Here is some info I found.
Double-Blind, Controlled Trial of Inositol Treatment of Depression
Joseph Levine, M.D., Yoram Barak, M.D., Mirtha Gonzalves, M.D., Henry Szor, M.D., Avner Elizur, M.D., Ora Kofman, Ph.D., and R.H. Belmaker, M.D.
Received Aug. 26, 1993; revision received Feb. 3, 1994; accepted April 22, 1994. From the Yehuda Abarbanel Mental Health Center, Bat Yam, Israel; and the Ministry of
Health Mental Health Center, Faculty of Health Sciences and Depamnent of Behavioral Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. Address reprint
requests to Dr. Belmaker, Beer-Sheva Mental Health Center, P.O. Box 4600, Beer-Sheva, Israel.
Supported by contract 263-MD-340-3442 from the NIMH New Medications Development Office.
OBJECTIVE: CSF levels of inositol have been reported to be lower than normal in depressed subjects. The authors administered inositol to depressed patients in a
double-blind, controlled trial. METHOD: Under double-blind conditions, 12 g/day of inositol (N=13) or placebo (N=25) was administered to depressed patients for 4 weeks.
RESULTS: The overall improvement in scores on the Hamilton Depression Rating Scale was significantly greater for inositol than for placebo at week 4. No changes were noted
in hematology or in kidney or liver function. CONCLUSIONS: This may be the first use of the precursor strategy for a second messenger rather than a neurotransmitter in
treating depression. Although inositol had a significant antidepressant effect in this study, replication is crucial. (Am J Psychiatry 1995; 152:792-794)
Inositol is a simple isomer of glucose that is a key metabolic precursor in the phosphatidylinositol cycle. Unlike L-dopa and tryptophan, which are amino acid precursors of
monoamine neurotransmitters and which have been reported to have antidepressant properties, inositol is a precursor of an intracellular second messenger system. The
phosphatidylinositol cycle is a second messenger system for numerous neurotransmitters (1).
Barkai et al. (2) reported that depressed patients, both unipolar and bipolar, had markedly low levels of inositol in CSF. In an open study of 11 depressed patients who had been
resistant to previous antidepressant treatment (3), inositol treatment led to a decline in mean Hamilton Depression Rating Scale score from 31.7 (SD=6) to 16.2 (SD=9). Levine et
al. (4) showed that 12 g/day of inositol raised CSF inositol levels by 70%. We report here the results of administering 12 g/day of inositol to depressed patients in a double-blind,
controlled trial.
METHOD
The diagnostic entry criteria for the study were DSM-III-R major depression or bipolar disorder, depressed. Each of the patients who were referred to the study and gave
informed consent had not re- sponded to antidepressant treatment, had dropped out of treatment because of side effects, or, in the case of the bipolar depressed patients, were
lithium prophylaxis patients who had had few problems with mania but intolerable continuation of depression. All medications other than study drugs were stopped at least 3 days,
and usually 1 week, before the subjects entered the study. No medications other than inositol or placebo were permitted during the trial, except for oxazepam, up to 15 mg/day,
or an equivalent benzodiazepine if the patient had been taking it before the study. The study was approved by the Helsinki Committee institutional review board and the Ministry of
Health. Each patient gave written informed consent before participation.
Thirty-nine patients entered the trial. Of these, 11 dropped out within 1 week of starring the trial. Four of these patients were taking placebo, and their reasons for dropping out,
respectively, were headache, hypomania, insomnia, and lack of desire to continue in the study. Seven patients taking inositol dropped out within 1 week; two had mild psychotic
symptoms, one had weakness and tremor, one had a cutaneous burning sensation, and three did not want to continue in the study. These 11 patients are not included in the data
analysis. One patient taking inositol dropped out after 3 weeks because of total remission of symptoms, and her 2-week score was used as a last value carried forward.