MAC wrote:Sorry, what I meant, is that the tHcy studies do not absolutely prove a dementia root mechanistic neurodegenerative cause. I have absolutely no theory, just trying to filter for absolute proven mechanisms that gives hope to improved targetted therapeutic result.
Ok I understand. No offence taken.
MAC I have said before that biochemistry is extremely complex. IMO scientists are still at the information gathering stage. Nothing is proven in black and white. We have no black and white root cause identified. Not one single one. I have said to you previously several times that I see you searching for certainty where there cannot be at this stage of the game. In your first posts you wanted black and white risk reduction numbers. And of course as a 4/4 woman I have much skin in this game so I want certainty at least as much as anyone.
However - at present I personally feel, and I know at least Bredesen is on the same page, in the absence of neurotoxin exposure (like the mould situation), glycaemic control and inflammation are likely to be the biggest players. But this is still an informed guess, as the evidence strongly points to this but is not conclusive.
There has to logically be other players because there are plausible biological mechanisms, in vitro and animal studies as well as observational data for aspects such as D3, Omega3, thyroid hormone, oestradiol, and yes homocysteine as well amongst others.
Of course questions are good. We are here for discussion. Everything we discuss here is unproven in terms of a large, decades long gold standard double blind RCT, which I predict will never see in our lifetimes. The body is the most complex system you will encounter as an engineer, and it is still only partially understood.
Welcome to my world as a mainstream, coalface doctor. I've worked with shades of grey and no certainty for over 30 years. And this field of dementia prevention is the greyest I have ever encountered.