The origin of the endogenousÂ depression vs exogenous/reactive depression dichotomy.
In the early nineteen eighties, researchers and practicing psychiatrists alike were looking for ways to classify mood disorders in general and depression types in particular. This was driven by a number of considerations. Firstly, since there are no definitive clinical tests for the presence of depression (a urine or blood test that would confirm the presence of the disease) and the symptoms of depression can be varied, contradictory and the set of symptoms each patient presents with is rarely the same as another, it was thought that segmenting depression in this manner would make precise diagnoses easier and improve diagnostic consistency. Secondly, with some patients responding very well to tricyclic antidepressants or monoamine oxidase inhibitorsÂ and some not at all (or indeed adversely), this was expected to be helpful in both determining the cause of such inconsistencies in treatment outcomes and helping to identify the patients who would respond favourably to such treatment ahead of time.
Endogenous depressionÂ was then defined as related to the patient’s physiology and independent of external conditions, therefore being amenable to treatment with antidepressantsÂ with talk therapyÂ being no more effective for this type of depressionÂ than for a broken foot (the principle being that thought can not shape matter). Exogenous depressionÂ was considered to be reactiveÂ in nature – precipitated by life events and as such best treated with talking therapy, since you could scarcely expect the precipitating life event such as the death of a loved one and the consequent grief to go away after the patient swallowed some pills (the principle that pharmacology can’t influence the world outside the subject organism).
Disputes about the difference between endogenous depression and reactive depression.
Since then, the fundamental assumptions on which the utility of differentiating between these two types of depressionÂ rests have been hotly disputed. There have been a growing number of claims, supported by research, that the likelihood of an endogenous depression suffererÂ experiencing an adverse life event prior to an episode is similar, if not identical, to the likelihood of that being the case for a reactive depression patient. Moreover, the efficacy of depression treatment with antidepressantsÂ does not appear to correlate anywhere as neatly as has been expected to the patients based on exogenous vs reactiveÂ diagnoses.
In addition to the above-mentioned empirically based critiques, some researchers held that this dualistic view of depression, when taken to its logical conclusion, would result in an irreconcilable conflict with what little we do know about the chemistry of the brain. Specifically, they claimed that this sort of classification necessarily implies that while some behaviours were all to do with brain chemistry (in the case of an endogenous depression diagnosis), others were somehow exempt (reactive depression diagnosis).
Additionally, some clinicians and quite a few sufferers have held that endogenous depressionÂ was being used as a default, catch-all diagnosis similar to ‘idiopathic’ diagnoses in other diseases. If a neurologist, for example, can’t figure out why someone is trembling, it’s diagnosed as idiopathic tremor. “Idiopathic”, of course, roughly means “arising spontaneously from no known cause” and as such is the absence of a diagnosis, but the Greek tag often misleads the patient into thinking that the doctor has finally put his finger on the problem. Similarly, when a talk therapistÂ didn’t succeed in determining the circumstances which led to the depressive episode, the temptation was there to write it off as endogenous depression. This had long been a source of complaints from patients before the various bodies started discouraging the use of this classification.
Modern understanding of endogenous depression.
While it is widely accepted that the split classification of depression as either endogenousÂ or reactiveÂ is not valid or useful for the original purposes for which it was conceived, there is a growing body of research that indicates it to be of value, albeit in a different way. Endogenous depressionÂ is viewed by these researchers as a disregulation of the endogenous opioid system.
The sufferer’s view of endogenous depression.
While researchers argue about things in theory, those of us in the trenches so to speak have an entirely different view. It may very well be that both reactive depressionÂ and endogenous depressionÂ sufferers can experience aÂ depressive episodeÂ as a result of life events, but those of us with endogenous depressionÂ often experience episodes of depressionÂ not caused by life events or any other external factor. While this evidence is anecdotal and thus not appropriate for scholarly work, it is very appropriate indeed in other settings. Incidentally, the reason it is purely anecdotal at this time is both the lack of interest among researchers and the difficulty, length and expense involved in a statistically sound study to support this claim.
The existence of endogenous depressionÂ is important for the patients to determine the viability of treatment options, since we feel that talk therapy is not effective for us in the absence of exacerbating external facors. Secondly, it is important in raising both awareness and understanding of our condition. As difficult as coping with depressionÂ is, it is doubly difficult to deal with people disregarding our suffering and doubting the validity of our condition because they can’t see the “reason” for the depression. If we can’t differentiate between reactiveÂ and endogenousÂ depression, we can’t inform and educate people on the idiosyncrasies of our subtype of depression.
The fact is, our understanding of brain chemistry and psychiatry today is somewhat akin to our understanding of the rest of medicine in the nineteenth century. We can’t penetrate the blood-brain barrier, measuring things in the brain non-intrusively has severe limitations no matter how much our technology improves and measuring intrusively is rarely a viable option. As a consequence, for a large number of compounds, we only know that they have certain effects without knowing why or exactly how they work. Antidepressants, for example, become bioavailable and start affecting neurotransmitter levels very quickly, yet they take quite some time to make a difference in the state of the patient being treated. We routinely discover that a certain compound has positive effects on brain function or mood when we test them for something else entirely (that’s how a lot of sleep medication was discovered). The reason I bring this up is that unlike the hard sciences or even the better understood fields of medicine, psychiatry does not currently have the last word on what is what and first-hand experience is not only valid and matters, but must always hold primacy. After all, it’s our mind and we darn very well know best if it’s messed up and in what way.
Depression-related (hopefully not depressing) quote of the day.
“Well, it may be all right in practice, but it will never work in theory.”
- Warren Buffett talking about how academics view his investment approach
I thought this was appropriate to sum up our discussion of how to sum up the dispute around whether endogenous depressionÂ exists (and we with it).
- “Endogenous Versus Exogenous: Still Not the Issue”, Medscape Psychopharmacology Today Journal Article,Â Â Thomas AM Kramer, MD
- “Does the antidepressive response to opiate treatment describe a subtype of depression?”,Â European Neuropsychopharmacology Journal Article