Stuttering Devices

'The start of a journey reflections on the gene discovery. Real science is encroaching on stuttering research and stuttering is now being cornered from two sides: the symptoms and the genes.

Mark asks the very crucial question that every sane person must now ask: How does a failure in a lysosomal transfer protein affect speech production? Genes are physical objects. No more hiding of your sloppy thinking behind the curtains of abstract psychological concepts.

You can point with the finger to them, and they deliver the instructions for the cells on how to build proteins. Three mutant genes were identified in people who stutter. Such a mutant gene results in the failure to produce a standard lysosomal transfer protein. If you have one, you very likely stutter.

Let's re-examine those glorious statements of early intervention in the lights of kids with one such mutant gene. How exactly should that work? Behavioural work à la Lidcombe or parental work lets them fully recover?

Oh, I once dared to ask the question on how such therapy can work if there is a neurobiological basis. The answer was of course: Brain Plasticity.

The magic word, yet again a curtain to hide behind your sloppy thinking. Let's be clear: How can early intervention change the mutant gene or provide the body with the right lysosomal transfer proteins. The answer is very clear: It cannot. The damage is done, and the brain of the kids are damaged.

Tell me that you try to install new behaviours and cognitive schemes in the young children in order for them to better cope with a life-long neurobiological deficit. Great, I wish you would have worked with me as a kid. But don't tell me that early intervention makes more kids recover fully. You are being fooled by the natural
recovery rate and slow relapse rate. And don't blame natural recovery on your abilities.

I also throw the gauntlet to those who are scientists. We need to come up with an over-arching framework on how to build theories on stuttering. We need cause-specific models, e.g. a model on how the found mutations lead to stuttering. But we also need an effective model that explains us the diversity of symptoms and their situation dependency.

We need the commonality to all cause-specific models. I would argue for a jam in the language-to-speech areas common to all subtypes of stuttering. Honestly, I have very little confidence in the modeling abilities of the eminent scientists, most of them are experimentalists and their modeling attempts are naive at best.
I also challenge the stuttering community not to chase into the gene-neurobiological corner.

Conditioning and cognitive beliefs are very clearly responsible for the modulation of the symptoms, its frequency and severity, and so is the well-being of the person. Yes, I cannot blame you for having a neurobiological deficit (or the mutant gene).

However, I can tell you that a decrease of your symptoms and an increase of your well-being is within your control. And yes it's not easy. It is very tough. And I have failed so far on the symptom side.

Am I just too lazy, do I just don't listen, do I have the wrong personality or is my brain too messed up? I don't know. But I do know that my well-being has considerably increased with regards to my speaking.


We are at the start of a real scientific journey. Let's take it together.byTom Weidig