Bilirubin has potent antioxidant properties in vitro and raised serum levels have been associated with lower rates of respiratory disease.
The enzyme uridine diphosphate glucuronosyltransferase polypeptide 1A1 is solely responsible for clearing bilirubin from the blood.
Homozygosity for 7 thymine-adenine (TA) repeats in the TATA box regulatory element of the UGT1A1 gene underlies a mild hereditary unconjugated hyperbilirubinemia (Gilbertís syndrome).
Dr Laura Horsfall and colleagues investigated whether this genetic variation is associated with differences in respiratory health.
|The odds of respiratory disease were half in those with Gilbertís syndrome genotype |
|Journal of Hepatology|
The relationship between the promoter genotype underlying Gilbertís syndrome, and respiratory outcomes assessed at ages 43, 53, and 60Ė64 were examined in 2190 members of the 1946 British birth cohort.
The (TA)7/7 genotype, present in 9% of the cohort, was associated with higher forced expiratory volume (FEV1) and forced vital capacity (FVC).
The researchers found that the relationship was strongest for heavy smokers at age 53 with mean FEV1 409 ml higher, and mean FVC 530 ml higher for UGT1A1 (TA)7/7 Gilbertís syndrome participants than for all others, indicating a protection from the pulmonary consequences of heavy smoking.
The team noted that the odds of respiratory disease were half in those with Gilbertís syndrome genotype compared to those without this genotype.
Dr Horsfall's team commented, "Genetically raised unconjugated serum bilirubin is associated with higher adult respiratory function and protection from respiratory disease."