I see where you’re coming from, and I agree with you. I’m pretty sure Brocklehurst would agree as well, at least in principle. I think the main misunderstanding between you and him comes down to how you both define certain terminologies. I mean, for instance, what you describe as "auditory corrupted feedback" is what Brocklehurst might categorize as "stuttering-like disfluencies" (speech planning difficulty disfluencies, formulation difficulty dysfluencies, or even neurogenic execution-difficulty dysfluencies) rather than true stuttering. According to Paul, "Neurogenic stuttering is stuttering that appears to have been caused by a neurological injury of some sort. Usually, late-onset stuttering is presumed to be neurogenic, but there is no logical reason why **early childhood stuttering** cannot be neurogenic as well. Indeed, Alm and Risberg postulate that about 40% of all stuttering has a neurogenic component to it. It is quite possible that the percentage is much higher, including among young children." So you could see it like this, from his perspective, if these stuttering-like disfluencies—influenced by genetics—lead to a maladaptive mindset, such as the belief in the need to speak more perfectly, fluently or error-free before speech execution should proceed, this could trap 20% of children who continue to stutter in a vicious cycle. So this might prevent them from naturally outgrowing stuttering, what what he's implying. Do you think this alignment of definitions could clear up some of the perceived differences in your views? Regarding your statement that dopamine may not have anything to do with improved fluency.. I mean, I kinda agree with you here, and I think Paul agrees with you here. But more in the sense of, tonic (long-term dopamine) simply does not have direct influence on a moment-to-moment or word-to-word basis - that occur on a millisecond timeframe, I'm sure you can agree?! I wrote about it in this [comparative table ](https://docs.google.com/document/d/1WHq599nouADIqkVlAPIXgHECLhwaGvMq5BVnVYI087s/edit?usp=sharing)in Google drive. But on the other hand, phasic dopamine (that works on a milli-second timeframe in response to conditioned stimuli and triggers), found in [research](https://chatgpt.com/share/6783f992-66e4-800f-8426-3bfecacd7a70).. I think that such abnormal phasic dopamine release is the effect or result of an underlying subconscious mechanism - that regulates (or manages) speech execution - primarily based on things that occur on the psychosocial level (higher-order level). Of course, I think that this can only imply responses on a psychosocial level to auditory impairments (i.e., lower level feedback). To clarify, I'm referring to execution difficulty stuttering in response to conditioned stimuli (not the other types of *stuttering-like dysfluencies* such as the ADHD mechanical type of dysfluencies), I'm speaking about what Paul considers the true stuttering (or perhaps you could call it advanced stuttering due to the vicious circle that is **hard to recover from**?) rather than the mechanical type of stuttering like disfluencies Your thoughts?