Depression is a term that has been used to describe a variety of ailments ranging from minor to incapacitating. Clinically significant depression, termed major depression, is a serious condition characterized not only by depressed mood, but a cluster of somatic, cognitive, and motivational symptoms. Major depression can be differentiated from a normal and transient sad mood by several factors:
intensity, as major depression causes impairment in social or occupational functioning and persists across time and situationsrelationship to antecedent events, as major depression either occurs without any identifiable antecedent event or is clearly in excess of what would be considered an expected reactionquality, with the quality of the emotion being different from that experienced in a normal sad moodassociated features, as the mood co-occurs with a group of other cognitive and somatic symptomshistory, with major depression typically appearing after a history of other such episodes (Whybrow et al 1984).Individuals who are suffering from major depression often report feeling overwhelmed, helpless, despairing, suffocated, or numb. Major depression can range from mild sadness to complete hopelessness and is often accompanied by frequent crying spells. Those with more severe depression may feel like crying but be unable to do so. Severely depressed individuals often believe that no one can help them.
Depression is defined according to specific criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) (American Psychiatric Association (APA) 1994).
The DSM-N details the diagnostic criteria for nearly 300 mental dis-orders, and nearly 100 other psychological conditions that might be the focus of professional attention. While many individuals experiencing a debilitating depression will meet criteria for one of the disorders within the DSM-IV, some will nonetheless elude classification using this system. The following sections detail the different disorders within the DSM-IV that may involve depressive symptoms, following which an overview of etiology and treatment — for the non-specialist — is provided.
In order to be diagnosed with a major depressive episode according to the DSM-IV, an individual must have at least five out of nine possible symptoms, which must be present during the same 2-week period and represent a change from a previous level of functioning. One of the symptoms must be either depressed mood for most of the day on nearly every day, or loss of interest or pleasure (anhedonia) in all or almost all activities for most of the day on nearly every day. Additional symptoms that may accompany the depressed mood or anhedonia are:
significant weight loss (when not dieting) or significant weight gain (i.e. more than 5% of body weight in 1 month), or a decreased or increased appetite nearly every dayinsomnia or hypersomnia nearly every dayobservable psychomotor agitation or retardation nearly every dayfatigue or loss of energy nearly every day, feelings of worthlessnessor excessive or inappropriate guilt nearly every daydiminished ability to think or concentrate, or indecisiveness nearly every dayand recurrent thoughts of death (not just fear of dying) or suicide.‘Depression is also often diagnosed according to criteria outlined in the ICD-10 Classification of Mental and Behavioral Disorders (World Health Organization 1992). ICD-10 criteria overlap substantially, but are not identical to, those of the DSM-IV. This post focuses on the criteria of the DSM-IV because the studies reviewed here have predominantly relied on these criteria for diagnosing depression.
The symptoms must be present for at least 2 weeks and cause clinically significant distress or impairment in social, occupational, or other areas of functioning. Additionally the mood disturbance should not be the direct physiological effect of a substance (e.g. street drug or medication) or general medical condition (e.g. hypothyroidism) (APA 1994). Individuals who meet criteria for a major depressive episode and have never experienced any manic or hypomanic episodes (see below) then meet criteria for major depressive disorder.
Unipolar Versus Bipolar Depression
The DSM-IV distinguishes two broad classes of mood disorder: unipolar and bipolar disorder. Unipolar disorders involve only the depressed dimension of mood and do not include periods of above-average mood such as manic or hypomanic episodes. There are two unipolar mood disorders: major depressive disorder and dysthymic disorder. Bipolar disorders include those in which the individual experiences both depressed moods and manic or hypomanic episodes. The three bipolar disorders described in DSM-IV are bipolar I disorder, bipolar II disorder, and cyclothymic disorder.
Dysthymia
Another form of depression that is less intense but more chronic than major depressive disorder is dysthymia. Distinguishing between a diagnosis of major depressive disorder and dysthymia is difficult because the two share many symptoms and the differences in onset, duration, persistence, and severity are difficult to evaluate retrospectively. In order to meet DSM-IV criteria for dysthymic disorder, an individual must experience depressed mood for most of the day, more days than not for at least 2 years. In children and adolescents, irritable mood would also suffice to meet the criteria, and must last for at least 1 year. Two or more additional symptoms must also be present: poor appetite or overeating, insomnia or hypersomnia, low energy or fatigue, low self-esteem, poor concentration or difficulty making decisions, and feelings of hopelessness. At no time during the 2-year period has such a person been without the depressive symptoms for more than 2 months at a time. If the person has met criteria for major depression at any point during the 2-year period, the diagnosis would be considered as major depression instead of dysthymia. However, an individual who has met criteria for dysthymia for at least 2 years and then subsequently meets the criteria for an episode of major depression superimposed on the dysthymia (without an intervening remission) would be given both diagnoses. This condition is referred to as double depression. It is particularly difficult to differentiate double depression from simple major depressive disorder or chronic major depressive disorder for the reasons mentioned above, combined with the fact that all three meet criteria for a major depressive episode and they differ only in onset, duration, and persistence. A history of mania (at least one manic episode) would rule out a diagnosis of both major depression and dysthymia (APA 1994).
Mania and Bipolar Disorder
Mania is the mood state that is the apparent opposite of depression. Mania involves a euphoric or elated mood that lasts for at least 1 week. A manic episode is more than just a normal good mood; rather, the person feels like he or she is on top of the world and there is nothing he/she can’t do. The euphoric mood is accompanied by at least three other symptoms, including: inflated self-esteem or grandiose beliefs (e.g. that the patient is President or some other famous person of importance), a decreased need for sleep (i.e. feels rested after only 3 h of sleep), a pressure to keep talking, the subjective experience that one’s thoughts are racing, distractibility, increase in activity (either socially, at work or school, or sexually), and excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g. unrestrained buying sprees, sexual promiscuity, etc.). In addition, the mood disturbance must cause impairment in functioning (either social or occupational), or require hospitalization to prevent harm to self or others, or involve psychotic features (e.g. hallucinations). Furthermore, a manic episode is not diagnosed if the symptoms are caused by street drugs, medication or other treatment, or a general medical condition (APA 1994).
A person who has experienced at least one manic episode would meet the criteria for bipolar I disorder. Most individuals who meet criteria for bipolar I have also experienced episodes of major depression in addition to manic episodes; however, this is not necessary for the diagnosis.
Some individuals experience a mood disturbance called hypomania that is similar to a manic episode, but not as severe. The criteria for hypomania are the same as the criteria for a manic episode (described above); however, hypomania must only be present for at least 4 days (versus 1 week for a manic episode), and the episode must not cause impairment in functioning or require hospitalization. Individuals who have experienced at least one major depressive episode, at least one hypomanic episode, and no fully developed manic episodes would be give a diagnosis of bipolar II disorder (APA 1994).
Cyclothymia
Cyclothymia is a more chronic but less intense form of bipolar disorder. To meet criteria for cyclothymia, an individual must experience numerous periods of hypomania and depressed mood over a period of at least 2 years. In fact, the person cannot show the absence of both hypo-manic and depressive symptoms for a period of more than 2 months. Moreover, in cyclothymia there are no major depressive episodes or manic episodes during the first 2 years of the disorder (APA 1994).
Although it is possible that acupuncture may prove effective in treat-ing many varieties of depression, our previous clinical trial (Allen et al 1998) examined only major depressive disorder, and this manual is designed for use with major depressive disorder. With modifications, it is possible that the framework detailed in the subsequent posts could be adapted for use with other depressive disorders.
Specifiers of Major Depression
To capture more adequately the range of mood disorders, the DSM-IV additionally provides for the inclusion of specifiers, which can be used to describe the current or most recent major depressive episode included. These specifiers include chronic, with melancholic features, severe with psychotic features, postpartum onset, and atypical. In addition, the course of the disorder can be specified as `with seasonal pattern’, which is considered a subtype of major depression also known as seasonal affective disorder. The bipolar disorders can be specified as rapid cycling.
The costs of major depression are substantial, and exceed those of other chronic diseases such as diabetes and hypertension in terms of personal distress, lost productivity, interpersonal problems, and suicide. A recent study estimated that these annual costs of depression in the United States exceeded $40 billion (Hirschfeld & Schatzberg 1994), and similar findings have emerged from a worldwide study (Murry & Lopez 1996) that ranked unipolar major depression as the number one cause of disability in the world. Over 80% of individuals who committed suicide were clinically depressed in the months before their death, and the lifetime risk for suicide among those with clinical depression is 15% (Hirschfeld & Schatzberg 1994). Furthermore, depressed individuals appear to be at increased risk of death from all causes. A 16-year prospective study found that mortality rates for depressed individuals are 1.5-2 times those of nondepressed individuals (Murphy et al 1987). Clearly, depression is a prevalent disorder with costly and potentially lethal consequences (Gotlib & Beach 1995).
Comorbidity of Major Depression with other Mental Disorders
Comorbidity is the presence of two or more disorders simultaneously. Comorbid conditions are generally more chronic, do not respond as well to treatment, and have a poorer prognosis than single disorders. It is important to be aware of the issue of comorbidity because a large proportion of individuals in the general population have more than one mental disorder concurrently (Kessler et al 1994). Outcome studies usually examine efficacy for individuals with only one disorder. Therefore, the average clinician deals with much more complicated cases than outcome research addresses (Greenberg & Fisher 1997). In fact, the National Comorbidity Survey found that it was more common to have two or more mental disorders than to have only one (Kessler et al 1994).
Dysthymia is present before the onset of a major depressive dis-order in approximately 10% of epidemiological samples. Other forms of mental illness may be present concurrent with major depressive disorder, such as: alcohol abuse or dependence disorder, personality disorders (e.g. borderline personality disorder), panic disorder, and other anxiety disorders (APA 1994). The literature demonstrates that 33-59% of people who are dependent on alcohol eventually meet criteria for depression at some point during the dis-order (Merikangas & Gelernter 1990). The comorbidity of personality disorders in clinically depressed individuals is 50% or greater (Zimmerman et al 1991). The comorbidity of anxiety disorders with depression is particularly high, in the range of 30% (Hiller et al 1989) to 57% (Mannuzza et al 1989). Research demonstrates that between 15 and 30% of individuals with acute major depression also suffer from panic disorder concurrently (Brown & Barlow 1992). The diagnostic criteria of anxiety and depression overlap, which increases the probability of meeting criteria for both disorders simultaneously. This overlap makes it difficult to know whether there exist two separate classes of conditions — anxiety and depression — or whether there may exist a single underlying predisposition that manifests with both depression and anxiety symptoms (see Frances et al 1992). In addition, the overlap increases lifetime comorbidity (i.e. meeting criteria for both depression and an anxiety disorder) between the disorders (Klerman 1990). The comorbidity of anxiety disorders with depression poses a taxonomic enigma (see Frances et al 1992) for diagnosticians and those interested in etiology.
In addition, 20-25% of individuals with general medical conditions such as diabetes, myocardial infarction, carcinoma, and stroke meet criteria for major depressive disorder at some point during the course of their illness (APA 1994). Depression may occur in the context of medical illness for three reasons: (1) the depression appears to represent a reaction to the burden and limitations associated with having a disease, (2) the depression is unrelated to the disease, but is a recurrence of a long-standing history of depression, or is in response to some other event in the person’s life, or (3) the depression occurs as a direct physiological consequence of the medical condition (e.g. mul-tiple sclerosis, stroke, hypothyroidism). In this latter case the diagnosis is technically not major depressive disorder, but rather mood disorder due to a general medical condition. A mood disorder can also be directly etiologically related to the use of a medication or a drug of abuse. In that case a diagnosis of substance-induced mood disorder (e.g. cocaine-induced mood disorder) is made instead of major depressive disorder. However, this diagnosis is reserved for depression that is a direct physiological consequence of the drug abuse or medication use; for example, the depressed mood is only present following withdrawal from cocaine (APA 1994).
This latter determination is often difficult to make because of the high rates of comorbid substance abuse or dependence disorders and mood disorders. In some cases individuals may begin using substances in response to depression, in an unfortunate attempt to cope with their pain. In such a case, major depression would be comorbid with sub-stance abuse, and both diagnoses would be given. In other cases, it could be that a pre-existing substance abuse disorder appeared to cause the depression through direct physiological means (e.g. cocaine withdrawal), in which case the diagnosis would be substance-induced mood disorder (see DSM-IV for further clarification of these diagnostic issues).
A variety of well-researched treatments exist for depression, and most have rather favorable results. These treatments include both psychotherapies and drug therapies. Unfortunately, however, the effectiveness of these traditional treatments is hampered by high rates of dropout, recovery failure, and relapse, suggesting that these traditional treatments may provide insufficient or transient symptom relief for many.
The National Institutes of Mental Health Treatment of Depression Collaborative Research Program was a clinical trial designed to investigate the efficacy of two brief psychotherapies (interpersonal psychotherapy and cognitive behavior therapy) and a drug treatment (pharmacotherapy with imipramine hydrochloride, a tricyclic antidepressant), all compared with a control group consisting of clinical management combined with pill-placebo as treatments for major depression. In this NIMH treatment study, 32% of patients who were randomized to treatment discontinued treatment prematurely. Excluding patients who dropped out for external reasons or because they had improved, 25% of all patients entering treatment terminated due to negative effects of the treatment such as dissatisfaction with treatment, desire for another treatment, intolerable side effects, and noncompliance (Elkin et al 1989). Among patients who had completed 15 weeks of pharmacotherapy or psychotherapy (not including the placebo group), 43-49% failed to recover to the point of having few symptoms, and among all patients including completers and non-completers 30-64% did not have significant symptom relief at the end of treatment (Elkin et al 1989).
Advocates of standard antidepressant medications (e.g. tricyclics such as imipramine) generally acknowledge that about one-third of patients do not improve with medication, one-third display improve-ment with placebos, and the remaining third demonstrate improve-ment that would not occur with placebo (Greenberg & Fisher 1997). In a meta-analysis (a statistical literature review that has compressed the results of large numbers of studies) of antidepressant outcome in which clinician bias was minimized, Greenberg et al (1992) found that effect sizes were approximately one-half to one-quarter as large as those found in previous studies in which clinician bias was not minimized. Clinician bias was reduced by examining the effectiveness of standard antidepressant tricyclic medications compared with newer antidepressants (serotonin reuptake inhibitors; SSRIs) as well as a placebo control. Presumably, in studies with such a design there is less motivation to establish the efficacy of the standard antidepressants, yet their effects can still be compared with those of a placebo control. With the advent of a new generation of antidepressants (SSRIs), it was hoped that they would be superior in treating depression to the older medications. A meta-analysis of all of the double-blind placebo-controlled efficacy studies of fluoxetine (Prozac) found that it was modestly effective in treating depression and resulted in response rates similar to those obtained in previous meta-analyses of tricyclic antidepressants (Greenberg et al 1994). Other meta-analyses and reviews have also found that new-generation antidepressants have equivalent outcomes to tricyclics (e.g. Anderson & Tomenson 1994, Edwards 1992, 1995, Kasper et al 1992).
It has been suggested that there may be some preference for SSRIs over tricyclics because they cause less sedation and fewer anticholinergic effects and cardiac complications than the standard tricyclics; however, they are associated with other side effects such as nausea, diarrhea, weight loss, agitation, anxiety, and insomnia (Edwards 1995; see below for details about the side effects of tricyclics, monoamine oxidase inhibitors (MAOIs), and SSRI antidepressants). Although drop-out rates from medication treatment studies are high regardless of the type of antidepressant used, the side effects of SSRIs may be slightly better tolerated by some people. These differences in tolerability are very small and may not be clinically meaningful. Furthermore, the number of patients completing each type of treatment is approximately equivalent (Greenberg & Fisher 1997).
The average effect in psychotherapy outcome research is one standard deviation, which is statistically large. An effect size of one standard deviation means that the average person receiving psychotherapy is better off than 84% of the people in the control condition who did not receive psychotherapy. In five meta-analyses of outcome with depression, psychotherapy outperformed no-treatment and wait-list controls (Lambert & Bergin 1994). Effect sizes produced by psychotherapy are equal to or greater than effects produced by various medical and educational interventions (Lambert & Bergin 1994).
For example, psychotherapy is as effective as or more effective than antidepressant medication (Dobson 1989, Robinson et al 1990, Steinbrueck et al 1983). When the allegiance of investigators and the differences between treatments are taken into account, the effectiveness of psychotherapy and pharmacotherapy is equivalent (Robinson et al 1990, Steinbrueck et al 1983). The results of the NIMH Collaborative Depression study, the largest and most well-controlled psychotherapy study conducted to date, support this notion. The NIMH study utilized investigators who were committed to each type of therapy compared and found little evidence for significant differences between therapies (Elkin et al 1989).
These findings are significant because antidepressants are often considered the treatment of choice for depression. Evans and colleagues (1992) found that psychotherapy may have an advantage over antidepressants in terms of decreased vulnerability to relapse. In addition, psychotherapy is not accompanied by the somatic side effects that occur with antidepressants. However, there is some evidence that antidepressants may start to work faster than psychotherapy and may be more effective with endogenous depressions ( Lambert & Bergin 1994 ).
Relapse, Recurrence and the Role of Maintenance Treatments
Depression tends to be a chronic and recurrent disorder. A naturalistic study of depression found that 70% of people recover from depression after 1 year and 81% after 2 years. Unfortunately, 12% of depressed individuals do not recover until 5 years after the onset of the episode and 7% of individuals suffering from depression remain chronically depressed (Hirschfeld & Schatzberg 1994).
Even once successfully treated, depression is likely to recur. Without further treatment, one-fifth of previously recovered persons once again meet criteria for major depression 6 months after the completion of treatment, and nearly one-quarter will develop new depressive symptoms. Within 18 months, over one-third of those persons who were remitted will once again meet criteria for full depression (Shea et al 1992). Ten years after an initial episode, 76% of patients will have a recurrence of depression. For those who have experienced two episodes, there is an 80-90% chance of experiencing a third episode (Hirschfeld & Schatzberg 1994). A growing consensus among those who treat depression is that, after recovery, some form of continued maintenance treatment is necessary.
Whereas research into the pharmacotherapy of depression has provided ample data concerning response to acute treatment, much less is known about the long-term efficacy of antidepressants. The available data suggest that a substantial proportion (10-34%) of patients who have responded to pharmacotherapy experience a return of depression during continued treatment (Belsher & Costello 1988, Doogan
Caillard 1992, Evans et al 1992, Frank et al 1990, Montgomery et al 1988, Prien & Kupfer 1986, Prien et al 1984, Robinson et al 1991, Thase 1990). Even greater recurrence rates are reported during long-term treatment for more severe depression. For example, Prien et al (1984) reported a 52% recurrence rate in patients on imipramine and Glen (1984) reported 68-70% recurrence rate in those on amitrip-tyline or lithium. Taken together, these data highlight the recurrent nature of mood disorders even during the course of long-term treatment and magnify the importance of developing alternative approaches for both short- and long-term treatment of depression.
Only a few studies have examined the effectiveness of psychotherapy maintenance — continued treatment designed to help keep a person from returning to a depressed state. These studies indicate that maintenance psychotherapy (alone or in combination with pharmacotherapy) helps to prevent or delay relapse or recurrence of depression. Based on a limited number of studies, cognitive therapy appears to be an effective maintenance treatment and may delay the onset of subsequent episodes of depression (Blackburn et al 1986). Although following a 6-month continuation phase relapse rates did not differ between cognitive therapy, cognitive therapy plus antidepressant drug of choice (typically amitriptyline or clomipramine), and antidepressant-alone groups, those participants receiving cognitive therapy (alone and in combination with antidepressants) had a significantly lower relapse rate than patients receiving antidepressants alone. Even without maintenance, similar results were obtained in a 2-year follow-up (Evans et al 1992). At the end of a 2-year follow-up in which no maintenance treatments were provided, patients who had received cognitive therapy (with or without medication) had significantly lower relapse rates (21% and 15%) than those who had received antidepressants only (50%) during a 3-month acute treatment phase. Another group that was continued on antidepressants for the first year of follow-up had an intermediate relapse rate (32%), which did not differ significantly from that of the other groups. Limited sample sizes (10 to 13 per group), however, make interpretation of the nonsignificant difference precarious. Collectively, these findings suggest that cognitive therapy is at least as effective as antidepressant medication in preventing relapse or recurrence.
There are also indications that interpersonal psychotherapy (IPT) provides some benefit as a maintenance treatment. An 8-month maintenance study (Klerman et al 1974) found that weekly IPT produced lower relapse rates (17%) than placebo combined with monthly 15-min IPT sessions (31%). The group receiving IPT weekly performed almost as well as the groups receiving amitriptyline and monthly IPT (12% relapse) and the amitriptyline combined with weekly IPT group (12.5% relapse). A 3-year maintenance study (Frank et al 1990) found that IPT alone, given once a month, had a recurrence rate of 60%, a rate between that of the medication groups and the placebo group. It should be noted, however, that imipramine maintenance was given in a much higher dosage than in any previous maintenance study and IPT was given in a much lower dosage (monthly) than found effective in previous studies. Nonetheless, the IPT maintenance treatments significantly lengthened the mean time of remission (survival rate) to over 1 year, compared with the placebo group with a mean duration of remission of 38 weeks.
Psychological Theories
Depression undoubtedly has many causes, and no single cause is likely to provide an adequate explanation. Different individuals may have different factors that contribute to their depression, and for any given individual multiple factors will contribute. Below we discuss some of the most widely researched factors that are thought to contribute to depression.
Learned Helplessness
The learned helplessness model posits that feelings of helplessness underlie depression. This model is based on research with both humans and animals, and has detailed how animals and humans learn that their efforts do not affect their situation and as a result they give up. Learning that behavior does not influence the situation causes motivational, cognitive, and emotional changes that resemble those in depression (Seligman 1975). Humans learn to feel helplessness not only by being in an uncontrollable situation, but also by coming to expect that their behavior will not affect important outcomes. When individuals stop expecting their responses to have an effect, they may cease trying. They have little motivation to try to escape or change situations because they have learned that nothing will change, despite their efforts. Learned helplessness also diminishes the chances that a person will later learn that responses do alter a situation. For example, dogs that were placed in a shuttle box and exposed to unavoidable inescapable shock later failed to attempt an escape when they were placed in a shuttle box in which they could escape the shock by jumping over the barrier. Learned helplessness produces affective deficits because an individual experiences negative cognitions as a result of learned helplessness (Abramson et al 1978).
The theory was revised when research demonstrated that most people do not become depressed when they experience an uncontrollable negative event. According to the reformulated theory (Abramson et al 1978), some people demonstrate a `depressogenic’ attributional style in which they explain negative events using internal, stable, and global reasons. Individuals can make either internal or external attributions about the reasons for negative events (e.g. it was my fault versus it was someone else’s fault). Those who make internal attributions are likely to suffer a loss of self-esteem because they feel that the uncontrollable situation stems from their inadequacy, whereas those who make external attributions believe their helplessness is a result of the situation and realize that the situation will change (Abramson et al 1978).
Another factor that affects an individual’s emotional reaction to an event is whether he or she generalizes the helplessness to all situations (makes a global attribution) or specifies that the helplessness occurs only in this particular situation (makes a specific attribution) (Abramson et al 1978). If individuals believe the negative event is due to a transitory factor (e.g. they failed the test because they did not feel well), they will make an unstable attribution that will result in only a short-lived depressive reaction. In contrast, a stable attribution about something that is unlikely to change will result in prolonged negative feelings about the event; for example, they failed the test because they are stupid (Abramson et al 1978). Research has demonstrated that an internal, stable, and global attributional style is a marker for vulnerability to depression (Seligman & Nolen-Hoeksema 1987).
Cognitive Model of Depression
According to the cognitive model of depression (Beck 1976), individuals become depressed because of inaccurate information processing that causes them to interpret events in a biased way. These negative but incorrect beliefs involve negative views of self, a negative world view, and pessimistic future expectations. These beliefs lead to behaviors that serve to reaffirm the beliefs. Furthermore, once they become depressed, individuals tend to focus selectively on negative thoughts, which cause them to perceive themselves and their situation in the worst possible light. This negative bias contributes to the maintenance of the depressed mood (Hollon & Garber 1988). Negative cognitions are viewed as necessary but not sufficient to trigger depression. They interact with other predisposing factors such as genetics, developmental factors, and traumatic events to trigger depression in certain individuals.
Gender Differences in Depression
The incidence of unipolar depression in women is approximately twice as high as the rate in men. According to Nolen-Hoeksema (1987), women tend to ruminate in response to depressed mood, amplifying and sustaining it, and men tend to cope with depressed mood by engaging in active behavior, which serves to inhibit their dysphoria. These differences in coping style may stem from social pressure on men to be active and ignore their moods, whereas women are socialized to be emotional and contemplative (Nolen-Hoeksema 1987).
Rumination contributes to depression by interfering with problem-solving behavior, which can lead to failure, feelings of helplessness, and exacerbation of the depressed mood. In contrast, active behavior can increase feelings of control, create reinforcement, and dampen depression. Furthermore, rumination increases an individual’s focus on negative memories, and activates depressive explanations of the negative feelings, which in turn lead to decreased activity, increased chances of subsequent failure, and a perpetuation of feelings of depression and helplessness (Nolen-Hoeksema 1987).
Interpersonal Factors and Social Skills
Another factor believed to be important in buffering an individual from the effects of loss and other stressful life events is social support. Having few supportive social relationships, a small social network, and few close relationships are associated with increased depression. In addition, there is evidence to suggest that the supportiveness of the most intimate relationship plays the biggest role in buffering an individual from depression, and that other supportive relationships cannot make up for deficiencies in one’s closest relationship (Coyne et al 1991).
Depression arises when negative life events lead to disappointment in expectations, personal goals, or plans. Marital discord is one example of such a stressor. Hammen (1991) has conducted longitudinal research in which she investigated individuals who were achievement focused and individuals who were socially focused. She found that individuals who experienced a life event that was considered a setback in the area of self-esteem focus were more likely to become depressed than those who experienced a setback in a domain that they were less invested in. One of the risk factors for depression is whether an individual experiences a negative life event that leads to a loss of self-esteem in an important area (e.g. an individual who derives most of her self-esteem from interpersonal relationships may become depressed when she experiences marital difficulties with her partner).
The negative life event may, in turn, cause the individual to experience reduced positive reinforcement and an increase in negative mood.
The negative experience can trigger a negative self-focus that leads to self-criticism, unfavorable evaluations of one’s own performance, blaming oneself for negative events, and negative expectations for the future.
There are behavioral consequences of self-focused attention, such as social withdrawal and interpersonal difficulties. Moreover, negative expectations may cause decreased effort and persistence on tasks. The overall effect of the self-esteem-damaging event can create conditions that perpetuate depression (Lewinsohn et al 1985).
Coping skills, such as the ability to see setback as opportunity (e.g. individuals who view losing their job as an opportunity to find a better job), can buffer the individual from loss of self-esteem. In addition, individuals who are able to decrease their self-focus by engaging in a distracting activity may be able to activate problem-solving skills rather than becoming caught up in rumination. Therefore, individuals who have predisposing characteristics (e.g. a confiding relationship or high learned resourcefulness) that permit them to cope effectively with a stressor will be able to stop the depressed feelings before they lead to a depressive episode, whereas those who lack these immunity factors or who have vulnerability factors may not be able to interrupt the depression feedback loop.
There is a complex interaction between predisposing characteristics and negative life events such that the presence of certain immunities may protect an individual from depression in spite of other vulnerability factors and, conversely, a particular combination of vulnerabilities may counteract the positive effect of an immunity factor. An individual’s predisposing characteristics, both immunities and vulnerabilities to depression, mediate the reaction to stressful life events so that in some individuals these events lead to a disruption in expectations or plans and create depression, whereas other individuals can compensate for losses and interrupt the path to depression.
Biological Theories
Research suggests that both psychological and biological factors are important in contributing to the onset of depression. People who are depressed often show signs of dysregulation of circadian rhythms (e.g. greater depression at certain times of the day), sleep disturbance, and alteration of eating habits. Psychological events can trigger this dysregulation and the depression that follows may be accompanied by altered psychological thought processes as well as maladaptive biological changes (Shelton et al 1991). It can be challenging, however, to establish whether depression is linked to a particular event. Even when there is a precipitating event, this can change as the depression continues. There are frequently clear triggers for an initial episode of major depression but not for later episodes (Brown et al 1994). Currently there is no solid evidence that certain types of depression are caused ‘biologically’ and others ‘psychologically’, and there is some evidence to the contrary (Rush & Weissenburger 1994). There is, however, evidence that treatments that alter biological rhythms, such as sleep deprivation, decreasing time spent in rapid eye movement (REM) sleep, and receiving light therapy, can relieve symptoms in many depressed individuals (Shelton et al 1991). These findings led to the development of the dysregulation hypothesis of depression.
Depression as Dysregulation
Individuals have `zeitgebers’ (time-givers): personal relationships, social demands, and behaviors that keep biological rhythms regulated normally. For example, one has to wake up at a certain time to go to work. Ehlers et al (1988) believe that these social interactions are the important link between psychological and biological aspects of depression. If a person loses social reinforcement — perhaps through death of a loved one or loss of a job — there is a resulting dysregulation of biological rhythms resulting in symptoms (e.g. mood disturbance, sleep disturbance, eating disturbance, psychomotor changes, and fatigue) that we call depression. In addition, treatments that reset the ‘biological clock’ are effective in alleviating depression in many individuals. Moreover, there are high rates of depression in people who work swing shift or night shift, who are more likely to experience disturbances in their biological rhythms.
Genetics
There is a hereditary component contributing to the predisposition to develop a mood disorder. Family studies demonstrate that first-degree relatives of those with major depressive disorder are 1.5-3 times more likely to develop depression than the general population. The risk for first-degree relatives of patients with bipolar disorder is 10 times the risk for the general population (Strober et al 1988).
Twin studies indicate that bipolar disorder is more heritable than major depressive disorder. In addition, the fact that there is a higher concordance rate between monozygotic (identical) twins than between dizygotic (fraternal) twins for major depression (40% versus 11%) and bipolar disorder (72% versus 14%) supports the heritability of depression in general (Allen 1976). An adoption study conducted by Mendlewicz & Ranier (1977) found that 31% of biological parents of bipolar adoptees had mood disorders, compared with 2% of the bio-logical parents of normal adoptees. Another study (Wender et al 1986) found that biological relatives of those with a broad range of mood disorders were eight times more likely to have major depression than biological relatives of individuals who were not diagnosed with any mood disorders.
Neurotransmitter Function
It has been hypothesized that abnormal levels of, or function of, neurotransmitters such as norepinephrine (NE), dopamine, and serotonin are a possible cause of depression. It was originally believed that decreased levels of NE contributed to the development of depressive symptoms. This is unlikely to be the mechanism, however, because most antidepressant medications take several weeks to have an impact on depression, but they have an immediate effect on blocking the reuptake of NE and other neurotransmitters. Research suggests that antidepressants may work by increasing the sensitivity of the postsynaptic receptors for NE, which appear to be under-sensitive in depressed individuals (Siever & Davis 1985). Furthermore, research indicates that serotonin dysregulation is also involved in the onset of depression. L-Tryptophan, an amino acid involved in the synthesis of serotonin, is an effective treatment for both mania and depression (Prange et al 1974). Prange and col-leagues have proposed a combined norepinephrine—serotonin hypothesis which states that: (1) a serotonin deficiency increases vulnerability to mood disorder, and (2) when there is a serotonin deficiency, too much NE will result in mania, and too little NE will trigger depression (Prange et al 1974).
Psychological Treatments
The most widely used treatments for depression include psychotherapy and antidepressant treatment. Until recently, antidepressants were considered to be a more effective treatment than psychotherapy. Psychotherapy, however, appears to produce outcomes equivalent to those obtained with antidepressants (Elkin et al 1989), and with fewer side effects. In addition, there is some evidence that psychotherapy may protect against or delay relapsing after treatment has stopped (Evans et al 1992).
When choosing a treatment for a patient, it is important to keep in mind his or her preferences and personality characteristics. Individuals are more likely to respond to a preferred treatment because they believe that it will work, and are less likely to discontinue the treatment. Certain individuals may be more likely to respond to one or another treatment, although the current state of knowledge does not assist in selecting the most effective treatment on the basis of assessing patient characteristics.
Interpersonal Psychotherapy
IPT is directed towards helping individuals interact more effectively with others. It focuses on the individual’s history of maladaptive behaviors that have created negative interactions, and seeks to alter those behaviors, thoughts, and feelings in order to result in more positive relationships. It also looks for links in the present behavior to past experiences in childhood that may have caused the patient to learn those ineffective social skills. Together, the patient and therapist explore the problems and attempt to alter the behavior and consequently relationships over time (Ehlers et al 1988). Research suggests that IPT is an effective treatment for depression and is as effective as antidepressant treatment and other forms of psychotherapy (Elkin et al 1989).
Cognitive Therapy
Cognitive therapy aims to change patients’ maladaptive belief systems to create more acceptable reactions to people and healthier interpretations of situations (Ehlers et al 1988). The patient and therapist explore the patient’s negative beliefs and the patient engages in hypothesis-testing activities to disconfirm his or her erroneous views (Hollon & Garber 1988).
The patient and therapist engage in a dialogue to define the problem, help the patient identify his or her assumptions, determine the importance of events to the patient, and point out the disadvantages of retaining the biased beliefs and maladaptive behaviors. The patient develops new skills that teach him or her to alter negative thoughts and become more independent (Corsini & Wedding 1989).
The main goal of cognitive therapy is to teach patients to alter their faulty information processing so that they interpret events in an adaptive way. The therapist aims to help patients develop new skills which they can use to prevent a recurrence of the depression. In final sessions the patients are asked to imagine themselves in difficult situations and decide what they would do if such an instance arose (Hollon & Garber 1988). Research suggests that cognitive therapy is as effective as antidepressant treatment and other forms of psychotherapy in treating depression (Elkin et al 1989).
Biological Treatments
Antidepressant Treatment
Tricyclic medications are commonly used to treat depression (e.g. imipramine and amitriptyline). The mechanism of tricyclic agents is to block the reuptake of neurotransmitters (especially NE and dopamine) from the space between the neurons in the brain (synaptic cleft). Numerous controlled double-blind research studies have demonstrated that tricyclics have efficacy in the treatment of depression (Goodwin 1992). Like most antidepressant medications, tricyclics take approximately 2-3 weeks to affect the depression (Delgado et al 1992).
Monoamine oxidase inhibitor (MAOI) antidepressants began to be used about the same time as tricyclics, but they are not as widely used. MAOIs may cause high blood pressure when used in conjunction with foods that contain tyramine (e.g. cheese and chocolate). Some early research indicated that they are not as effective as tricyclics; however, a recent review concluded that when used with a proper diet they are an effective treatment for depression (Larsen 1991).
Selective serotonin reuptake inhibitors (SSRIs; e.g. Prozac and Zoloft) are a relatively new class of drugs synthesized in the early 1980s. They work by blocking the reuptake of serotonin so that increased levels remain in the synaptic cleft. They have a high selectivity for blocking serotonin reuptake receptors, whereas tricyclics affect to a greater extent both NE and other neurotransmitters. SSRIs are currently the most frequently prescribed medication. Controlled trials suggest that they are equivalent in effectiveness to the tricyclics; however, they have fewer side effects, are more easily adjusted to the proper dosage level, and are less toxic if the patient overdoses (Greenberg & Fisher 1997). Table 3 summarizes each type of medication, side effects, and mechanism of action.
Electroconvulsive Therapy (ECT)
ECT is usually administered to inpatients in a series of treatments. Treatment frequency is approximately twice a week. Many people demonstrate marked improvement after six to eight sessions, but some need more. Electrodes are placed either on both sides of the head or at the front and back of the skull on one side of the head. ECT remains an effective treatment according to several studies (Consensus Conference 1985), although the mechanism through which it works is still unknown (Sackheim 1989). ECT is usually reserved for severely depressed patients who have not responded to other forms of treatment or who are at immediate risk of suicide. ECT may also be more effective than medication with rapid cycling bipolar patients and depressed patients with psychotic symptoms. Although infrequent, ECT can result in pervasive and persistent memory loss. More frequently, it results in minor memory loss for events that happen shortly before receiving treatment, but does not result in persistent memory loss.
Some clinicians believe that certain types of depression have a biological etiology and others have a psychological etiology. The literature suggests, however, that there are a number of different possible causes of depression, each involving a complex interaction between biological, psychological, and social factors. No one perspective provides a complete explanation for how depression develops. Regardless of how the episode appears to be precipitated, the causal mechanisms are affected at all three levels: biological, psychological, and social. While medications seem to intervene at a biological level and psychotherapy treats depression at a psychosocial level, both interrupt the chain of events that maintains the depression and both facilitate changes in the other domains. For example, antidepressants affect neurotransmitter receptor sensitivity but also affect how individuals interact with others once they begin to feel better. Psychotherapy initially targets behavior change or cognitive change (e.g. socializing with others or learning not to make minor setbacks into devastating events), which then triggers physiological changes as well.
It is important to remember that the cause of depression cannot be explained with a simple biological or psychological explanation alone. The likelihood that any given individual becomes depressed is the result of a complex interaction of heredity, physiology, environmental events, cognitive representations, and situational factors. Treatment can intervene at any point in this complex web and have effects on function across all arenas. In this early stage of research into the effectiveness of acupuncture, it is important to keep in mind that the impact of acupuncture may be seen in physiological, psychological, and social domains, but that such effects do not address the ultimate question of precisely how acupuncture works in the treatment of depression.
