Key result
In healthy individuals, additive genes accounted for 35% of the variance in plasma EC-SOD levels (P<0.00002), with significant pleiotropy observed between EC-SOD and apoA-I.
Population
610 healthy Australians (family data)
Design
Cross-sectional
Authors
Loading...
Genetic EC-SOD variance with apoA-I is hypothesis-generating; leaves open clinical cardiovascular applications.
Observational (n=610)
p-value: p=<0.00002
Over a third of the variance in EC-SOD plasma levels in healthy individuals is due to additive genetic effects, with shared genes influencing both EC-SOD and apoA-I levels.
Mahaney et al. (2000) conducted an observational in Healthy (n=610). Additive genes was evaluated on Variance in plasma EC-SOD levels accounted for by additive genes (p=<0.00002). In healthy individuals, additive genes accounted for 35% of the variance in plasma EC-SOD levels (P<0.00002), with significant pleiotropy observed between EC-SOD and apoA-I.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: