Background
When I first started learning about the pathology of sensory overload in autistic people, I thought that it was due to a potassium channelopathy. This was because I had learned that sensory overstimulation is caused by intracellular hypokalaemia, and at the time, research had just been published about the importance of inwardly-rectifying potassium channels in autism. My friend Benjine Gerber sent me information and explained things to me in simple ways. I understood about one-twentieth of it, but I was able to make a pretty good video explaining sensory overload in layman’s terms. This was screened at the South Asia International Autism Conference of 2015.
I subsequently learned that the problem is more likely to be a congenital voltage-gated calcium channelopathy.
New learning
Several possible starting points for the same end-problem
More recently, I learned that (in theory) a variety channelopathies could end up yielding similar symptoms, because the problem, when you think about it, is electrolyte dysregulation, and there are several ways in which you could end up with that. (Obviously under adverse conditions such as severe gastroenteritis, or war plus starvation, you could end up with an intracellular potassium deficiency and sensory overload too, but that’s another story.) So, that potassium channel study from a few years ago (subsequently updated) once again became relevant. And it’s on my reading list as I try to piece all this together.
Meanwhile, please bear in mind that the treatment isn’t merely to eat bananas (drives me nuts when people say this!) or take potassium pills, because this is not the whole problem, and it also doesn’t address the cause.
The scope of my project does not include treating the cause and all the co-factors, because I fear that if we go directly there, we won’t get doctors on board, because they tend to balk at complexity. I just need them to be aware that when taking the first step in treatment, they are only treating the condition which is the end result of a chain of events. It will at least provide rapid relief and several other knock-on benefits for patients. It’s better than doing nothing.
Hyperkalaemic versus hypokalaemic sensory overstimulation
This was quite a surprise to me. I learned this from someone who followed the approach we generally use for treating sensory overload, except that with this person, everything got significantly worse on treatment. A typical treatment protocol for sensory overload includes (inter alia) upping the magnesium and potassium and reducing carbodydrates; but for this person, it was necessary to reduce the potassium and increase the carbohydrates!
A bit of further reading taught me that whereas this is uncommon, it’s not unheard of. See also this overview, which mentions both hypo- and hyperkalaemic periodic paralysis stemming from channelopathies.
I will now have to add this to my paper.
Update 31 August 2020
I have put the writing of this paper on hold indefinitely. I cannot keep it up now that there are so many other things I need to focus on to help people survive. I am frustrated by the prominent autism researchers in my country who do not help autistic people’s own priorities reach the top of the autism research agenda, but who instead pander to the goals of donors who violate disability rights. The work on documenting treatment for sensory overload needs doing, but I cannot do it. Please support Benjine in any way you can. This remains a health issue for millions of people. I will continue lobbying for change.
Update 24 September 2021
Well, I tried to give up, but I couldn’t let go. This is a major development, which adds a whole new factor. Some people don’t benefit from either the hypokalaemia treatment regime or the hyperkalaemia regime. This may be why: