Исследование SAM-e при депресии

A total of 73 adults were enrolled in this six-week study and randomly assigned to the placebo control group or the SAM-e treatment group.

SAM-e, in combination with standard depression treatment, was more effective than antidepressant treatment alone in improving measures of depression and remission rates of patients with significant clinical depression. SAM-e-treated subjects had a greater response and remission rate to treatment than the placebo-treated group. SAM-e was well-tolerated with no reported adverse reactions.

Dietary Supplement SAM-e Aids Treatment of Depression

Альтернативные методы лечения депрессий

#

Although there is strong evidence that light therapy can counter seasonal depression, the efficacy of light therapy as a treatment for major depression is less well established. Also, it looks as if light therapy might be more effective against major depression if it is combined with an antidepressant than if used alone.

In one randomized, controlled trial, for instance, 102 subjects were treated with the SSRI sertraline (50 mg/d). Subjects also received randomized augmentation treatment with 30 minutes of either bright morning (10,000 lux) or dim red (50 lux) light for five weeks. All clinician and self-report measures significantly favored active light augmentation.
#

Regarding St. John's wort, trials suggest that it is more effective for mild to moderate depression than for the severe form of the illness.
#

Studies have failed to demonstrate the efficacy of acupuncture compared with a control condition for the treatment of major depression.
#

And as for folate, its efficacy as a monotherapy for major depressive disorder has yet to be adequately tested. A few trials have found folate to be efficacious and well tolerated, although the best dose and form of folate remain unclear.

Alternative Treatments May Have Some Use in Depression

S-Аденозилметионин при депрессии

The actions of S-adenosyl methionine in the central nervous system have been reviewed previously (3, 7, 8). SAMe acts as a major methyl donor for the synthesis of brain amines and maintenance of phospholipid cell membranes. Low levels of SAMe have been reported in the cerebrospinal fluid (CSF) of severely depressed patients. Oral and parenteral administration of SAMe result in a rise in CSF SAMe concentrations, indicating the compound crosses the blood-brain barrier. An increase in SAMe levels has been positively correlated with improvement in depression. SAMe concentrations also appear to rise in patients who respond to other antidepressants such as desipramine. SAMe is produced in the one-carbon cycle involving folate, homocysteine, and vitamin B12 and abnormalities of each of these compounds has been associated with depression. In short, the hypothesis is that abnormalities in the one-carbon cycle may result in low concentrations of SAMe that in turn may limit the synthesis of brain neurotransmitters such as serotonin, norepinephrine, and dopamine. This may directly contribute to depressive symptoms or interfere with or limit the action of other antidepressants. Administration of SAMe may ameliorate these deficiencies or augment antidepressants and facilitate neurotransmission.

In this issue, Papakostas and colleagues (1) report the results of an adjunctive trial of S-adenosyl methionine (SAMe) in 73 patients with major depression who had failed a prior selective serotonin reuptake inhibitor trial at an adequate dose for at least 6 weeks. Patients were randomly assigned to SAMe, with a targeted dose of 800 mg twice a day, or placebo. Both were added to the ongoing antidepressant regimen and continued for 6 weeks. Response according to the primary outcome, the Hamilton Depression Rating Scale (HDRS), was more likely with SAMe (36.1%) than with placebo (17.6%), as was remission (HDRS score ≤ 7): 25.8% versus 11.7%, respectively. Differences were statistically significant and clinically meaningful.

S-Adenosyl Methionine (SAMe) Augmentation in Major Depressive Disorder