Blue Jefe
Member
- Joined
- Sep 24, 2017
- Messages
- 22
Hey all,
First post. Tagging @haidut
I would have made this a PM but the forum was denying me saying it was spam. So here I am.
I have ME/CFS which the latest research is showing to be a hypometabolically driven autoimmune condition. I'm trying Mitolipin and plan on buying Gonadin soon. So thanks so much for providing these unique products @haidut!
Here is a great paper from last year that breaks down the specific hypometabolic features of ME/CFS.
Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome
tldr; ME/CFS is characterized by upregulated PPAR delta, SIRT4, PDK1,2,4 and inhibited Pyruvate Dehydrogenase Enzyme Complex. Also we have CD8+ T cell clonal expansion and B cell driven autoantibody production (as you pointed out 95% of CFS patients have anti-cardiolipin antibodies).
Personally I have anti Ganglioside, Acetylcholine Muscarinic and alpha Adrenergic antibodies. I take Rapamycin, the quintessential mTorC1 inhibitor (I had a theory that overactive mTorC1 was involved and Rapamycin has improved my condition probably by 33% and therefore a relative major success).
My personal theory is the Liver X Receptor (of which Squalene is essentially the endogenous ligand) is being suppressed in ME/CFS and we have some sort of hypercholesteremia and liver/bile acid dysfunction. The Liver X Receptor has recently been elucidated to be suppressed during a viral infection and then reactivated to commence resolution of the immune response. My understanding is that if LXR does not resolve the immune response a state of hypometabolically driven autoimmunity can occur. No one has been able to connect this to ME/CFS yet but I'm trying to bring this to researchers attention.
Anyways, I believe @haidut is in a much better position to research/develop/market a product for ME/CFS (I know you cannot claim it's specifically for ME/CFS) than researchers who are strapped for cash and have to rely on patient donations. It's a horrible system that probably won't produce any treatments for us for many years.
Thanks for taking the time to consider this @haidut or anyone else who has any insight here. I'd love to discuss with anyone with a better understanding of metabolism (Econ major here before getting sick).
First post. Tagging @haidut
I would have made this a PM but the forum was denying me saying it was spam. So here I am.
I have ME/CFS which the latest research is showing to be a hypometabolically driven autoimmune condition. I'm trying Mitolipin and plan on buying Gonadin soon. So thanks so much for providing these unique products @haidut!
Here is a great paper from last year that breaks down the specific hypometabolic features of ME/CFS.
Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome
tldr; ME/CFS is characterized by upregulated PPAR delta, SIRT4, PDK1,2,4 and inhibited Pyruvate Dehydrogenase Enzyme Complex. Also we have CD8+ T cell clonal expansion and B cell driven autoantibody production (as you pointed out 95% of CFS patients have anti-cardiolipin antibodies).
Personally I have anti Ganglioside, Acetylcholine Muscarinic and alpha Adrenergic antibodies. I take Rapamycin, the quintessential mTorC1 inhibitor (I had a theory that overactive mTorC1 was involved and Rapamycin has improved my condition probably by 33% and therefore a relative major success).
My personal theory is the Liver X Receptor (of which Squalene is essentially the endogenous ligand) is being suppressed in ME/CFS and we have some sort of hypercholesteremia and liver/bile acid dysfunction. The Liver X Receptor has recently been elucidated to be suppressed during a viral infection and then reactivated to commence resolution of the immune response. My understanding is that if LXR does not resolve the immune response a state of hypometabolically driven autoimmunity can occur. No one has been able to connect this to ME/CFS yet but I'm trying to bring this to researchers attention.
Anyways, I believe @haidut is in a much better position to research/develop/market a product for ME/CFS (I know you cannot claim it's specifically for ME/CFS) than researchers who are strapped for cash and have to rely on patient donations. It's a horrible system that probably won't produce any treatments for us for many years.
Thanks for taking the time to consider this @haidut or anyone else who has any insight here. I'd love to discuss with anyone with a better understanding of metabolism (Econ major here before getting sick).