Highlights
- •Y chromosome haplogroup I is associated with increased coronary artery disease risk.
- •Associations between haplogroup I and 10 male-/sex specific phenotypes were examined.
- •Neither aggression nor sex steroids are associated with Y chromosome haplogroup I.
Abstract
Objective
Amongst middle-aged men, haplogroup I is associated with ≈50% higher risk of coronary
artery disease than other paternal lineages of Y chromosome. We hypothesised that
carriers of haplogroup I had higher levels of aggression and estrogens and/or lower
levels of androgens early in life and thus might be more prone to cardiovascular disease
than men with other lineages of Y chromosome.
Methods
We reconstructed phylogenetic tree of the Y chromosome in >1000 young apparently healthy
white men from the general population. Each Y chromosome was classified into one of
13 most common European lineages. Androgens (DHEA-S, androstenedione, total testosterone)
and their metabolites (total estradiol, estrone) were measured by radioimmunoassays.
Information on five dimensions of aggression (total, physical, verbal, anger and hostility)
was collected using Buss and Perry questionnaire.
Results
Approximately 17% men inherited haplogroup I from their fathers. Carriers of haplogroup
I showed lower scores of verbal aggression than men with other haplogroups (β = −0.72, SE = 0.29, P = 0.012) and when further compared to carriers of most common R1a lineage and other
haplogroups (β = −1.03, SE = 0.34, P = 0.003). However, these associations did not survive a correction for multiple testing.
Sex steroids did not show even nominal level of association with haplogroup I.
Conclusion
Our data show no overall association between haplogroup I and sex-related phenotypes
in young white men. These results also suggest that the previously identified association
between haplogroup I and coronary artery disease is not likely mediated by unfavourable
profile of sex steroids or heightened aggression early in life.
Keywords
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Article info
Publication history
Accepted:
December 3,
2013
Received in revised form:
November 26,
2013
Received:
October 28,
2013
Identification
Copyright
© 2014 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.
