Saying that oxygen homeostasis is impaired is the same as saying that overactive neuroinflammation is the cause of OCD. I mean, there is obviously neuroinflammation in specific parts that contribute a lot to OCD. Patients probably have the genetic susceptibility to be in a pro-inflammatory state easier and maybe some sodium-channel mutation that causes that part of the brain to be hyper (or hypoactive). So it's part a cause and part sustaining it. I'm not going against any of those things. I'm saying by acknowledging that those pathological states only come up depending on what social or physical environment people are in. There's plenty of evidence surrounding the interference effect of social cognition in stuttering and other mental states (for example 'Stuttering in relation to anxiety, temperament, and personality: Review and analysis with focus on causality'. Look for paragraph 8.5.2). Maybe the label social anxiety was not accurate enough, as I put social cognition and clinical social anxiety under a same label (social interference). Stuttering is the end product of a chicken and egg situation where you don't know what caused what anymore at some point. But the fact that more than 70% of stutterers can talk way more fluently when alone tells you that the circuits do function! What I'm trying to learn people is that processes like these are not irreversible and have to learn a way to FEEL more deeply into themselves as to what part of their social cognition is disrupting their speech. It worked for me, I helped many others in the hospital with this kind of reasoning (fibromyalgia, POTS, OCD, as I focus on integrative rehabilitation of complex patients). Peoples brains are so much more flexible than they think.