Brain hyperserotonemia causes autism-relevant social deficits in mice.
Miho Tanaka, Atsushi Sato, Shinya Kasai and 12 others
PMID 30498565WHAT IT FOUND
In mice with reduced serotonin transporter function, a tryptophan-free diet lowered striatal serotonin and increased social interaction.
This is animal evidence, not a human autism treatment.
Key findings
01In mice, Sert heterozygous and knockout animals showed reduced active social interaction compared with wild-type animals.
02In mice, a tryptophan-free diet lowered extracellular serotonin in the striatum in all genotypes.
03In mice, the tryptophan-free diet increased active social interaction in Sert heterozygous and knockout animals.
STILL TO COME
How it was doneWhat they found
Read the rest of this summary
You get three full summaries a month, free, and we do not ask for a card. Search, the TL;DRs and your library stay unlimited either way.
What it does not show
The study was done in mice, not humans, so it does not show what happens in patients. The tryptophan-free diet was tested in mice, not as a clinical intervention, and no human social communication outcome was measured. The paper does not state the total number of mice, so the reader cannot judge the sample size. The authors note that the effect of the diet on locomotor activity was not fully evaluated.
The easy way to misread this
Do not conclude that a tryptophan-free diet is a treatment for autistic patients. The study tested mice, not humans, and it did not evaluate speech, occupational, or physical therapy outcomes.