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DepressionAlpert, Silva, Pouget Depressed geriatric patients have lower levels of folate (FOL)
than controls. Also, FOL supplement can reduce depressive morbidity.
One hypothesis consistent with this is that FOL deficiency causes
a lowering of CNS serotonin that contributes to depression. The
present report is from one site of a multicenter study that compared
an SSRI (sertraline) with a nonspecific tricyclic antidepressant
(nortriptyline) in geriatric depressed patients. We added measures
of FOL at baseline and outcome for 22 depressed patients older than
60 years. Both treatments were effective. At baseline, FOL levels
were within the normal range. Higher FOL levels at baseline predicted
greater improvement. Further study of FOL interaction with SSRI
is warranted. For the group treated with the SSRI, baseline FOL
level was a more efficient predictor of improvement, especially
for results on a self-rating depression scale (POMS). Tiemeier, van Tuijl, Hofman, Meijer, Kiliaan, Breteler OBJECTIVE: The associations of vitamin B(12), folate, and homocysteine with depression were examined in a population-based study. METHOD: The authors screened 3,884 elderly people for depressive symptoms. Subjects with positive screening results had psychiatric workups. Folate, vitamin B(12), and homocysteine blood levels were compared in 278 persons with depressive symptoms, including 112 with depressive disorders, and 416 randomly selected reference subjects. Adjustments were made for age, gender, cardiovascular disease, and functional disability. RESULTS: Hyperhomocysteinemia, vitamin B(12) deficiency, and to a lesser extent, folate deficiency were all related to depressive disorders. For folate deficiency and hyperhomocysteinemia, the association with depressive disorders was substantially reduced after adjustment for functional disability and cardiovascular disease, but for vitamin B(12) this appeared independent. CONCLUSIONS: The association of vitamin B(12) and folate with depressive disorders may have different underlying mechanisms. Vitamin B(12) may be causally related to depression, whereas the relation with folate is due to physical comorbidity.
OBJECTIVE: To describe 5-year changes of mental health in SENECA participants, and to examine whether mental health is associated with the status of vitamin B12 and folate. DESIGN: A longitudinal, multicentre study including a Baseline study, a Follow-up study, and a Finale study. SUBJECTS: Inhabitants of 11 European towns, born between 1913 and 1918, were randomly selected at baseline to participate in the SENECA study. Of the 1099 enrolled subjects in the Follow-up study, 586 participated in the Finale study. INTERVENTION: Mental health status was assessed by the Mini-Mental State Examination (MMSE, cognitive impairment defined as MMSE<23) and the 15-item Geriatric Depression Scale (GDS, depression defined as GDS>5). RESULTS: In the Finale study, mean overall MMSE score was 26.1 for men and 25.6 for women, while mean overall GDS score was 3.1 for men and 4.1 for women. Among subjects that participated in both the Follow-up and the Finale study, MMSE scores decreased with 0.9 points (P<0.0001) and 1.0 points (P<0.0001) among men and women respectively. The GDS scores decreased with 0.7 points (P<0.0001) for men and 0.8 points (P<0.0001) for women. Among subjects that participated in the Finale study, no significant correlations have been observed between mental health and vitamin B12/folate status. CONCLUSION: In the Finale study, mental health of the majority of the SENECA participants remained intact. In contrast to the Follow-up study, no associations between mental health and vitamin B12/folate status were emerged.
The possible role of folate supplementation in reducing hyperhomocysteinemia in dialysis patients has been reported in several recent papers. However, scant data are available for peritoneal dialysis patients; besides, none of these studies investigated either the role of intraerythrocyte folate concentration or the presence of side effects caused by folate administration. Sixty-six peritoneal dialysis patients with hyperhomocysteinemia (>15 micromol/l) and normal folate status (as assessed by erythrocyte folate level >600 nmol/l) were randomly allocated to receive either oral folate (5 mg/day) or no vitamin supplementation. After 2 months of therapy, patients were requested to answer a questionnaire investigating the occurrence of symptoms possibly related to folate supplementation. Twenty-nine treated patients and 30 untreated controls completed the study. In the treated patients, serum and erythrocyte folate increased significantly (p < 0.0001) (respectively from 10.6 +/- 4.9 to 237 +/- 231 nmol/l and from 1,201 +/- 297 to 2,881 +/- 294 nmol/l) to levels at the uppermost limit of detection by laboratory methods. Serum vitamin B(12) levels did not change. Plasma homocysteine levels decreased from 54 +/- 32 to 23 +/- 14 micromol/l after folate supplementation and remained unchanged in the control group. After 4 months of folate therapy, homocysteine concentration was within the normal range in 5 patients (17%) and below 30 micromol/l in the other 21 (72%). Folate therapy resulted in a decrease in homocysteine of more than 50% in 45% of the patients and decrease of more than 20% in a further 38%. No significant symptoms were reported. Thus, serum and erythrocyte folate increase confirms that normal folate levels are inadequate in dialysis patients, even if serum and erythrocyte levels before folate supplementation cannot predict the effect on homocysteine plasma levels. BACKGROUND: A consistent finding in major depression has been a low plasma and red cell folate which has also been linked to poor response to antidepressants. The present investigation was designed to investigate whether the co-administration of folic acid would enhance the antidepressant action of fluoxetine. METHODS: 127 patients were randomly assigned to receive either 500 microg folic acid or an identical looking placebo in addition to 20 mg fluoxetine daily. All patients met the DSM-III-R criteria for major depression and had a baseline Hamilton Rating Scale (17 item version) score for depression of 20 or more. Baseline and 10-week estimations of plasma folate and homocysteine were carried out. RESULTS: Patients receiving folate showed a significant increase in plasma folate.This was less in men than in women. Plasma homocysteine was significantly decreased in women by 20.6%, but there was no significant change in men. Overall there was a significantly greater improvement in the fluoxetine plus folic acid group. This was confined to women where the mean Hamilton Rating Scale score on completion was 6.8 (S.D. 4. 1) in the fluoxetine plus folate group, as compared to 11.7 (S.D. 6. 7) in the fluoxetine plus placebo group (P<0.001).A percentage of 93. 9 of women, who received the folic acid supplement, showed a good response (>50% reduction in score) as compared to 61.1% of women who received placebo supplement (P<0.005). Eight (12.9%) patients in the fluoxetine plus folic acid group reported symptoms possibly or probably related to medication, whereas in the fluoxetine plus placebo group 19 (29.7%) patients reported such symptoms (P<0.05). LIMITATIONS AND CONCLUSIONS: Folic acid is a simple method of greatly improving the antidepressant action of fluoxetine and probably other antidepressants. Folic acid should be given in doses sufficient to decrease plasma homocysteine. Men require a higher dose of folic acid to achieve this than women, but more work is required to ascertain the optimum dose of folic acid.
OBJECTIVES: Previous studies suggest that folate deficiency may occur in up to one third of patients with severe depression, and that treatment with the vitamin may enhance recovery of the mental state. There are, however, difficulties in interpreting serum and red cell folate assays in some patients, and it has been suggested that total plasma homocysteine is a more sensitive measure of functional folate (and vitamin B12) deficiency. Other studies suggest a link between folate deficiency and impaired metabolism of serotonin, dopamine, and noradrenaline (norepinephrine), which have been implicated in mood disorders. A study of homocysteine, folate, and monoamine metabolism has, therefore, been undertaken in patients with severe depression. METHODS: In 46 inpatients with severe DSM III depression, blood counts, serum and red cell folate, serum vitamin B12, total plasma homocysteine, and, in 28 patients, CSF folate, S-adenosylmethionine, and the monoamine neurotransmitter metabolites 5HIAA, HVA, and MHPG were examined. Two control groups comprised 18 healthy volunteers and 20 patients with neurological disorders, the second group undergoing CSF examination for diagnostic purposes. RESULTS: Twenty four depressed patients (52%) had raised total plasma homocysteine. Depressed patients with raised total plasma homocysteine had significant lowering of serum, red cell, and CSF folate, CSF S-adenosylmethionine and all three CSF monoamine metabolites. Total plasma homocysteine was significantly negatively correlated with red cell folate in depressed patients, but not controls. CONCLUSIONS: Utilising total plasma homocysteine as a sensitive
measure of functional folate deficiency, a biological subgroup of
depression with folate deficiency, impaired methylation, and monoamine
neurotransmitter metabolism has been identified. Detection of this
subgroup, which will not be achieved by routine blood counts, is
important in view of the potential benefit of vitamin replacement.
Levitt, Wesson, Joffe Antidepressant response is associated with a rise in red cell folate (RCF) and a reduction in thyroxine (T4). Since T4 levels may directly influence folate status, it is possible that the increase in folate with recovery results from the decline in T4. To examine the possible role of thyroid hormones in the observed change in folate status during antidepressant therapy, T4, tri-iodothyronine (T3) or placebo was given in a double-blind fashion to 25 depressed subjects at the initiation of standard antidepressant treatment. Folate levels and mood [using the Hamilton Rating Scale for Depression (HAMD), Montgomery-Asberg Depression Rating Scale (MADRS) and Beck Depression Inventory (BDI)] were measured at baseline and following 4 weeks of therapy. Using MANOVA for repeated measures, there was a significant interaction between response status and time for vitamin and hormone levels. Univariate analysis confirmed that response was associated with a significant change in red cell folate, but not a significant change in T4 or T3. The mean change in RCF across the 4-week trial was significantly greater in the 14 responders than the 11 non-responders. Change in RCF, and not change in T4 or T3, was significantly correlated with change in HAMD and contributed significantly to the variance in change in HAMD. These results suggest that change in RCF is closely tied to response to antidepressant treatment, and this effect is not inhibited by exogenous administration of thyroid hormones or the changes in T4 that the exogenous hormones produce. These findings support the possible role of folate, independent of thyroid function, in the modulation of mood. OBJECTIVE: The authors examined the relationships between levels of three metabolites (folate, vitamin B12, and homocysteine) and both depressive subtype and response to fluoxetine treatment in depressed patients. METHOD: Fluoxetine, 20 mg/day for 8 weeks, was given to 213 outpatients with major depressive disorder. At baseline, depressive subtypes were assessed, and a blood sample was collected from each patient. Serum metabolite levels were assayed. Response to treatment was determined by percentage change in score on the 17-item Hamilton Depression Rating Scale. RESULTS: Subjects with low folate levels were more likely to have melancholic depression and were significantly less likely to respond to fluoxetine. Homocysteine and B12 levels were not associated with depressive subtype or treatment response. CONCLUSIONS: Overall, the results are consistent with findings linking low folate levels to poorer response to antidepressant treatment. Folate levels might be considered in the evaluation of depressed patients who do not respond to antidepressant treatment. Godfrey, Toone, Carney, Flynn, Bottiglieri, Laundy, Chanarin,
Reynolds
Husemann, Kugler, Frank
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