Overabundance of reactive oxygen species (oxidative distress) leads to redox homeostasis disturbance and is associated with many pathological conditions. Accumulating evidence suggests that oxidative distress may contribute to osteoporosis. This review thoroughly outlines the relationships among osteoporosis, redox homeostasis, and alcohol addiction, since these relations are not sufficiently known and subsequently summarized. The brain-bone axis plays a crucial role in alcohol-induced damage to the nervous and skeletal systems. Alterations in the nervous system can lead to osteoporosis because the central nervous system is involved in bone remodeling through various neural pathways. Conversely, as an endocrine organ, bone secretes a number of bone-derived factors (osteokines), which can influence brain function and behavior. As a result, osteoporosis is more common in individuals with neurological disorders, and sudden neurological events can rapidly increase the risk of osteoporosis. Excessive alcohol consumption is linked to many neurological complications, as well as osteoporosis, which are manifested by disrupted redox homeostasis, inflammation, neurodegeneration, inhibition of neurogenesis, decreased bone mineral density, impaired bone microarchitecture, altered mineral homeostasis, raising fracture risk, hormonal dysregulation, and altered gut microbiota composition. Compared to men, alcohol dependence has more negative consequences for women, including an increased risk of liver, cardiovascular, metabolic, mental disorders, and breast cancer. Abstinence has been demonstrated to improve bone and brain health in alcohol addiction. The discovery of the brain-bone axis may lead to the development of new therapeutic approaches for alcohol and other substance addictions. Further research is needed in this direction, as many questions remain unanswered.