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closeI think that it cannot be said from this data alone that LDL does not affect cerebral and cardiovascular disease.
Posted by tak_k0417 on 23 Apr 2023 at 14:08 GMT
As described in this paper, high blood levels of Lp(a) and that HDL1 leads to arteriosclerosis and causes cerebral and cardiovascular disease are consistent with existing reports. Also, I myself have requested LipoSearch from Skylight Biotech many times for analysis, so I understand its characteristics. As you say, we also understand the drawback that ultracentrifugation does not preserve the individual lipoprotein components.
Incidentally, in your paper you say: "This may be the reason why LDL cholesterol is not always a significant risk factor, even in large cohort studies". I would like you to confirm again that this effect has been confirmed in clinical trials. Also, please consider that in patients with familial hypercholesterolaemia, which is still a problem, some efficacy has been achieved with the above-mentioned drugs, as well as with MTP inhibitors and LDL apheresis.
In addition, in Figure 1 of Reference 11, which you have already published, there is an accumulation of ApoB48 in the WB of the "LAC2" fraction. This may indicate an accumulation of chylmicron remnants rather than LAC2 particles. If it is LAC2, then ApoB100 should accumulate. The paper also mentions chylomicron TG/cholesterol, but as you know, TG in chylomicron secreted from the small intestine is rapidly degraded by LPL in the vessel wall and converted to TG-poor chylomicron remnants. Therefore, if TG/cholesterol is to be used as an index, it would be difficult to say that it is necessary to measure the subject's meal content and postprandial time, as well as LPL activity, and to prepare the conditions. In addition, several papers have been published in the past on the high arteriosclerosis-inducing potential of chylomicron remnants, so please check these as well.
The prospect of looking at blood lipoprotein particles is very interesting, and we believe it can make a significant contribution to reducing the residual risk of cardiovascular events.
In Akita, where the accumulation of CETP deficiency was once discovered and was one of the reasons for the futility of CETP inhibitors, I hope that a firm new discovery will be made that will lead to the treatment of cardiovascular events. I'm sorry for the high expectations.