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I can't answer your other questions, but figuring out why and how Abilify seems to be beneficial to (a subset of) pwME is an area of active investigation at the OMF. Ron mentioned it a few times in update videos and presentations.

That's correct. Three out of five IDO2 mutations that Dr Phair identified in his metabolic trap presentation(s) are on the 23andMe v4 chipset. Here's some n=1: I have all three. I am severe.

Quite right. "Publish or perish" is a common turn of phrase in academia. Gotta meet your quota of peer-reviewed published papers or risk losing your job! These pressures have trickle-down effects from research risk adversity (negative results are hard to get published) to pro forma studies...

The more I look at this paper, the less I know what to make of it. HPA axis* dysfunction and oxidative & nitrosative stress are (very) old ideas for the etiology of MECFS. Most of the treatments proposed in the paper - DHEA, NAC, and NADH, for instance - are known quantities. Yet MECFS is still...

That's fantastic! Carpe diem! (Well, you know, within the limits of your energy envelope!)

How are things, @leokitten ?

@Jessie 107 @chelby Hope you're both doing okay! We've not heard from you in a little while. How are your Abilify trials going?

They are indeed. FGF-21 - I was told in writing - is under ongoing investigation as a potential biomarker for certain mitochondrial disorders where it is found in elevated levels. FGF-21 is also found elevated in some patients with *defined* respiratory chain defects. Which, taken together...

My serum FGF-21 was tested some three years ago by a London, UK immunology lab as part of a study on mitochondrial dysfunction. My serum FGF-21 levels were found to be "very low". I was told that Oxford had also seen very low levels in adult patients with MECFS. The researchers had no explanation.

I'll take to answering my own question! :jimlad: I don't see how it does. The MetS study finds enrichment of indole pathway metabolites in urine, which are thought to result from bacterial metabolism of tryptophan. This is an entirely different pathway from the kynurenine pathway. It doesn't...

Does it? How?

Interesting. This is a Dutch study. The Netherlands experienced a "Q Fever epidemic" (link) between 2007-2011. Some 20% of patients went on to develop so-called "Q Fever Fatigue Syndrome" (QVS). I took a look at the official government guidelines on QVS (link to document, in Dutch). It describes...

Hmm. Abilify does not eliminate trapped cells' elevated tryptophan content, so it cannot push a patient out of the trap. Abilify also does nothing about kynurenine pathway inhibition in trapped cells. But, if I read the hypothesis correctly, it predicts that secondary effects on TPH1/2 will...

@Sid I know, I know. My point is that all dopaminergic drugs are not equal, and your friend's experience with bupropion can therefore not necessarily be extrapolated into a warning about Abilify. It's also worth noting that the present interest in Abilify is coming from the exact opposite...

I'm sorry to hear that. Important caveats though are: - Abilify is a serotonergic drug as much as a dopaminergic drug; - Even within the subclass of atypical antipsychotics, Abilify is atypical in that it acts as a partial agonist at D2, D3, and D4 receptors. This means it can correct high as...

It's no clearer in the original language (Dutch), most likely because the main article is effectively one long citation that seems to use the literal spoken or written words of Eline. The article's gray-box inset at the bottom briefly touches upon the experiences of fellow patient Marleen. It...

Gosh, the article by Dutch newspaper AD is a tricky one. It does not use the word degenerative ("degeneratief"), nor does it explicitly describe CCI as degenerative. In fact, it doesn't use the term CCI at all, speaking only of "neck instability" ("nekinstabiliteit"). The article strongly...