No association between two candidate markers of prenatal sex hormones: Digit ratios (2D:4D and other) and finger-ridge counts

2010 ◽  
Vol 53 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Stefan G. Dressler ◽  
Martin Voracek
2021 ◽  
Vol 129 ◽  
pp. 104929
Author(s):  
Gareth Richards ◽  
Tess Beking ◽  
Baudewijntje P.C. Kreukels ◽  
Reint H. Geuze ◽  
Alan A. Beaton ◽  
...  

2012 ◽  
Vol 132 (4) ◽  
pp. 415-421 ◽  
Author(s):  
Adam J. Lawrance-Owen ◽  
Gary Bargary ◽  
Jenny M. Bosten ◽  
Patrick T. Goodbourn ◽  
Ruth E. Hogg ◽  
...  

The Lancet ◽  
1974 ◽  
Vol 303 (7867) ◽  
pp. 1168 ◽  
Author(s):  
JohnJ. Mulvihill ◽  
CharlotteG. Mulvihi ◽  
CatherineA. Neill

2020 ◽  
Vol 287 (1941) ◽  
pp. 20201756
Author(s):  
Boris van Leeuwen ◽  
Paul Smeets ◽  
Jeanne Bovet ◽  
Gideon Nave ◽  
Jonathan Stieglitz ◽  
...  

Economic preferences may be shaped by exposure to sex hormones around birth. Prior studies of economic preferences and numerous other phenotypic characteristics use digit ratios (2D : 4D), a purported proxy for prenatal testosterone exposure, whose validity has recently been questioned. We use direct measures of neonatal sex hormones (testosterone and oestrogen), measured from umbilical cord blood ( n = 200) to investigate their association with later-life economic preferences (risk preferences, competitiveness, time preferences and social preferences) in an Australian cohort (Raine Study Gen2). We find no significant associations between testosterone at birth and preferences, except for competitiveness, where the effect runs opposite to the expected direction. Point estimates are between 0.05–0.09 percentage points (pp) and 0.003–0.14 s.d. We similarly find no significant associations between 2D : 4D and preferences ( n = 533, point estimates 0.003–0.02 pp and 0.001–0.06 s.d.). Our sample size allows detecting effects larger than 0.11 pp or 0.22 s.d. for testosterone at birth, and 0.07 pp or 0.14 s.d. for 2D : 4D ( α = 0.05 and power = 0.90). Equivalence tests show that most effects are unlikely to be larger than these bounds. Our results suggest a reinterpretation of prior findings relating 2D : 4D to economic preferences, and highlight the importance of future large-sample studies that permit detection of small effects.


2007 ◽  
Vol 38 (1) ◽  
pp. 6-15 ◽  
Author(s):  
Cornelieke van de Beek ◽  
Stephanie H. M. van Goozen ◽  
Jan K. Buitelaar ◽  
Peggy T. Cohen-Kettenis

2020 ◽  
Vol 33 (3) ◽  
pp. 403-408
Author(s):  
Anna Kasielska-Trojan ◽  
Marian Danilewicz ◽  
Aneta Sitek ◽  
Boguslaw Antoszewski

AbstractBackgroundJuvenile breast hypertrophy is characterised by massive enlargement of the breast in the peri-pubertal period. We aimed to analyse body size measurements (body mass index [BMI], waist-to-hip circumference ratio [WHR]), digit ratio (ratio of II and IV digits’ length [2D:4D]) and oestrogen receptor (ER) alpha (ERα) and progesterone receptors (PRs) in the breast gland in women with juvenile gigantomastia.MethodsThe study involved 30 women (mean age 25.7 years) (mean age of onset – 14.8 years). ERα and PR expressions were detected immunohistochemically in breast gland samples. For comparison, 100 controls (50 women and 50 men) were included.ResultsBMI and WHR in women with gigantomastia were higher than in control women and the former had a higher WHR than expected for their BMI. 2D:4D in the examined women did not differ from that in control women. However, left 2D:4D was negatively related to the age of gigantomastia onset. There were no correlations between ER and PR expressions and the analysed body and digit ratios.ConclusionsThe lack of a relationship between 2D:4D and juvenile breast hypertrophy may suggest that foetal exposure to sex hormones may not be crucial in its aetiology. However, the link between high left 2D:4D and early development of gigantomastia suggests that prenatal sex hormones have a role in its development timing. High WHR, and particularly high WHR relative to BMI, may indicate that these women had at some stage of development higher circulating androgens, which may have been converted to oestrogens in breasts due to local aromatase activity. Verification of this hypothesis could allow consideration of the role of aromatase inhibitors in juvenile breast hypertrophy.


Neurology ◽  
2015 ◽  
Vol 85 (14) ◽  
pp. 1193-1194
Author(s):  
Robyn M. Lucas ◽  
Brenda Banwell

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