a poor lipid profile. So, I would urge that E4 carriers do not try to induce ketosis by use of coconut oil. I would stick with MCT oil.
You are doing the right thing by trying to induce ketosis by diet. I think this is most important for E4 carriers to lower risk of Alzheimer's.
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