This study examines foetal testosterone (fT) levels (measured in amniotic fluid) as a candidate biological factor, influencing sex differences in systemizing. Systemizing is a cognitive process, defined as the drive to analyze or construct systems. A recent model of psychological sex differences suggests that this is a major dimension in which the sexes differ, with males being more drawn to systemize than females. Participants included 204 children (93 female), age 6–9 years, taking part in a long-term study on the effects of fT. The systemizing quotient – children’s version was administered to these mothers to answer on behalf of their child. Males (mean = 27.79 ± 7.64) scored significantly higher than females (mean = 22.59 ± 7.53), confirming that boys systemize to a greater extent than girls. Stepwise regression analysis revealed that fT was the only significant predictor of systemizing preference when the sexes were examined together. Sex was not included in the final regression model, suggesting that fT levels play a greater role than the child’s sex in terms of differences in systemizing preference. This study suggests that the levels of fT are a biological factor influencing cognitive sex differences and lends support to the empathizing–systemizing theory of sex differences.
Bonnie Auyeung, Simon Baron-Cohen, Emma Chapman, Rebecca Knickmeyer, Kevin Taylor and Gerald Hackett
Serena Khoo, Greta Lyons, Anne McGowan, Mark Gurnell, Susan Oddy, W Edward Visser, Sjoerd van den Berg, David Halsall, Kevin Taylor, Krishna Chatterjee and Carla Moran
Familial dysalbuminaemic hyperthyroxinaemia (FDH), most commonly due to an Arginine to Histidine mutation at residue 218 (R218H) in the albumin gene, causes artefactual elevation of free thyroid hormones in euthyroid individuals. We have evaluated the susceptibility of most current free thyroid hormone immunoassay methods used in the United Kingdom, Europe and Far East to interference by R218H FDH.
Different, one- and two-step immunoassay methods were tested, measuring free T4 (FT4) and free T3 (FT3) in 37 individuals with genetically proven R218H FDH.
With the exception of Ortho VITROS, FT4 measurements were raised in all assays, with greatest to lowest susceptibility to interference being Beckman ACCESS > Roche ELECSYS > FUJIREBIO Lumipulse > Siemens CENTAUR > Abbott ARCHITECT > Perkin-Elmer DELFIA. Five different assays recorded high FT3 levels, with the Siemens CENTAUR method measuring high FT3 values in up to 30% of cases. However, depending on the assay method, FT4 measurements were unexpectedly normal in some, genetically confirmed, affected relatives of index FDH cases.
All FT4 immunoassays evaluated are prone to interference by R218H FDH, with their varying susceptibility not being related to assay architecture but likely due to differing assay conditions or buffer composition. Added susceptibility of many FT3 assays to measurement interference, resulting in high FT4 and FT3 with non-suppressed TSH levels, raises the possibility of R218H FDH being misdiagnosed as resistance to thyroid hormone beta or TSH-secreting pituitary tumour, potentially leading to unnecessary investigation and inappropriate treatment.