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ADC Fetal and Neonatal Edition Letters and ADC Education and Practice Letters
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James M. Howard, Biologist independent
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jmhoward{at}anthropogeny.com James M. Howard
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Dear Editor, It is my hypothesis that the "secular trend," the increase in size and earlier puberty of children, is caused by an increase in the percentage of women of higher testosterone within the population with time. Maternal testosterone has been connected with autism. I suggest the increase in autism, and other increasing disorders, that are occurring is due to the secular trend; I suggest increasing exposure of fetuses to increasing maternal testosterone is increasing autism. (http://www.anthropogeny.com/increase in autism.htm) This increase in maternal testosterone occurs in different groups of women of differing levels of testosterone. Therefore, the consequences of this fetal exposure will manifest as increases in different ways. For example, I suggest obesity, diabetes, and breast cancer are increasing because of this exposure in different women. Dr. Baron-Cohen has demonstrated "mothers of autistic children often show patterns of brain activity more associated with men." (BBC comments on the internet). I suggest the connection of these types of mothers is that they may produce increased levels of testosterone. |
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Simon Baron-Cohen, Scientist Cambridge University
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sb205{at}cam.ac.uk Simon Baron-Cohen
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Dear Editor, I welcome James Howard's eLetter prompted by my article on autism in your Journal. The hypothesis that one risk factor for autism may be maternal levels of testosterone (T) has several pieces of supportive evidence. First, second-to-fourth digit (2D:4D) ratios show sexual dimorphism related to T levels, and mothers of children with autism have masculinized 2D:4D ratios. Second, mothers of children with autism have a hypermasculinized pattern of brain activity (measured by blood flow during fMRI whilst performing tasks which demonstrate sexual dimorphism in the typical brain) (Baron-Cohen et al, in press). Whether this reflects T levels is not known, but there is a large literature from animal research demonstrating foetal testosterone (FT) levels shape sexual dimorphism in the brain. Finally, and most directly relevant to the maternal T hypothesis, we have just completed a study surveying mothers of children with autism for T-related medical conditions. These mothers show elevated rates of these (Ingudomnukul et al, submitted). It is of interest that FT levels (measured following amniocentesis) correlate inversely with social behaviour and directly with narrowed attention postnatally (Knickmeyer et al, 2005). If it turns out that a foetus who later develops autism has high T levels, and their mother does too, this could reflect shared susceptibility genes, or maternal T acting as an environmental risk factor by crossing the placenta, or both. It is important to highlight that at present we only have a set of clues for both the FT and maternal T hypotheses in relation to autism, and that considerably more research is needed in this area. Key references Baron-Cohen, S, Knickmeyer, R, & Belmonte, M (2005) Sex differences in the brain: implications for explaining autism. Science, 310, 819-823. (A review of the relevant clues mentioned above). Baron-Cohen, S, Wheelwright, S, Williams, S, Ring, H, Bullmore, E, Brammer, M, Gregory, L, & Chitnis, X, (in press) fMRI of parents of children with Asperger Syndrome: a pilot study. Brain and Cognition. Ingudomnukul, E, Baron-Cohen, S, Knickmeyer, R, & Wheelwright, S (submitted) Elevated rates of testosterone-related disorders in a sample of women with autism spectrum conditions. Unpublished ms, University of Cambridge. Knickmeyer, R, Baron-Cohen, S, Raggatt, P, & Taylor, K (2005) Foetal testosterone, social relationships, and restricted interests in children. Journal of Child Psychology and Psychiatry. 46,198-210. |
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