Elevated ACE activity is not associated with asthma, COPD, and COPD co-morbidity

SummaryThe angiotensin-converting enzyme (ACE) gene is a potential candidate gene for risk of asthma, COPD, and COPD co-morbidity. In 9034 Danish adults, we determined whether individuals homozygous or heterozygous for the ACE D allele are at greater risk of asthma, COPD, or COPD co-morbidity compared with ACE II homozygous individuals. In the general population, serum ACE activity increased with the number of D alleles (Kruskal-Wallis ANOVA: II vs. ID, p < 0.001; ID vs. DD, p < 0.001); however, this did not translate into altered risk of asthma or COPD. In the general population, the odds ratio (95% confidence interval) for asthma was 1.2 (0.9–1.4) for ID individuals and 1.2 (0.9–1.5) for DD individuals compared with II individuals. In the general population, the odds ratio for COPD was 0.9 (0.8–1.1) for ID individuals and 1.0 (0.8–1.2) for DD individuals compared with II individuals. Among patients with COPD, the odds ratio for ischemic heart disease was 1.1 (0.8–1.6) for ID individuals and 1.2 (0.8–1.7) for DD individuals compared with II individuals; corresponding odds ratios for hypertension were 1.1 (0.7–1.5) and 0.8 (0.5–1.2), and for low physical activity 0.9 (0.5–1.4) and 0.7 (0.4–1.2). The results were similar upon adjustment for sex, age, smoking status, body mass index, total cholesterol, and ACE inhibitor/angiotensin II type 1 receptor blocker use. These data suggest that lifelong genetically elevated ACE activity is not a major risk factor for asthma or COPD, or for ischemic heart disease, hypertension, and low physical activity in COPD patients.