Ethanol consumption has minimal effects on cancellous bone architecture in femur and lumbar vertebra in two species of non-human primates

Alcohol abuse is a risk factor for atraumatic fractures. Our previous work using a non-human primate model of voluntary ethanol consumption showed that chronic ethanol intake for 6 months to 2.5 years decreased global bone turnover and tibial cortical porosity but did not result in changes in distal tibia cancellous architecture. However, bone remodeling varies among skeletal sites. Here, we extended this analysis to include 3 additional cancellous bone compartments (distal femur metaphysis, distal femur epiphysis, lumbar vertebra). Specifically, we applied a machine learning framework to data from 155 monkeys (100 ethanol and 55 controls) to identify the bone features associated with chronic ethanol use. In concordance with our prior findings, we did not find that ethanol consumption resulted in population-level changes in cancellous bone architecture. These findings support the concept that ethanol consumption similarly decreases bone formation and bone resorption across sites, resulting in minimal changes in bone remodeling balance. • Alcohol abuse is a risk factor for atraumatic fractures in humans. • Alcohol may lower bone turnover without altering cancellous bone architecture. • Machine learning detected no effects of alcohol use on bone architecture in monkeys. • The absence of architectural changes was consistent across cancellous bone sites.