COVID-19 Vaccination and Alcohol Consumption: Justification of Risks

Abstract

Since the beginning of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, pharmaceutical companies and research institutions have been actively working to develop vaccines, and the mass roll-out of vaccinations against COVID-19 began in January 2021. At the same time, during lockdowns, the consumption of alcoholic beverages increased. During the peak of vaccination, consumption remained at high levels around the world, despite the gradual relaxation of quarantine restrictions. Two of the popular queries on search engines were whether it is safe to drink alcohol after vaccination and whether this will affect the effectiveness of vaccines. Over the past two years, many studies have been published suggesting that excessive drinking not only worsens the course of an acute respiratory distress syndrome caused by the SARS-CoV-2 virus but can also exacerbate post-COVID-19 syndrome. Despite all sorts of online speculation, there is no specific scientific data on alcohol-induced complications after vaccination in the literature. Most of the published vaccine clinical trials do not include groups of patients with a history of alcohol-use disorders. This review analyzed the well-known and new mechanisms of action of COVID-19 vaccines on the immune system and the effects of alcohol and its metabolites on these mechanisms.

Keywords: COVID-19; SARS-CoV-2; alcohol; immune system; spike protein; vaccines.

Figure 1

Ethanol-induced overexpression of angiotensin-converting enzyme 2 (ACE2) activates pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling pathway and exacerbates the “spike effect” of COVID-19 vaccines.

Figure 2

Alcohol consumption affects the immune response to adenovirus-vector-based vaccines and vaccine-associated immune thrombosis and thrombocytopenia (VITT). Physiologically relevant concentrations of alcohol lead to endothelial dysfunction, which, in combination with stasis and hypercoagulability, could increase venous thromboembolism (VTE) formation. At the same time, small or moderate doses of alcohol have an inhibitory effect on secondary platelet aggregation responses.