Clinical signs of rickets include craniotabes, palpable enlargement of the costochondral junctions, and thickening of the wrists and ankles. Diagnosis is based on nutritional history and clinical observation and confirmed by chemical analysis and radiography. Nonrachitic craniotabes can occur in the immediate postnatal period but disappear before rachitic softening of the skull becomes manifest. Congenital epiphyseal dysplasia, cytomegalic inclusion disease, syphilis, rubella, and copper deficiency are further differential diagnoses. In most cases in Western countries, there is a combination of different risk factors, such as maternal vitamin D deficiency, no vitamin D supplementation, long-term breastfeeding, and insufficient sunlight exposure.3 Occult rickets has been reported in Asian immigrant children in the United Kingdom.4 Dagnelie et al5 compared the vitamin D metabolism in white 10- to 20-month-old children receiving a macrobiotic diet with children on omnivorous diets. The low availability of calcium in the macrobiotic diet was an independent factor in causing the high prevalence of rickets in infants with macrobiotic diets.5 Nutritional rickets by child neglect without signs of child abuse has received little attention.6 The mother of this patient was an alcoholic; alcohol abuse is present in many families with abused or neglected children. In these families, marital problems, unemployment, and drug abuse may play a role as trigger factors.7,8 Prevention and treatment measures for problems related to alcohol have been proposed, such as home visitation services.