Is Depression a Disease? — Part I II III

By Jonathan Rottenberg, Ph.D.
Created Oct 12 2009 – 6:05am

The symptoms of depression –despondency, lethargy, nightly insomnia, an inability to concentrate–are bewildering. The person with depression wonders, “What is wrong with me?…Why do I feel this way?” and if the symptoms persist, he or she will pose these questions to a doctor or therapist. Mainstream approaches to depression say that these symptoms reflect a defect or disease. While this model of depression is intuitive and virtually inescapable, it may be time to reconsider its clinical and scientific usefulness.

By Jonathan Rottenberg, Ph.D.
Created Oct 12 2009 – 6:05am

The symptoms of depression –despondency, lethargy, nightly insomnia, an inability to concentrate–are bewildering. The person with depression wonders, “What is wrong with me?…Why do I feel this way?” and if the symptoms persist, he or she will pose these questions to a doctor or therapist. Mainstream approaches to depression say that these symptoms reflect a defect or disease. While this model of depression is intuitive and virtually inescapable, it may be time to reconsider its clinical and scientific usefulness.

For example, mainstream psychiatry presents the idea of a correctible biological defect, a ‘chemical imbalance.’ With 27 million people taking antidepressant medicines in the US, the media, patient groups, and mental health professionals have widely embraced this comforting and optimistic notion. Sadly, the efficacy of antidepressants is often overstated: Two-thirds of those who are treated with antidepressants continue to be burdened with some degree of depressive symptoms. In fact, current antidepressant treatments are no more effective than those developed 60 years ago. Even diehard biological psychiatrists acknowledge that the quest for a physical cause for all cases of depression has proven elusive. Without a clear target of what is being treated, the search for a magic pharmacological bullet for depression verges on the quixotic.

Likewise, cognitive approaches answer the depressed person in the same terms-your symptoms reflect a defect. This time, it is faulty thinking that is to blame. This approach, too, has spawned an influential therapy, one that corrects thought. But the evidence that one or more of these cognitive defects causes depression is modest, and the resulting therapy is only about as effective as treatment with antidepressants-beneficial for many, but far from a cure.

In fact, just about anywhere a depressed patient turns in contemporary society, the answer remains much the same: Your symptoms signal a deficiency. That deficiency may lie in the person’s childhood (says the psychoanalyst), in the person’s soul or relationship with god (says the priest, pastor, or rabbi), or in the person’s relationships with significant others (says the marital or family therapist). While each idea may capture a part of why some people become depressed, for most these will not be final answers that lead to fully effective treatment.

In the end, the depressed person all too often faces a triple indignity. (1) You experience distressing and crippling symptoms; (2) treatments deliver you less relief than is promised; and (3) professionals interpret the failure of a treatment as a sign that your defect is more serious than initially thought.

If results are this frustrating, why do we cling to the idea that depression is a disease or defect?

Dear Blog Readers, this very question has been on my mind lately.

More to come…


Is Depression a Disease? — Part II

By Jonathan Rottenberg, Ph.D.
Created Oct 17 2009 – 1:03pm

The disease (or defect) model of depression represents a mainstream view of this condition. In my last post, I started the series by asking whether this approach should go unchallenged. In this post, I briefly debunk four commonly held arguments that are used to support the disease model.

(1) Depression must be a disease because it is disabling and aversive. Yes, depression is horrible and undesirable and associated with impairments. Many real diseases are undesirable and associated with impairments. However, just become something is bad does not make it a disease. As Randolph Nesse has so nicely argued, fever and cough and pain are unpleasant and undesirable but far from being diseases, these responses are actually protective of health (without a capacity for pain, you are prone to become severely injured or dead!). Number one is a phony argument. 

(2) But haven’t scientists discovered the brain areas or regions that are responsible for depression? This one is easy. No. Although there is research that correlates patterns of brain structure or function to the symptoms of depression, almost no evidence establishes that any brain pattern is a cause of depression, as opposed to just being an effect of depression (i.e., feeling sad all the time changes brain function. Is that interesting or surprising?). In fact there are no laboratory tests of any kind, including brain images, that are truly diagnostic of depression! One common metaphor that is used to support the disease model of depression is that it is like diabetes. Leaving aside the question of whether a depressed person needs their prozac as the diabetic needs their insulin, one problem with the metaphor is that unlike diabetes (and most physical diseases), there are no diagnostic tests or even reliable signs of the disorder that are independent of the person’s own report of symptoms.

(3) But isn’ t it accepted that depression is genetic? If so, isn’t it just a matter of time before they discover the disease genes? Yes, there is evidence that depression has substantial heritability. But this does not mean that depression is a disease.  Intelligence, extraversion, and just about every trait that has been ever studied has been found to be substantially heritable but I hope you would agree that the heritability of intelligence and extraversion does not make these traits diseases! In other words, just because something is heritable (i.e., is related to genetic variation) this does not make it a disease. As far as the search for specific ‘disease genes’ for depression,  this venture is not going well at all. Perhaps the most celebrated depression candidate gene involved the ‘serotonin transporter gene.’ However, the scientific evidence favoring a relationship between the serotonin transporter gene and depression has almost completely unraveled. Most behavioral genetics experts do not expect a single gene of large effect will ever be discovered to explain depression vulnerability.

(4) What about the efficacy of antidepressant medicines? Doesn’t that clinch the idea that depression must be a disease? Yes, antidepressants are effective at reducing the symptoms of depression for a majority of depression sufferers. This is a good thing. However, this is not a strong clincher argument. First off, the efficacy of antidepressants is somewhat overstated. Second, these medications do not appear to have any specific efficacy for depression per ce. They are used for the treatment of a wide variety of different clinical problems including, OCD, eating disorders, and pain. If these drugs address a depressive disease, they are also addressing an OCD disease, an eating disorders disease, and a pain disease. Unless these different conditions are all the same disease it is more likely, these drugs are not treating any specific disease process per ce; rather they are having a beneficial nonspecific effect, such as improving a person’s overall hedonic tone. Third, it is unwise to assume that a remedy ever tells us about original causation. Do you agree that it would be absurd to argue that because aspirin is useful for treating a headache, a headache is caused by a lack of aspirin? How different is the argument that because prozac is useful for treating a depression, a depression is caused by a lack of …….

More to come.

Is Depression a Disease? — Part III

By Jonathan Rottenberg, Ph.D.
Created Oct 26 2009 – 9:42am

Mainstream approaches to depression view it as resulting from a disease or defect (the defect can be biological or psychological). In my last post, I debunked several of the main arguments that are advanced in favor of the disease model.

In this post, (the last on this particular topic for a while) I consider some of the challenges of creating a better explanation of why people become depressed. Specifically, here are five key facts that an explanation of depression, must, somehow, explain. Again, these are facts that the disease model does not handle especially well, but I will not belabor that now.

(1) Syndromal and subsyndromal depression have extraordinarily high lifetime prevalence. Recent estimates project that up to 1/5th of the population will have an episode of major depression at some point. If one includes people who have significant depressive symptoms that fall just short of a diagnosis, about 40 percent of the population will have significant depression at some point in the life course. This is an extraordinarily high prevalence! When this high prevalence is coupled with the often young age of onset (late adolescence and early adulthood), one could say that the epidemiology of depression does not resemble that of a typical medical malady. Any explanation of depression must account for its extraordinarly high prevalence.

(2) Rates of depressive illness are accelerating. Good cross-cultural and cross-national evidence indicates that the prevalence of depression is increasing. This increase is a problem for the idea that depression reflects the operation of a fixed biological deficit (like a genetic defect), since the change in the prevalence of depression is occurring on a much more rapid timescale than could our biological makeup. And no, I do not think there is something in the water! Change in the psychological environment rather than the physical environment is the most likely candidate explanation.

(3)  Depression is more prevalent in younger birth cohorts than in older birth cohorts. Again, there is strong epidemiological data that shows not only increasing rates of depressive illness overall, but that this acceleration is much more pronounced in young people. Several studies demonstrate that today’s young adults have accumulated as much or more depression risk as people born much earlier (say people in their 50s and 60s). It is very unlikely that these effects are due to younger people simply being more comfortable reporting mild episodes of depression because of reduced depressive stigma. We see also increases in rates of very severe incapacitating depression in the young, including depression that requires hospitalization.  The acceleration and concentration of illness among young people poses another challenge for defect models of depression.

(4) Depression is twice as common among adult females than adult males. Interestingly, we don’t see this pattern in childhood. It emerges only in the middle-school years in adolescence. Again, if one holds to the defect model, one would have to explain why women have a special propensity to a deficit as well as why the deficit in question would come to light only at a particular stage in the life course. The gender difference in depression is one of the big facts of depression that has not been well-accounted for by most of the major models of depression.  

(5) There are several empirically-supported treatments for depression but they appear to have plateaued in their effectiveness. The good news is that there are supported pharmacological and psychologically based treatments for depression (biological: antidepressants; psychological: cognitive-behavioral and interpersonal therapies). The bad news is that most of these treatments leave the majority of patients (even patients who respond) with residual symptoms. It is good that people are encouraged to seek treatment. However, one of the big facts of depression, which any good explanation of depression must explain is why the condition is often so recalcitrant to treatment. Once we acknowledge that depression is often treatment-refractory and focus efforts on explaining why this is, it will be much easier to develop treatments that manage the condition more effectively.


 reviewed by Forum Admin 2-4-10

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