GH deficiency (GHD) in adults is associated with abnormalities in body composition, metabolic derangements, sub-optimal physical performance, high incidence of adverse cardiovascular risk factors and poor quality of life. GHD adults are insulin resistant and have reduced hepatic glycogen stores, reduced insulin stimulated glucose utilization and reduced glycogen synthesis in muscle. GH replacement results in either no change or slight reduction in insulin sensitivity. Hence, it is important to monitor for the development of glucose intolerance in patients on long-term GH replacement. GHD is associated with a lipid profile known to predispose to premature atherosclerosis and cardiovascular disease, i.e. increased total and LDL cholesterol, decreased HDL cholesterol, increased small dense LDL particles and increased triglycerides. LDL-cholesterol abnormalities appear to improve with GH replacement even if maintained within physiological dose range; the greatest improvement occurs in those subjects with higher baseline total and LDL cholesterol values and in female patients with adult onset GHD compared with male patients with childhood onset GHD. In contrast, hypertriglyceridaemia is not corrected by GH replacement. The majority of the reports suggest GH replacement increases Lipoprotein-a levels. Long-term observation will be required to determine whether GH replacement reduces cardiovascular morbidity and mortality in GHD adults. The reduced muscle mass and strength associated with GHD has been shown to improve after GH replacement. GH treatment also improves maximal and sub-maximal exercise performance in GHD adults. The effects on protein metabolism, energy expenditure and thyroid metabolism in GHD adults are also critical.