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Really thoughtful piece. As a clinician scientist, I love seeing the autism conversation move from “behavior only” to biology + behavior, without reducing a heterogeneous condition to a single pathway. The taurine signal here is especially intriguing because it’s not just an “antioxidant” story: taurine touches inhibitory tone (GABA/glycine modulation), neurodevelopmental signaling, mitochondrial energetics, and even osmoregulation; exactly the kinds of fundamentals you’d expect to influence circuits like the ACC that govern cognitive flexibility and repetitive behaviors. That said, this is still an association (cross-sectional MRS), so the key question becomes: marker, mediator, or consequence? Diet selectivity, sleep/circadian disruption, inflammation, meds, and broader metabolic context could all push taurine and symptoms in the same direction. The registered RCT you mention is the right next step, and I’m very curious whether responders cluster by phenotype (diet pattern, GI features, baseline taurine, sensory profiles, etc.). Practical take-home I’d echo: food-first (seafood/dark meats if appropriate), caution against “miracle molecule” framing, and keep supplementation firmly in the “adjunct/under study” bucket, not a replacement for established supports. If taurine ends up being a modifiable lever for a subset, that would be a genuinely meaningful win.

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