Dr Jesper Mehlsen - Towards a uniform treatment regimen
There is knowledge in the Pathobiology of MECFS - using that to direct treatment
Neuro inflammation and human herpes virus - removal of EBV, cmv, hhv6. ; also decrease inflammation with mono/doxy (#remissionbiome ), LDN, aripripazol, SSRI, PEA, cox 2 inhibitors; ATR1 blockers - not one size fits all
Areas of TRx for mito dysfunction: anti oxidants, L carnitine, Dribose, ketogenic amino acids.
Other areas to address mito dysfunction through energy transport is Coq10 and NAD
Gastro dysfunction: dietary adjustments, pro kinetics, bile binders, probiotics, fecal transplants.
Cardiovascular control - sympathetic nervous system- aferente and efferent inputs focus .
Focus on neuro inflammation, mito dysfunction, GI dysfunction and cardiovascular control. All systems are involved in ME and often in LC. Some trx exist but few have been subject to placebo control.
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All of them are risk factors and we need to understand the interrelationships of complex disease and the possibilities for differentiated treatment by patient stratification. Biomarkers remain elusive and clinical subtypes need phenotype & system biology approach
We have just started to define the edges of the puzzle, we need to be able to complete the puzzle by understanding the big picture and what pieces are the components.
How do you determine molecular cause of MECFS and how do you treat and cure it ?
There are many crossroads in the maze of trying to treat MECFS. The decision taken had to do with the experience and perception of the person taking the decision
Before MECFS: a virus, bacteria, physical trauma, childbirth, vaccination, surgery.
TCA cycle - itaconate not discussed prevalently within this cycle. The transformation with CoA-SH was believed to be the end of that part of the process.
Every carbon is avoiding the processes that lead to NAD. The shunt will reduce the amount of ATP depending on the amount of carbon going in the different directions.