Genetic analyses have suggested a causal association between alcohol intake and cardiovascular diseases, questioning the purported cardioprotective effects of modest intake. Though traditional approaches to genetic epidemiology are limited in ability to assess association shapes, we hypothesized that any alcohol may increase risk of cardiovascular disease. In 371,463 participants from the UK Biobank, we first examined for confounding in epidemiological associations between alcohol intake and cardiovascular diseases. Next, using traditional and non-linear genetic approaches (Mendelian randomization), we assessed for causal links of alcohol consumption with several cardiovascular diseases and evaluated the shapes of all causal associations identified. Study participants consumed 9.2 (SD, 10.6) standard drinks per week on average; 121,708 (32.8%) and 27,667 (7.5%) subjects had hypertension and CAD, respectively. Modest consumers of alcohol demonstrated healthier lifestyles - such as lower BMI and greater physical activity - than abstainers, and adjustment for lifestyle factors attenuated the observed benefits of light alcohol intake. Traditional and non-linear Mendelian randomization demonstrated consistently risk-increasing and quadratic associations between alcohol consumption and both clinical and subclinical cardiovascular disease, with exponential increases in risk across levels of drinking; relative to abstainers, consumption of 7, 14, 21, and 28 drinks per week conferred 1.2, 1.7, 3.4, and 8.9-fold odds of hypertension and 1.2, 2.3, 6.2, and 25.9-fold odds of CAD, respectively (both models p