During lactation, mammals resorb mineral from the maternal skeleton to provide calcium to milk. Rodents lose 25% to 35% of skeletal ash weight, ash calcium content, and bone mineral content as measured by dual‐energy X‐ray absorptiometry (DXA), and have compromised material properties of bone as assessed by crushing vertebrae and 3‐point bend tests of femora or tibias. The strength, stiffness, and toughness of vertebrae, femora, and tibias are reduced by as much as 60%. The effects of lactation are not uniform throughout the skeleton, but instead resorption is much more marked in the trabecular‐rich spine than in the appendicular skeleton or whole body. Women who breastfeed exclusively lose an average of 210 mg calcium in milk each day, whereas nursing of twins or triplets can double and triple the output of calcium. Clinical data are also consistent with skeletal calcium being released during lactation to provide much of the calcium needed for milk production. Lumbar spine bone mineral density (BMD), as assessed by DXA, declines by a mean of 5% to 10% among numerous studies during 3 to 6 months of exclusive lactation, whereas largely cortical sites (hip, forearm, whole body) show half that loss or no significant changes. Micro‐CT of rodents and high‐resolution peripheral quantitative computed tomography (HR‐pQCT) imaging of women confirm that lactation causes microarchitectural deterioration of bone. These skeletal losses occur through two pathways: upregulated osteoclast‐mediated bone resorption and osteocytic osteolysis, in which osteocytes remove mineral from their lacunae and pericanalicular spaces. After weaning, the skeleton is fully restored to its prior mineral content and strength in both animal models and humans, despite persistent microarchitectural changes observed in high‐resolution imaging. Osteoblasts upregulate to lay down new osteoid, while osteocytes remineralize their surroundings. The factors that stimulate this post‐weaning skeletal recovery remain unclear. In most studies, a history of lactation does not increase the risk, but may protect against, low BMD and fragility fractures. © 2017 American Society for Bone and Mineral Research.