Lithium - a continuing story in the treatment of bipolar disorder.

OBJECTIVE: To review the literature on the use of lithium in the treatment of bipolar disorder and highlight the evidence base supporting its efficacy and safety. METHOD: A selective literature review. RESULTS: Lithium is widely believed to be effective against acute mania, acute bipolar depression and in relapse prevention to either mania or depression. In fact, the data supporting efficacy in acute treatment are less impressive than is often claimed, whereas for relapse prevention and suicide prevention no other agent has comparable depth of support. Lithium is best described as the bench mark treatment for bipolar disorder, rather than the gold standard, because only a minority of patients show major clinical benefit. There is a developing need for further trials against new alternatives and in combination studies. CONCLUSION: Lithium has a continuing important role in the clinical management of bipolar disorder. Its under-utilization in North America reflects opinion rather than evidence and the demonstrated anti-suicide effects should help to reignite interest in its use.

Effects of zinc and vitamin A deficient diets on the hepatic mobilization and urinary excretion of vitamin A in rats.

Weanling rats were fed diets deficient in zinc (ZD), vitamin A (AD), or both (ZAD) for 3 weeks. Each then received 20 mug of 11,12-3H-retinyl acetate. Plasma retinol was monitored for radioactivity for 5 hours and urine for 6 days. Rats were killed and measurements made of plasma and liver vitamin A and plasma zinc. Plasma vitamin A was depressed but growth was not affected in AD rats compared to pair-fed controls. Radioactivity appeared most rapidly in the plasma retinol fractions of the two vitamin A-depleted groups (AD and ZAD) and was excreted most rapidly in the urine of these same groups. Zinc-deficient diets (ZD and ZAD) caused depressed plasma levels of zinc and vitamin A and growth retardation greater than in pair-fed controls. However zinc deficiency had no effect on mobilization of newly-ingested vitamin A or urinary excretion of labeled metabolites. Liver stores of vitamin A were lower for ZD rats than for controls. The data indicate that zinc deficiency is not a limiting factor in hepatic vitamin A release except as it influences growth and body demand for the vitamin. The data also suggest that newly-absorbed vitamin A is mobilized and utilized in preference to that previously stored in the liver.