Would you take an experimental drug to stop your desire to stim?
I get a mid-week email from the National Association of Special Education Teachers (NASET) each week. These emails gather up what NASET’s editors think is relevant in the week’s news. In this morning’s collection, I found the following headline (source):
Building a better drug.
Iama Therapeutics is hoping a new class of molecule will prove successful against an old target in autism.
In the opening paragraph, the author sets up the premise. The researchers, it seems think that they may have found a way to “test whether dialing down inhibitory brain activity by modulating chloride ion transport” so that they can “treat the repetitive behaviors and social challenges that are associated with autism.” For them, “treat” equates to “stop.”
Imagine that for a moment. Would you take an experimental drug that may stop your stims? If so, why?
Before you run out the door to your doctor, demanding this new drug, read the article. You’ll find some shocking quotes like the following:
The autism mouse data align with other animal studies suggesting that manipulating NKCC1 may change social behavior, and they provide support for testing the hypothesis in people, Veenstra-VanderWeele says.
But mouse models, and especially behavioral tests in mice, often do a poor job of predicting a drug’s effect in people, says John Jay Gargus, director of the Center for Autism Research and Translation at the University of California, Irvine. He agrees that the company’s results so far lay the groundwork for a clinical trial.
But wait, there’s more …
The company plans to test the drug in two age groups of autistic children: 7 to 14 years and 14 to 18 years. Malizia, meanwhile, is building connections with advocacy groups and within the broader autistic community. He’s well aware that clinical trials are notoriously challenging for autism drugs, which often fail in late-stage trials. “Bumetanide is proof of this,” he says.
Another issue before Iama is how to best select participants for trials. Although manipulating NKCC1 to boost GABA activity makes sense for epilepsy, where hyperexcitability is a core part of the disease mechanism, says Veenstra-VanderWeele, in autism that mechanism will likely only be relevant for a subset of autistic people.
And it gets worse …
He also notes that the behavioral assessments that are used in clinical trials for autism drugs “are very difficult to define objectively.” That makes autism a risky place to start, compared with refractory epilepsy, where success or failure is much clearer to see, he says.
Read the article. See for yourself how we are viewed by the medical establishment and BigPharma. Ask yourself, is reducing your desire to stim worth risking your health by taking a drug whose mechanisms aren’t all that well understood by the people developing it? Let me know in the comments below.