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Somali women at high lattitudes may be at even greater risk of vitamin D deficiency if they observe the tradition of covering their skin.

In 2006 your lab published a paper in Nature Neuroscience linking a mirror neuron dysfunction to autism. How might reduced mirror neuron activity explain the symptoms of autism?

Reduced mirror neuron activity obviously weakens the ability of these patients to experience immediately and effortlessly what other people are experiencing, thus making social interactions particularly difficult for these patients. Patients with autism have also often motor problems and language problems. It turns out that a deficit in mirror neurons can in principle explain also these other major symptoms. The motor deficits in autism can be easily explained because mirror neurons are just special types of premotor neurons, brain cells essential for planning and selecting actions. It has been also hypothesized that mirror neurons may be important in language evolution and language acquisition.

Thus, a deficit in mirror neurons can in principle account for three major symptoms of autism, the social, motor and language problems.

There is convincing behavioral evidence linking media violence with imitative violence. Mirror neurons provide a plausible neurobiological mechanism that explains why being exposed to media violence leads to imitative violence.

I think there are two key points to keep in mind. The first one is the one we started with: mirror neurons are brain cells specialized for actions. They are obviously critical cells for social interactions but they can’t explain non-social cognition. The second point to keep in mind is that every brain cell and every neural system does not operate in a vacuum. Everything in the brain is interconnected, so that the activity of each cell reflects the dynamic interactions with other brain cells and other neural systems.

Pervasive Developmental Disorders, including Autistic Disorder, Asperger Disorder, Pervasive Developmental Disorder Not Otherwise Specified, and Childhood Disintegrative Disorder.

For autistic disorder, Fombonne says: The correlation between prevalence and year of publication was statistically significant and studies with prevalenceover 7/10,000 were all published since 1987. These findings point towards an increase in prevalence estimates in the last 15-20 years.

recent autism surveys have consistently identified smaller numbers of children with AS than those with autism within the same survey.

How much lower is difficult to establish from existing data, but a ratio of 3 or 4 to 1 would appear an acceptable,

We therefore used for subsequent calculations an estimate of 6/10,000 for AS, recognizing the strong limitations of available data on AS.

Eight studies provided data on childhood disintegrative disorder (CDD). Prevalence estimates ranged from 0 to 9.2/100,000.

The upper-bound limit of the associated confidence interval (4.0/100,000) indicates that CDD is a very rare condition, with about 1 case to occur for every 103 cases of autistic disorder.

Current evidence does not strongly support the hypothesis of a secular increase in the incidence of autism but power todetect time trends is seriously limited in existing datasets.

Whilst it is clear that prevalence estimates have gone up over time, this increase most likely represents changes in the concepts, definitions, service availability and awareness of autistic-spectrum disorders in both the lay and professional public.

The possibility that a true change in the underlying incidence has contributed to higher prevalence figures remains, however, to be adequately tested.