SEX DIFFERENCES IN VERBAL AND SPATIAL ABILITY RECONSIDERED IN RELATION TO BODY SIZE, LUNG VOLUME, AND SEX HORMONES

2003 ◽  
Vol 96 (3) ◽  
pp. 1347
Author(s):  
ONER TAN
2003 ◽  
Vol 96 (3_suppl) ◽  
pp. 1347-1360 ◽  
Author(s):  
Üner Tan ◽  
Mukadder Okuyan ◽  
Tugba Albayrak ◽  
Ahmet Akgun

Sex differences in verbal and nonverbal abilities were reconsidered in relation to bodily measures and sex hormones in Turkish university students. Perceptual-verbal ability was evaluated using As Test. To assess the nonverbal abilities, the mental rotation test and Cattell's Culture Fair Intelligence Test were used. As expected, the 53 women performed better than men on the As Test; 79 men had a higher mean than the 53 women on the mental rotation task; there was no sex difference on Cattell's IQ Test. Cattell IQs correlated only with tidal volume of lungs. Scores on the As Test did not show significant correlations with body size and lung capacities. Mental rotation was significantly correlated with height, weight, and lung volume. With covariates of height, weight, and vital capacity, sex differences in mental rotation completely disappeared, but the difference on the As Test increased while Cattell IQ remained sex-neutral. With testosterone as covariate, the sex difference on the As test increased but on the mental rotation task disappeared; Cattell IQ was sex-neutral. With covariates of estradiol and progesterone, sex differences on the As test disappeared; mental rotation scores and Cattell IQ were not influenced. Under a combined covariation of height, weight, and testosterone, sex differences in mental rotation reversed, women scoring better than men; after adding estradiol or progesterone instead of testosterone to this model, sex differences on mental rotation completely disappeared, but verbal ability and Cattell IQ were not changed. These results suggest that Cattell's Culture Fair Intelligence Test is unique in resistance to sex differences; perceptual-verbal ability was the most sex-specific mental trait but with dependence on estradiol; mental rotation, on the contrary, was least sex-specific, depending on body size, lung volume, sex hormones, and their combined actions, which explains women's better performance.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 8.1-8
Author(s):  
G. Robinson ◽  
K. Waddington ◽  
J. Peng ◽  
A. Radziszewska ◽  
H. Peckham ◽  
...  

Background:Males and females have altered immune responses resulting in variation in autoimmune and cardiovascular disease risk (CVR). Recently, these differences have played a role in the inflammatory response to COVID-19. Sex differences exist in the frequency and activity of immune-cell subsets but mechanisms underlying sexual dimorphism remain unknown. Juvenile-onset systemic lupus erythematosus (JSLE) is an autoimmune disorder that commonly emerges during puberty, has a strong female prevalence (female:male ratio, 4.5:1) and results in an increased CVR. JSLE is characterised by chronic inflammation and dyslipidaemia, where cardiovascular disease is a leading cause of mortality for patients. Our previous work identified a link between immune cell function and lipid metabolism in adult-onset SLE. We hypothesised that sex hormones could influence both lipid metabolism and immune cell function and this could determine sex-specific susceptibility to JSLE and associated CVR.Objectives:We investigated the role of sex hormones in modifying systemic lipid metabolism and inflammation.Methods:Nuclear magnetic resonance spectroscopy based serum metabolomics measuring over 130 lipoproteins (14-subsets with lipid compositions), flow cytometry measuring immune-cells, and RNA-sequencing were used to assess the metabolic and immune profile in young, pre/post-pubertal males (n=10/17) and females (n=10/23) and in individuals with gender-dysphoria (GD) under cross-hormone treatment (trans-male/female, n=26/25). This analysis was also performed on a cohort of post-pubertal male (n=12) and female (n=23) JSLE patients. Data was analysed by logistic regression, balanced random forest machine learning (BRF-ML), differential gene expression (DEG) and pathway analysis.Results:Post-pubertal males had significantly reduced cardio-protective high-density lipoprotein (HDL) subsets (p<0.0001) and increased cardio-pathogenic very-low-density lipoprotein subsets (p<0.0001) compared to females. These differences were not observed pre-puberty and were reversed significantly by cross-hormone treatment in GD individuals, suggesting that sex hormones regulate lipid metabolism in-vivo.BRF-ML (28 immune-cell subsets) identified an increased frequency of anti-inflammatory regulatory T-cells (Tregs) in post-pubertal males compared to females (p=0.0097). These Tregs were also more suppressive in males compared to females. Differences in Treg frequency were seen pre-puberty and were not altered by sex hormone treatment in GD individuals. However, Treg DEGs and functional transcriptomic pathways altered between post-pubertal males and females, including those involved in inflammatory signalling, overlapped with those altered by hormones in GD, suggesting hormones may also drive Treg functional changes. In addition, HDL metabolites modified by hormones showed differential associations with Treg phenotypes between post-pubertal males and females.Strikingly, sex differences in lipoproteins and Tregs were lost in JSLE, suggesting hormone signalling could be dysregulated in the pathogenesis of autoimmunity and could increase CVR for patients.Conclusion:Sex hormones drive altered lipoprotein metabolism and functional transcriptomic pathways in Tregs. Males have a lipoprotein profile associated with increased CVR, but a more anti-inflammatory immune profile compared to females. Together, this could explain sex differences in inflammatory disease susceptibilities and inform future sex-specific therapeutic strategies for the management of both JSLE and CVR.Acknowledgements:Lupus UKRosetrees TrustVersus ArthritisNIHR UCLH Biomedical Research CentreDisclosure of Interests:None declared


2021 ◽  
Vol 22 (9) ◽  
pp. 4620
Author(s):  
Holly J. Woodward ◽  
Dongxing Zhu ◽  
Patrick W. F. Hadoke ◽  
Victoria E. MacRae

Sex differences in cardiovascular disease (CVD), including aortic stenosis, atherosclerosis and cardiovascular calcification, are well documented. High levels of testosterone, the primary male sex hormone, are associated with increased risk of cardiovascular calcification, whilst estrogen, the primary female sex hormone, is considered cardioprotective. Current understanding of sexual dimorphism in cardiovascular calcification is still very limited. This review assesses the evidence that the actions of sex hormones influence the development of cardiovascular calcification. We address the current question of whether sex hormones could play a role in the sexual dimorphism seen in cardiovascular calcification, by discussing potential mechanisms of actions of sex hormones and evidence in pre-clinical research. More advanced investigations and understanding of sex hormones in calcification could provide a better translational outcome for those suffering with cardiovascular calcification.


2021 ◽  
pp. 153537022110196
Author(s):  
Nathalie Fuentes ◽  
Miguel Silva Rodriguez ◽  
Patricia Silveyra

Lung cancer represents the world’s leading cause of cancer deaths. Sex differences in the incidence and mortality rates for various types of lung cancers have been identified, but the biological and endocrine mechanisms implicated in these disparities have not yet been determined. While some cancers such as lung adenocarcinoma are more commonly found among women than men, others like squamous cell carcinoma display the opposite pattern or show no sex differences. Associations of tobacco product use rates, susceptibility to carcinogens, occupational exposures, and indoor and outdoor air pollution have also been linked to differential rates of lung cancer occurrence and mortality between sexes. While roles for sex hormones in other types of cancers affecting women or men have been identified and described, little is known about the influence of sex hormones in lung cancer. One potential mechanism identified to date is the synergism between estrogen and some tobacco compounds, and oncogene mutations, in inducing the expression of metabolic enzymes, leading to enhanced formation of reactive oxygen species and DNA adducts, and subsequent lung carcinogenesis. In this review, we present the literature available regarding sex differences in cancer rates, associations of male and female sex hormones with lung cancer, the influence of exogenous hormone therapy in women, and potential mechanisms mediated by male and female sex hormone receptors in lung carcinogenesis. The influence of biological sex on lung disease has recently been established, thus new research incorporating this variable will shed light on the mechanisms behind the observed disparities in lung cancer rates, and potentially lead to the development of new therapeutics to treat this devastating disease.


PLoS ONE ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. e0191373 ◽  
Author(s):  
Antonio Aguayo ◽  
Camille S. Martin ◽  
Timothy F. Huddy ◽  
Maya Ogawa-Okada ◽  
Jamie L. Adkins ◽  
...  

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