Nevertheless, our study has some potential limitations. Self-reported alcohol consumption data are prone to bias and are challenging to harmonise across studies conducted over different time periods that used varying instruments and methods to record such data.20, 57 We did not, however, identify major differences in results across studies that used differing alcohol measurement instruments. Despite our study's access to extensive serial alcohol re-surveys from mid-life, our study could not investigate alcohol consumption during the entire life course. Misclassification in outcomes would have diluted dose-response associations, suggesting that true underlying associations of alcohol consumption with cardiovascular disease subtypes are stronger and more divergent than we observed. Because we did not generally have access to additional alcohol-related adverse outcomes (eg, non-fatal liver disease, injuries, or psychiatric comorbidities), we probably under-estimated potential benefits associated with lowering alcohol consumption. Because some individuals who reduced, but did not cease, alcohol consumption due to health complications were probably included in our analysis, we cannot exclude the effects of reverse causation (especially since some contributing studies did not record baseline chronic disease other than cardiovascular disease).
