RE:Re: PCSK9Hi imtesty.
Not sure where to post my current thinking but your reducing LDL comment sparked a thought for me. I believe BearDownAZ and perhaps fouremm have provided insight regarding treatment strategies directed at lowering LDL and certainly have done so in the context of describing the different target populations for rvx-208 vs. LDL lowering drugs.
My thought may be off target but I'd sure like to get a POV from science. I've been reading lately that healthy LDL (not sure of the wording but it might be LDL not impacted by free radicles or not inflammed) is an extremely important protein in the process of carrying important proteins such a beta-HBA and BDNF across the blood brain barrier and these proteins are essential for the health of neurons in the brain and particularly neurogensis. Therefore, it begs the question of a strategy directed at lowering LDL. Perhaps a strategy of sacrificing neurological function is a good trade off for reduced heart attacks?
Hopefully I've got some of the understanding reasonably correct but I sure want to be corrected.
So as humans we are all genetically unique. Yet for medical and scientific purposes norms (ranges of) are established for acceptable levels of LDL and HDL in whatever form they may take and whether they are "healthy" molecules or if they have been bent and twisted by other proteins and thus become dysfunctional.
What my curiousity is that if a drug is developed to reduce LDL then might it have a negative neurological impact in the healthy functioning of the brain, possibly leading to various forms of dementia? Please recognize that I understand that a drug could be designed to take LDL from a level that is too high(or even too low) to a more normal level or a drug could be designed to fix the non functional LDL. I'm just trying to get a bit of an understanding of the LDL strategy.
The reason I'm curious is that because there is a lot of bad science done and group think along with social norms dictate where the scientific $s get spent. It has only been very recently that the 7 Country Study by Ancel Keys is being refuted in terms of dietary habits and the role of cholesterol in the formation of various types of plaques.
Of course, once the plaques are there then something must be done and we are seeing the impact of rvx-208 on this very issue.
It does seem that the epigenetic strategy of building ApoA-I (and thus setting the epigenetic wheels in motion) and thus functional HDL seems more beneficial than lowering LDL, particularly when given the post hoc ASSURE/SUSTAIN MACE reductions of 55% and 77% respectively in the total and DM with CVD samples (respectively) traded off with potential neurological deterioration from LDL lowering strategies.
So my thinking remains in the rvx-208 camp and regarding epigenetics my htinking remains in the knowledge pool now sitting at Zenith (as well as RVX).
Any critiques and thoughts re lower LDL strategies are welcome. I am just trying to understand but as of now I remain long on the stock.
DYODD GLTA
Cheers
Toinv :)