Depression is often why people seek out therapy.  When depression is mild to severe, exercise can alleviate many symptoms.  However, if symptoms are severe, medication can be beneficial.  Below is an excerpt from a Medscape article addressing this issue.
In patients with mild-to-moderate major depression (operationally defined as HAMD17 scores of 12-25), aerobic exercise that expends at least 17.5 kcal/kg/week at least 3 days/week has been shown to reduce depression severity by nearly 50%, an effect described as comparable to that seen with antidepressants.[48] However, a Cochrane database analysis of exercise for major depression found only a moderate effect size — comparable to that of cognitive therapy — but no statistically significant difference from placebo or no treatment.[49] In patients who have major depression with incomplete remission with antidepressants, an adjunctive individualized exercise program showed significant reductions in residual depressive symptoms.[50] In more severe forms of major depression, aerobic exercise has not been demonstrated to exert a comparable effect to antidepressants.
Patty’s assertion that antidepressants “do not work for depression anyway” may have been a misreading of a recent meta-analysis comparing antidepressants with placebo for mild-to-moderate forms of depression, which indeed found no clear advantage of antidepressants in the absence of greater severity.[51] That meta-analysis, however, was confined to only 6 studies of 2 antidepressants — paroxetine and imipramine — and was limited in its generalizability by a number of methodologic shortcomings. There is little dispute that antidepressants are efficacious in more severe forms of major depression, and the premature cessation of antidepressants after an initial response carries a high likelihood for relapse.
High levels of expressed emotion in the spouses or significant others of depressed patients (such as perceived criticism, hostility, and emotional overinvolvement) were originally described as predictors of relapse in schizophrenia, although contemporary studies have also identified links between high expressed emotion and residual depressive symptoms after initial response[52] as well as subsequent relapse rates.[53] However well-intended Patty’s intentions may be with respect to Dennis’ depression and its treatment, appropriate family psychoeducation at this point would involve a discussion of the disease model of depression; that is, the recognition of Dennis’ depression symptoms as manifestations of an illness that arise within a vulnerability-stress model. One would review the signs and symptoms of major depression, the concept of a biologic predisposition to depression and the importance of treatment irrespective of possible etiologies, and the role of family members (Patty) with respect to relapse prevention. The latter includes ways to recognize signs of impending relapse and seek treatment, as well as efforts to encourage Dennis’ adherence to treatment recommendations. Should it appear that Patty’s attitudes, beliefs, and attributions about Dennis’s illness may be interfering with Dennis’ treatment, it may then be appropriate to undertake a more focused intervention that addresses communication enhancement training, which involves teaching skills for active listening, delivering positive and negative feedback, and requesting changes in behavior.
There are a number of basic tenets worth addressing when educating a family member about major depression in a loved one, including the following points:
- Depression attains clinical importance when it involves a collection of signs and symptoms affecting not only mood but also the sleep-wake cycle, energy, appetite, thinking, motivation, capacity to feel pleasure, behavior, and outlook or perspective about life and one’s future.
- Genetics may sometimes contribute to an individual’s inherent vulnerability for depression but hereditary factors alone do not fully explain the lifetime risk for depression.
- Life stresses (such as losses, separations, or difficulty adapting to change) may or may not catalyze or precede the onset of a depression. However, because the exact causes of depression remain unknown, efforts to differentiate “situational” from “biologic” causes of depression may not be informative. Depression will not develop in all individuals who endure the same life stresses, and it is thought that predisposing genetic or other biologic susceptibilities may be necessary prerequisites for the occurrence of a major depression in the context of environmental interactions.
Patty also raises the issue of treatments for depression other than traditional antidepressant medicines. There has long been interest among patients as well as practitioners about the validity and utility of complementary and alternative medicine treatments for depression. Research rigor has not fully kept pace with clinical interest in this area, as evident from the plethora of small, underpowered proof-of-concept studies that limit the ability to draw broad conclusions. Recently, however, the Canadian Network for Mood and Anxiety Treatments published a consensus-based guideline on complementary and alternative medicine approaches to major depression, ranked by perceived levels of research support.[54] In the absence of a seasonal pattern of depression (where light therapy is accorded the highest level of evidence and a first-line recommendation), the identified interventions of sleep deprivation, exercise, and yoga are viewed as second- or third-line recommendations, all with evidence supported by at least 1 randomized trial with adequate sample size and/or meta-analysis with wide confidence intervals. The evidence base for acupuncture was viewed as lacking sufficient information from which to form any recommendations. Two nutraceutical remedies, omega-3 fatty acids and s-adenosylmethionine, were viewed as second-line recommendations as monotherapy supported by at least 2 adequately-powered randomized trials, while other remedies (notably, the steroid dehydroepiandrosterone and folic acid as monotherapy and adjunctive therapy, respectively) were identified as third-line treatments supported by at least 1 randomized trial. In addition, St. John’s Wort was identified by the study group as a first-line monotherapy treatment for mild-to-moderate depression (supported by 2 or more adequately-powered randomized trials) and a second-line treatment for more severe forms of depression with less extensive support from randomized trial data.
When should a structured psychotherapy be considered as an appropriate augmentation strategy to pharmacotherapy for depression — particularly if an initial medication response is poor? In STAR*D, 71% of depressed patients who did not respond to an initial SSRI trial declined the option of cognitive therapy for depression in favor of alternative medication strategies,[55] even though response and remission rates were comparable between augmentation of cognitive therapy and changing to an alternative antidepressant.[56]Cognitive therapy was a more acceptable treatment option among patients with higher education levels and a family history of a mood disorder.[55]