, Volume 21, Issue 1, pp 70-71
Date: 19 Jan 2011

Reply to Letter of Peter Good

This is an excerpt from the content

Authors Helt, Kelley, Boorstein, Pandey, and Fein, asked authors Kinsbourne and Herbert to respond to the Good letter because of their expertise in this area. Following is Dr. Herbert's response.

The most remarkable thing about fever-associated transient improvement of core features of autism (Curran et al. 2007) is the challenge it poses to the conception of autism as trait, as static encephalopathy (Herbert 2009). What neurobiological mechanisms might underlie autism as dynamic encephalopathy? Others have advanced various models; Good proposes that in the setting of fever the free amino acid taurine may reduce astrocytic enlargement and capillary compression, thereby improving brain blood flow, and may account for clinical improvement in this context. He also proposes that ASD individuals who do not respond in this way may be taurine deficient.

One problem with pinning an explanation on any one mechanism or agent, such as taurine, is the pleiotropic web of influences of the components ...