Evolutionary theory suggests that depression is an evolved adaptation that served to help resolve complex social problems in our ancestral past. Most episodes of depression resolve on their own in the absence of treatment (spontaneous remission) and it is only a subset of people who get depressed (likely those with inherited or acquired diatheses) that ever seek treatment. The bottom line is that while depression may be unpleasant it also may serve a functional purpose. To the extent that that is true then those interventions that facilitate the processes that depression evolved to serve (like cognitive therapy or behavioral activation or interpersonal psychotherapy) are likely to be preferred over antidepressant medications that suppress symptoms but do little to facilitate solving complex social problems (Hollon 2019).

At its core depression involves inaccurate beliefs and maladaptive information processing. CBT directly targets those etiological mechanisms. CBT has an enduring effect that reduces risk for relapse by more than half relative to ADM following treatment termination (Cuijpers 2013). This suggests that it may work because it targets important causal processes in a relatively enduring fashion.

CBT is as efficacious as ADM (on average) although some patients are more likely to respond to the other and vice versa (DeRubeis 2014). CBT does have an enduring effect not found for ADM that cuts risk for relapse following treatment termination (Cuijpers 2013). At least some of the somatic treatments are more efficacious than either CBT or ADM (ECT especially) although you would not go there unless the patient does not respond to psychosocial or antidepressant medications.

Very much so. We are twice as likely to medicate people with non-psychotic depressions than we were a quarter century ago or than they do in the United Kingdom or Western Europe where they have clinical practice guidelines that examine the relative efficacy and safety of the various interventions., ADM prescriptions really exploded in the early 1990s with the introduction of the SSRIs because they are believed to be relatively safe (you cannot overdose on them and they require no special dietary restrictions). General practitioners now write about 90% of the prescriptions for SSRIs and they are far more likely to put someone on medications and to under-medicate patients who ought to be on medications. Some patients will do better on medications than on psychotherapy but they rarely get to psychiatrists who are more aggressive in their dosing strategies and other patients will do better on psychotherapy than on medications but they rarely get referred on by their general practitioners.

All have their uses. SSRIs are relatively benign (you cannot overdose and side effects are minimal). SNRIs might be a little stronger but a little more problematic. Tricyclics might be a little stronger still but increase risk of death via overdose. MAOIs may be a little stronger still but have problematic interactions with certain foods and other medications. Most research psychiatrists start with SSRIs and only move through the progression just described from easier to manage to more difficult to manage medications as they have to (Hollon 2014). All that being said I much prefer going with one or more of the empirically-supported psychosocial interventions (cognitive therapy,, behavioral intervention, interpersonal psychotherapy) and bringing medications on board only if you have to. CBT does have an enduring effect that cuts risk for relapse by more than half relative to medication following treatment termination (Cuijpers 2013).

I would be very cautious about medicating preadolescent children. Antidepressant medications can trigger manic episodes in people in the bipolar spectrum and although the odds are about ten to one that someone who is depressed is in the bipolar spectrum that seems to be an unnecessary risk given that other comparably efficacious psychosocial interventions are available.

Recent advances in machine learning can be used to identify the optimal treatment for a given individual and that should allow us to make treatment delivery more efficient (DeRubeis 2014). There also are indications that depression may be an evolved adaptation that facilitates solving complex social problems (Andrews & Thomson 2009). To the extent that is true then psychosocial interventions that facilitate the process that depression evolved to serve are likely to be preferred over medications (Hollon 2019).

Adding ADM to CBT appears to enhance acute response at least to some extent (Hollon 1992; Hollon 2014) but may interfere with its long-term enduring effect (DeRubeis 2020) and CBT provided alone appears to cut risk for relapse by more than half relative to ADM following treatment termination (Cuipers 2013).

Antidepressants do suppress symptoms for most people but only separate from pill-placebo among patients with more severe depressions (Fournier 2010). Evolutionary theory suggests that depression is an evolved adaptation that facilitates solving complex social problems (Andrews & Thomson 2009). It may be that suppressing symptoms allows patients to better deal with life problems but although widely believed there is not that much evidence to support the supposition. CBT does increase the odds that patients improve their employment situation relative to ADM (Fournier 2014). CBT does have an enduring effect that reduces risk for relapse following treatment termination not found for ADM (Cuijper 2013). At the least CBT and other psychosocial interventions (like behavioral activation or interpersonal psychotherapy) likely teach the skills that depression evolved to serve (Hollon 2019)

That is widely believed but not all that well supported. CBT is as efficacious as ADM (on average) although there are indications that some people are more likely to respond to CBT than ADM whereas others show the opposite pattern (DeRubeis 2014). Combined treatment tends to be a little more efficacious than either single modality but not by all that much (Hollon 1992; Hollon 2014) but adding ADM may interfere with any enduring effect that CBT possesses (DeRubeis 2020) and the evidence that CBT alone has an enduring effect not found for ADM is quite compelling (Cuijpers 2013).

No. You would do the same things either way. The one concern is that at least one recent study suggests that adding medications may interfere with any enduring effect that CBT may possess (DeRubeis 2020) and the evidence that CBT provided in the absence of medications is quite compelling (Cuijpers 2013).

There are some differences in what the different interventions target although they are fairly minimal (Fournier 2013). Each intervention is efficacious and specific although CBT has an enduring effect not found for medications (Cuijpers 2013). There are indications that some people respond to the one who will not respond to the other and vice versa (DeRubeis 2014).

SSRIs are relatively safe short-term and side effects are relatively minimal (some nausea and loss of interest in sex). Longer-term is not so clear although mostly because it has not been all that well studied. Maslej 2017 reports a 30% increment in "all cause" mortality for all antidepressants regardless of type but those findings are open to multiple interpretations.

There are two established preventive methods. Cognitive therapy and perhaps the closely related behavioral activation cut risk for relapse by more than half (Hollon 2005; Dobson 2008). People who get better on antidepressant medications are well advised to stay on medications. That appears to be about as preventive as prior exposure to cognitive therapy (Cuijpers 2013).

Not everyone will respond to every different treatment even if it is adequately implemented. DeRubeis and colleagues found that just under a third of patients with more severe depression would have done better on antidepressant medications than on CBT whereas just under a third of the patients in that trial would have shown the opposite pattern (DeRubeis 2014). What he and others are trying to develop precision treatment rules that can predict in advance who will do better on which treatment. Getting the optimal treatment to each patient can make mental health delivery more efficient even before we improve our treatments and being able to predict what treatment is best for a given patient will help us figure out how to make our treatments more effective.

That is an episode of depression that has not responded to two more adequate courses of treatment. Some depressions are harder to treat than others but there are several different types of psychotherapy and at least four major classes of antidepressants each with several different specific medications and several different types of somatic treatments (ECT may be the strongest) so there are lots of options to try.

The evidence seems to indicate that it does. Antidepressant medications stimulate brain derived neurotrophic factor (BDNF) which seems to promote growth in synaptic connections and quite possibly neuronal growth in the hippocampus (Duman 1999; Duman & Monteggia, 2006 ). Whether that is unique to antidepressant medications or a more general phenomenon produced by any intervention (for example exercise) that relieves depression remains unclear.

It always fair game to suggest that someone talk with their physician about whether medications might be appropriate but if someone wanted to consideration medications I would encourage them to see a psychiatrist not a general practitioner. The number of patients treated with antidepressants has skyrocketed since the SSRIs were first introduced back in the early 1990's and the vast majority of prescriptions nowadays are written by general practitioners. Most psychiatrists know to dose to remission (becomes fully well). That means raising dosage until the patient either remits or reaches their maximally tolerated dose and if they do without remitting then augmenting or combining or switching medications. General practitioners medicate too many patients (only about half of the patients medicated show a "true drug" response over and above placebo) and under medicate the people who ought to be on medications and would do better if they were seeing a psychiatrist.

I suspect that folks are simply misinformed as to what it actually involves. Not everyone responds to CBT but it is at least as efficacious as any other type of intervention and has a long-term enduring effect that simply has not been established for other interventions (behavior activation may as well).

I work on both. Sleep typically responds fairly rapidly to simple sleep hygiene strategies (within a couple of days) whereas mood typically takes a couple of weeks to clear but I would start on both in the initial sessions. As sleep improves that usually helps to improve mood.

The therapeutic relationship matters in CBT just as it does in all types of therapy but in a somewhat different way than in most other approaches. Robert DeRubeis at the University of Pennsylvania tracked therapist behaviors and the quality of the working alliance across the course of treatment and found that adherence to specific cognitive and behavioral skills in early sessions drove rapid symptom change that in turn drove the rated quality of the working alliance (Feeley DeRubeis, & Gelfand, 1999). In brief, help patients improve quickly and you enhance the quality of the working alliance. When working with clients we go right after symptom change as rapidly as possible (not faster than the client wants to go but as rapidly as they are willing to tolerate) in a matter-of-fact business-as-usual fashion. I will answer any question and make it clear that we cannot predict how things will turn out but that but that we do know how to find out and that is to run experiments (try new things) and see how it goes. At the same time we are very much aware that it is the client who has to deal with the anxiety that trying new things can arouse so we do not push but rather facilitate. The analogy I like to use is that doing therapy with someone is like going off to war; the therapeutic relationship develops while you are sharing a foxhole and fighting together. The other analogy that I like to use is that I work with a client the same way that I train a promising new therapist; my goal is not just to do the therapy with them but rather to teach them how to do the therapy for themselves. I think that is why cognitive therapy gets such good enduring results; cognitive therapy cuts risk for relapse by more than half relative to medications following treatment termination (Cuijpers et al., 2013).

We know less about the long-term effects than we would like. SSRIs are thought to be relatively safe and non-addictive but there are indications that they increase "all cause" mortality by 30% among people without heart conditions (they are slightly protective for the latter) (Maslej 2017) and may be difficult to discontinue without triggering a relapse (Hollon 2019).

I simply talk with them about their prior experience(s) with the approach. CBT does not have to be regimented and it certainly should never be calloused. When I work with someone I make it clear that I work for them and not that they work for me. What I want to know is what they are trying to get out of therapy and I do my best to deliver.