The self-medication hypothesis posits that alcohol is consumed to cope with stress, but corresponding evidence (incl. its impact on physiological stress markers) is heterogeneous. Thus, this systematic review examined the relationship between acute stress, acute alcohol consumption, and cortisol levels in individuals with varying alcohol use disorder (AUD) statuses. Following PRISMA guidelines, records from PubMed/Medline, Web of Science, and PsycInfo up to 16/05/2025 were analysed. We included 53 experimental and 31 observational studies that reported alcohol consumption volume after stress versus control conditions or measured cortisol recovery (CMin) and reactivity (CMaxMin) following alcohol intake with or without concurrent stressor exposure. Samples were classified by AUD status (active AUD, previously diagnosed but abstinent, or no AUD). Additionally, the moderating effect of family history of AUD was investigated. Regarding effects of acute stress on alcohol consumption, stressor exposure only increased alcohol consumption when small-study effects were not accounted for (gREE = 0.25), but this effect disappeared with adjustments (gPEESE = 0.02). Acute alcohol consumption was associated with delayed cortisol recovery (CMin↑; gREE = 0.15), especially in active AUD individuals (gREE = 0.46) and those with a familial history of AUD (gREE = 0.16). However, alcohol intake did not significantly affect cortisol reactivity (β = -0.01), although contrasting effects were seen in active AUD individuals (CMaxMin↑) and those with familial AUD histories (CMaxMin↓). In conclusion, acute stress does not increase alcohol consumption, and alcohol consumption does not regulate cortisol peak responses. Since alcohol consumption altered cortisol recovery, minimal cortisol levels may be a sensitive marker of alcohol-related change in adrenal functioning contributing to AUD progression.