High winter mortality (28 per cent) in female Jersey calves (<one month) characterised by mild hepatopathy and enteropathy was investigated. Liver copper (Cu) was very high in casualties, but also high in culled, newborn males (19.2 ± 1.54 and 12.0 ± 2.74 sd mmol/kg dry matter (DM) respectively). Serum glutamate dehydrogenase (GLDH) was >80 IU/l in healthy females aged 3–24 weeks, and correlated with serum aspartate transaminase (AST). Copper supplementation of total mixed rations during lactation was excessive (40–60 mg added Cu/kg DM) and reduced to 16–28 mg Cu/kg, but supplementation of milk replacer and creep feed (10 and 35 mg added Cu/kg DM, respectively) continued. The syndrome recurred two years later, and liver Cu remained high in casualties (13.6 ± 2.6) and culled cows (6.38 ± 2.38 mmol/kg DM) prompting withdrawal of all Cu supplements. Mortality remained low (6–9 per cent) thereafter. Three years after removal of all Cu supplements, six culled newborn were examined postmortem; five had normal liver Cu (4.5 ± 1.73), but a sixth had 11.65 mmol/kg DM. In live, healthy calves (1-6 months old) sampled at the same time, GLDH and AST increased with age to levels found five years earlier, indicating possible subclinical hepatopathy. Causative links between Cu supplementation, high calf mortality and hepatopathy are plausible, and reductions in Cu supplementation may prove beneficial in other dairy herds.