Kitano wrote:Along the same lines, how critical is HCY, and with lowering HCY with B12/folate/TMG/NAC to an optimal level, can we lower AD risks? Some studies suggest that supplement lowered HCY does not alter CV outcomes.
We are THE known population with decreased cerebral glucose metabolism decades before cognition declines. What gets tricky for us is HOW to best create those ketones without driving up our risk for CAD/CVD as we also tend to hyper-absorb dietary cholesterol. Many of our members practice CR, IF, exercise, reduce starchy carbs, and use MUFAs to more safely create ketone bodies. Ketone supplements, like MCT, can also drive up LDL-P. As you've wisely ascertained, ketone esters MAY end up being our ticket... but even less research has been done there
We're kind of between a rock and a hard place. It's pretty clear that we could greatly benefit from ketones; but we're struggling with how to balance brain health with heart health.
Another consideration with regard to heterogeneity of LDL particles is their content of specific proteins and perhaps lipids that could refine assessment of pathophysiologic properties of lipoproteins, as proposed originally by Alaupovic.20 Of particular interest is apoCIII, a small molecular weight protein that has been found consistently to be strongly associated with risk of CVD when present on apoB-containing lipoproteins,21 likely because of the combined effects of increased very low density lipoprotein (VLDL) secretion,22 impaired VLDL remnant catabolism,23 and proinflammatory activity.24Recently, it has been reported that whereas LDL particles containing apoCIII are significantly associated with CHD risk, this relationship is substantially weaker for the majority of LDLs lacking apoCIII.25 Notably, apoCIII is particularly abundant in very small LDL particles.26 Other subspecies of sdLDL that may have particularly high atherogenic potential are those with increased content of glycated apoB27 and increased electronegative charge.
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