Allan–Herndon–Dudley syndrome (AHDS)[1] is a rare X-linked inherited disorder of brain development that causes both moderate to severe intellectual disability and problems with speech and movement.

[2] Allan–Herndon–Dudley syndrome, which is named eponymously for William Allan, Florence C. Dudley, and C. Nash Herndon,[3][4] results from a mutation of the thyroid hormone transporter MCT8 (also referred to as SLC16A2).

[citation needed] In X-linked recessive inheritance, a female with one altered copy of the gene in each cell is called a carrier.

[citation needed] The signature of low T4 and high T3 was for a long time assumed to be caused by either compensatory hyperdeiodination or impaired uptake of T3 in target tissues.

A third hypotheses suggested it to ensue from impaired outward transport of thyroxine from thyroid cells and subsequently substrate-mediated overactivity of intrathyroidal deiodinases.

[11] The authors of several studies noted that especially silychristin, one of the compounds of the silymarin mixture seems to be perhaps the most powerful and selective inhibitor for the MCT8 transporter.

Because the thyroid hormones and the MCT8 as well are known to play a critical role during early and fetal development, the administration of silymarin during pregnancy is especially thought to be dangerous, potentially leading to the Allan–Herndon–Dudley syndrome.

[citation needed] In May 2013, the US FDA granted Orphan drug status to Diiodothyropropionic acid (DITPA) in the treatment of MCT8 deficiency.

In 2014, a case was demonstrated in which therapy with TRIAC in early childhood led to significant improvement of cognition and mobility.