Figure 4.

Alcohol consumption, categorized as chronic mild–moderate, chronic heavy, or acute heavy (binge drinking), has varying impacts on ICH. ICH is divided into deep ICH, primarily caused by small vessel disease due to hypertension and platelet dysfunction as well as lobar ICH, influenced by cerebral amyloid angiopathy (CAA) and atherosclerosis. Both types involve SBI mechanisms like oxidative stress, neuroinflammation, mitochondrial dysfunction, endothelial dysfunction, and cell apoptosis. Chronic heavy alcohol consumption exacerbates all these SBI mechanisms. Acute heavy consumption contributes to oxidative stress, neuroinflammation, endothelial dysfunction, and apoptosis but not mitochondrial dysfunction. In contrast, chronic mild–moderate consumption can be protective, reducing neuroinflammation and CAA by lowering low-density lipoprotein-cholesterol (LDL-c).