126 CORRESPONDENCE lie for tragedieswheretherehasbeenno outreach, and previous carers may not even know about them? Conclusions from the three-year study await our final report this year. They will be based on the clinical and social outcomes, users' (patients and relatives) satisfaction, risk assessment, and an economic analysis. MA1-r MUUEN Research and Development for Psychiatry 134/138 Borough High Street London SEJ ILB Institute of Psychiatry De CrespignyPark London SE5 8AF by the fact that the point ofentry to the trial was the finding ofa low or borderline red cell folate level, at which point many of the patients were already on standard medication. We were studyingin a placebo controlledmanner the outcomeof an adjunct to treatmentand we had no wish, nor would it have been practical, to influence the normal treatment that thesepatientswere otherwisereceiving.We cannot exclude the possibility of baseline differences occurringduetochance, but nor haveweanyreason to believe that such differences exist. WeagreewithProcterandhavestressed for many years(Carney,1967;Reynolds,1967)that our obser vations are relevant to other psychiatric diagnostic categories. The influence of folate treatment in differentmentaldisordersmay bemediatedby an effect on mood, drive, initiative and sociability (ultimately cognition), as may also be the case for S-adenosylmethionine, a metabolitecloselyrelated to folate in methylation processes within the nervous system(Reynolds et a!, 1984). Procter and Anderson et a! discusspossiblecon nectionswith monoamineand biopterin metab olism, which we have emphasised since our earliest studiesof folate(Reynoldset a!, 1970,1984).In a recent study of 34 patients with a DSM—III diag nosis ofdepression (Bottiglieri et a!, 1992) we found significant positive correlations between red cell folateandcerebrospinal fluid5-hydroxyindoleacetic acid(CSF5-HIAA), homovanillicacid(HVA), and tetrahydrobiopterin (BH4). As expected, therewere alsosignificant correlationsbetweenthelatterthree CSF metabolites.Theseobservations further sup port the links between folate and monoamine theoriesof affectivedisorder.Thisandotherrecent studies(Carneyet a!, 1990)alsoemphasise the im portanceof studyingthemorestableredcellfolate in psychiatricdisordersand we wouldencourage Andersonet a! and Wing & Lee to do so in their own studies. BOTrIOLIERI, T., HYLAND, K., LAUNDY, M., el a! (1992) Folate deficiency, biopterin and monoamine metabolism in depression. Psychological Medicine (in press). CAR!€Y, M. W. P. (1967) Serum folate values in 423 psychiatric patients. British Medical Journal, iv, 512—516. —¿ , CHARY, T. K. N., LAut@inY, M., et a! (1990) Red cell folate concentrations in psychiatric patients. Journal of Affective Disorders, 19,207—213. GODFREY,P. S. A., TooNE, B. K., CARNEY, M. W. P., ci a! (1990) Enhancementof recoveryfrom psychiatricillnessby methyl folate.Lance:,336,392—395. Ramows, E. H. (1967) Effects of folic acid on the mental state and fit frequency of drug-treated epileptic patients. Lance:, i, 1086—1088. —¿ , PREscE, J. M., BAILEY, J., ci a! (1970) Folate deficiency in depressive illness. British Journal of Psychiatry, 117,287—292. ISAAC MARKS JOSEPHCONNOLLY Enhancement of recovery from psychiatric illness by methylfolate SIR: We are grateful to Dr Procter (Journal, August 1991, 159, 271—272), Dr Anderson et a! (Journal, January 1992, 160, 130) and Drs Wing & Lee (Journal, May 1992, 160, 714—71 5) for their interest in our studyreporting enhancementof recoveryfrom psychiatric illness by methylfolate (Godfrey et a!, 1990).Procter is sufficiently impressedby this and earlier literature to doubt the need for further controlled trials of treatment of folate deficiencyin psychiatric patients. Anderson eta! and Wing & Lee have some reservationsabout some aspectsof the design of our trial, while at the same time stressing the importance of the folate—mentaldisorder connection and drawing attention to their own interestingcontributions to the subject. To deal first with the design features of our methylfolate trial, we do not agree that it was inappropriate to use the Hamilton Rating Scale for Depression (HRSD) in schizophrenicpatients. The HRSD is as valid for depressionas a symptom in other psychiatric disorders as it is in depressive illness.Nor did we find the inconsistenciesbetween theHRSD andBeckscoressurprising. Many of our patients were psychotic,and self-reportin such patients, many of whom are without insight, is boundto beunreliable.Theobjectof ourstudywas to evaluatelong-term (six months) clinical outcome, and the use of clinical outcome scalesin such a contextiswell establishedin psychiatricresearch.We donotagreethatit isdifficulttodistinguishbetween residualsymptomsandpronounced impairment,or betweenfull socialrecoveryandnoor partialsocial recovery. Theabsenceof baselinescoreswasdictated