"Autism from A to Z"
The Mary Coleman lecture was introduced two years ago with the aim of highlighting prominent researchers in autism and similar areas. The lecture is given every other year and this year's edition was presented by senior professor Christopher Gillberg. Christopher Gillberg began his research career in the 1970's and has authored over 650 peer-reviewed scientific articles, nearly 400 of which concern autism. Christopher Gillberg has been awarded several grants for his research such as the Fernström award for young researchers, H.M. The King's Medal and the Söderberg award for medicine. The title of this year's lecture was "Autism from A to Z". Christopher Gillberg started off by describing what autism is and what it is not. He concluded that there are almost as many different causes behind autism as there are people with autism. Synapses and clock genes play an important part in cases of clear disorder, but there are also associated environmental factors (premature birth, exposure to toxins and certain medications during the foetal stage, infections, trauma, vitamin D deficiency) that contribute to disorders and that may also cause autism in some cases. Clinical autism virtually always comes with at least one other symptom such as learning difficulties, language difficulties, motor deficits, ADHD etc. People with autism but without any comorbid features are identified later in life and sometimes not at all, and if their autism goes unidentified they might instead be characterised as odd and/or loners. The core symptoms of autism are not increasing across the population, however in some places the number of autism diagnoses is increasing. There is no sharp delineation between autism and autistic traits and between autistic traits and what we call normal. Christopher Gillberg emphasised that it is abnormal to not have any autistic features. Four fifths of the population have at least one autistic trait. The autistic traits are not something that one outgrows, but the disorder caused by said traits can decrease or increase, and this in turn usually depends on the presence (or absence) of other conditions (disorders/illnesses). The members of the audience were then, in a pedagogic manner, taken on a tour of autism, from genetics to treatment via epidemiology and diagnostics, in alphabetical order. In the "A" section we learned, among other things, about a study showing that the amygdala (which might be described as the brain's "fight-and-flight centre") is activated when people with autism are forced to look other people in the eye, while the "B" section included a description of Bumetanide, a diuretic with promising potential in the treatment of autism, and so on. Christopher Gillberg finished the lecture by arguing why it is meaningless for research endeavours to study autism without any further specification. Autism is such a broad term with so many different causes and clinical presentations that it would be impossible to group all people with autism using one and the same term. Christopher Gillberg made a comparison with studies of cancer where studies of causes and treatment distinguish between separate cancer forms. Even if there may be a practical and societal utility to having a general autism diagnosis, there is still a need for a more specific description of autism (and of "comorbidity") in research contexts. The fact that more than seventy years of research of the broad autism term has failed to result in any targeted medical treatments serves as a compelling argument for this point.