British Journalof Psychiatry (1991), 159,271—272
The Current Literature
Enhancement
Illness by Methylfolate
of Recovery from Psychiatric ANDREW PROCTER
“¿41 (33%) of 123 patients with acute psychiatricdisorders(DSM Ill diagnosisof major
depression orschizophrenia) hadborderline ordefinitefolatedeficiency(red-cellfolatebelow 200 pg/I)andtook part in a double-blind,placebo-controlledtrial of methylfolate,15 mgdaily, for 6 monthsin additionto standardpsychotropic treatment.Amongbothdepressedand schizophrenic patientsmethylfolatesignificantly improvedclinicalandsocialrecovery.The differencesinoutcomescoresbetweenmethylfolateandplacebogroupsbecamegreaterwith
time.Thesefindingsaddtotheevidence implicating disturbances ofmethylation inthenervous systemin the biologyof someformsof mentalillness.― The summary quoted above is from an article by Godfrey et a! (1990). Andrew Procter was invited to
comment upon the study.
methylfolate. If this is more than merely reversal of a co-existing deficiency as a result of poor diet and self-care, other explanations may be considered. Methylation is a common biochemical step in many
The demonstration by Godfrey et al (1990) of significant and substantial effects of concurrent methylfolate treatment in psychiatric patients with
metabolic processes, and thus the bioavailability
borderline
by the methylfolate
and/or efficacy of both antipsychotic and anti depressant medication may conceivably be affected
folate deficiency differs from many
studies in biological psychiatry in that patients with different diagnoses show similar effects. Generally,
treatment.
More speculative is the interpretation that this may
indicate similar biochemical abnormalities under
lining both schizophrenia and depression, possibly significant effects are usually observed in subgroups providing some support for a biological basis to the of carefully defmed diagnostic groups (e.g. ‘¿psychotic' postulated ‘¿unitary psychosis'. Such biological evidence is not entirely without precedent, as has depression; see Jeste et al, 1988, for review). That the same effects of methylfolate-adjunct treatment been recently reviewed (Crow, 1990). Monoamine neurotransmitters have, to date, been the subject of can be seen in both depression and schizophrenia, long considered distinct disorders, raises the possibility the most intensive study in both of these conditions. that this fmding is being mediated through some non These transmitters share many features of their specific effect on psychological well-being common metabolism, and thus any treatment affecting the to both groups of subjects, and independent of the metabolism of one is likely to affect that of others. major psychiatric condition. To address this further However, abnormalities of the cerebral cortex have it may be helpful to consider what the effects of been described in both affective disorders and methylfolate are on the psychological function of schizophrenia and it must be remembered that other subjects with borderline folate deficiency monoaminergic nerve terminals are a small con including both patients with other diagnoses and the stituent of the cortex. With the development of new psychiatrically well. It must surely be expected that drugs and techniques for the study of the major given the existing knowledge of the psychological excitatory and inhibitory transmitters of the cortex effects of folate deficiency, subjects with any the position of the monoaminergic theory of affective in biological
studies of functional
psychiatric
illnesses,
psychiatric illness with co-existing definite or border line folate deficiency have a better outcome when this is corrected. The rationale for the placebo treatment of such a biochemically proven deficiency must perhaps be questioned.
This study has confirmed previous reports of fairly common folate deficienciesamong psychiatric patients (interestingly, these revert to normal on treatment of the psychiatric condition). Furthermore, it has also
demonstrated
an enhanced response to standard
psychiatric treatments in those patients treated with 271
disorders
and dopaminergic
theory
of schizophrenia
must be subject to constant critical review (Procter & Bowen, 1988; Reynolds, 1989). Independent of these more theoretical consider ations of the importance of this study and the light it sheds on the neurobiological
nature of psychiatric
illnesses, is the fact that one-third of the patients attending a psychiatric unit had borderline-low folate levels and that these patients were significantly improved by the co-administration of methylfolate with their normal psychiatric treatment. These fmdings
272
PROCTER
should surely warrant the attention of all practising psychiatrists and if confirmed may deserve wider general application.
Enhancement of recovery from psychiatric illness by methyl folate. Lancet, 336, 392—395. Jerrs, D. V., LOHR, J. B. & GooDwiN, F. K. (1988) Neuroanatoinical
studiesof majoraffectivedisorders.A reviewandsuggestions for further research. British Journal of Psychiatry, 153,444-459. PROCreR, A. W. & BOwEN, D. M. (1988) Aging,
Caow, T. J. (1990) The continuum of psychnds and its genetic origins:
pp. 3-20. Cold Spring Harbor: Cold Spring Harbor Laboratory.
thesixty-fifthMaudsleylecture.BritishJournalof Psychiatry, REmous, 156, 788—797. GODFREY,
P.
S. A.,
0. P. (1989) Beyond the dopamine hypothesis: the
neurochemical TooNs,
B. K.,
CARNEY,
the cerebral
neocortex and psychiatric disorder. In Mo@4arNouropzthoIogy of Aging (eds P. Davies & C. E. Finch). Banbury Report, 27,
References
M.
W.
P.,
et al(1990)
pathology
of schizophrenia.
British Journal
of
Psychiatry,155, 305—316.
Andrew W. Procter, MA, MBBS,MRCPsych,Senior Lecturer in Psychiatry,
UMDS - Guy's Hospital, London
SEJ 9RT, and Honorary Research Fellow in Neurochemistry, Institute of Neurology, London WCJN JPJ
Enhancement of recovery from psychiatric illness by methylfolate. A Procter BJP 1991, 159:271-272. Access the most recent version at DOI: 10.1192/bjp.159.2.271
References Reprints/ permissions You can respond to this article at Downloaded from
This article cites 0 articles, 0 of which you can access for free at: http://bjp.rcpsych.org/content/159/2/271#BIBL To obtain reprints or permission to reproduce material from this paper, please write to [email protected] /letters/submit/bjprcpsych;159/2/271 http://bjp.rcpsych.org/ on May 22, 2016 Published by The Royal College of Psychiatrists
To subscribe to The British Journal of Psychiatry go to: http://bjp.rcpsych.org/site/subscriptions/
The Current Literature
Enhancement
Illness by Methylfolate
of Recovery from Psychiatric ANDREW PROCTER
“¿41 (33%) of 123 patients with acute psychiatricdisorders(DSM Ill diagnosisof major
depression orschizophrenia) hadborderline ordefinitefolatedeficiency(red-cellfolatebelow 200 pg/I)andtook part in a double-blind,placebo-controlledtrial of methylfolate,15 mgdaily, for 6 monthsin additionto standardpsychotropic treatment.Amongbothdepressedand schizophrenic patientsmethylfolatesignificantly improvedclinicalandsocialrecovery.The differencesinoutcomescoresbetweenmethylfolateandplacebogroupsbecamegreaterwith
time.Thesefindingsaddtotheevidence implicating disturbances ofmethylation inthenervous systemin the biologyof someformsof mentalillness.― The summary quoted above is from an article by Godfrey et a! (1990). Andrew Procter was invited to
comment upon the study.
methylfolate. If this is more than merely reversal of a co-existing deficiency as a result of poor diet and self-care, other explanations may be considered. Methylation is a common biochemical step in many
The demonstration by Godfrey et al (1990) of significant and substantial effects of concurrent methylfolate treatment in psychiatric patients with
metabolic processes, and thus the bioavailability
borderline
by the methylfolate
and/or efficacy of both antipsychotic and anti depressant medication may conceivably be affected
folate deficiency differs from many
studies in biological psychiatry in that patients with different diagnoses show similar effects. Generally,
treatment.
More speculative is the interpretation that this may
indicate similar biochemical abnormalities under
lining both schizophrenia and depression, possibly significant effects are usually observed in subgroups providing some support for a biological basis to the of carefully defmed diagnostic groups (e.g. ‘¿psychotic' postulated ‘¿unitary psychosis'. Such biological evidence is not entirely without precedent, as has depression; see Jeste et al, 1988, for review). That the same effects of methylfolate-adjunct treatment been recently reviewed (Crow, 1990). Monoamine neurotransmitters have, to date, been the subject of can be seen in both depression and schizophrenia, long considered distinct disorders, raises the possibility the most intensive study in both of these conditions. that this fmding is being mediated through some non These transmitters share many features of their specific effect on psychological well-being common metabolism, and thus any treatment affecting the to both groups of subjects, and independent of the metabolism of one is likely to affect that of others. major psychiatric condition. To address this further However, abnormalities of the cerebral cortex have it may be helpful to consider what the effects of been described in both affective disorders and methylfolate are on the psychological function of schizophrenia and it must be remembered that other subjects with borderline folate deficiency monoaminergic nerve terminals are a small con including both patients with other diagnoses and the stituent of the cortex. With the development of new psychiatrically well. It must surely be expected that drugs and techniques for the study of the major given the existing knowledge of the psychological excitatory and inhibitory transmitters of the cortex effects of folate deficiency, subjects with any the position of the monoaminergic theory of affective in biological
studies of functional
psychiatric
illnesses,
psychiatric illness with co-existing definite or border line folate deficiency have a better outcome when this is corrected. The rationale for the placebo treatment of such a biochemically proven deficiency must perhaps be questioned.
This study has confirmed previous reports of fairly common folate deficienciesamong psychiatric patients (interestingly, these revert to normal on treatment of the psychiatric condition). Furthermore, it has also
demonstrated
an enhanced response to standard
psychiatric treatments in those patients treated with 271
disorders
and dopaminergic
theory
of schizophrenia
must be subject to constant critical review (Procter & Bowen, 1988; Reynolds, 1989). Independent of these more theoretical consider ations of the importance of this study and the light it sheds on the neurobiological
nature of psychiatric
illnesses, is the fact that one-third of the patients attending a psychiatric unit had borderline-low folate levels and that these patients were significantly improved by the co-administration of methylfolate with their normal psychiatric treatment. These fmdings
272
PROCTER
should surely warrant the attention of all practising psychiatrists and if confirmed may deserve wider general application.
Enhancement of recovery from psychiatric illness by methyl folate. Lancet, 336, 392—395. Jerrs, D. V., LOHR, J. B. & GooDwiN, F. K. (1988) Neuroanatoinical
studiesof majoraffectivedisorders.A reviewandsuggestions for further research. British Journal of Psychiatry, 153,444-459. PROCreR, A. W. & BOwEN, D. M. (1988) Aging,
Caow, T. J. (1990) The continuum of psychnds and its genetic origins:
pp. 3-20. Cold Spring Harbor: Cold Spring Harbor Laboratory.
thesixty-fifthMaudsleylecture.BritishJournalof Psychiatry, REmous, 156, 788—797. GODFREY,
P.
S. A.,
0. P. (1989) Beyond the dopamine hypothesis: the
neurochemical TooNs,
B. K.,
CARNEY,
the cerebral
neocortex and psychiatric disorder. In Mo@4arNouropzthoIogy of Aging (eds P. Davies & C. E. Finch). Banbury Report, 27,
References
M.
W.
P.,
et al(1990)
pathology
of schizophrenia.
British Journal
of
Psychiatry,155, 305—316.
Andrew W. Procter, MA, MBBS,MRCPsych,Senior Lecturer in Psychiatry,
UMDS - Guy's Hospital, London
SEJ 9RT, and Honorary Research Fellow in Neurochemistry, Institute of Neurology, London WCJN JPJ
Enhancement of recovery from psychiatric illness by methylfolate. A Procter BJP 1991, 159:271-272. Access the most recent version at DOI: 10.1192/bjp.159.2.271
References Reprints/ permissions You can respond to this article at Downloaded from
This article cites 0 articles, 0 of which you can access for free at: http://bjp.rcpsych.org/content/159/2/271#BIBL To obtain reprints or permission to reproduce material from this paper, please write to [email protected] /letters/submit/bjprcpsych;159/2/271 http://bjp.rcpsych.org/ on May 22, 2016 Published by The Royal College of Psychiatrists
To subscribe to The British Journal of Psychiatry go to: http://bjp.rcpsych.org/site/subscriptions/
