I think that the tricky thing is that a psychiatrist has to put statistics into perspective on two sides of the equation—both in regards to the medication, and then in regards to the diagnosis/presentation of the patient. In a nutshell, we diagnose patients based on their behaviour, not their brain chemistry and function, while we are using medication to treat their brain chemistry and function. We are not treating something that, in most cases, a doctor can see or quantify absolutely (in most instances doctors are not doing brain scans in order to medicate—I don’t even think at this point in our understanding they do).
Looking at the side effects for many psychiatric medications, it is fairly clear that the side-effects are vast and for a huge number also include non-temporary worsening of symptoms, including risk of suicide. To me that indicates that we do not understand nearly enough about brain chemistry or the cause of mental illness to medicate with reason—as much of it is intuition and experience and guesswork as formal training.
In this link it notes that “Gjedde explains we don’t really know what is wrong with people suffering from depression but looking at the symptoms we get a good idea of where the fault could lie within the brain”. Furthermore, major theories such as that the serotonin causes depression are suggested to be simplistic and innacurate, so while we have an idea that using medication to affect serotonin levels can help depression, it doesn’t mean that low serotonin levels are the cause. Those two articles are generally depression-specific, but considering that depression is probably the most studied mental illness (if not one of), if our understanding of that illness is vague, it seems likely that our understanding of other psychiatric illnesses are too (which is supported very much by the “we’ll try this medication and see if it works” approach, as opposed to “you have a hole in your leg, we’ll dose you up with morphine and you won’t feel it as much”).
I was going to reply to your direct examples, but an overarching response seems more appropriate.
I am not saying we should not medicate, as you seem to think. As a long-term psychiatric patient and the wife to another, I have seen the enormous benefits medication for depression can bring. I am saying that our understanding of this condition is relatively basic in regards to its complexity. A hole in the leg, or pain, do not need to be complexly understood to be dealth with sufficiently—pain medication hides the pain, that is the goal, and a suitable painkiller will do the job. It does not fix the hole in the leg, or the source of the pain.
With depression, the symptoms are treated, not the cause. Which is not a bad thing in itself, but it does not cure someone of their condition, which would be an ideal long-term goal. Painkillers are no use to a patient if the doctor cannot fix the wound or it cannot be healed; likewise with depression.
In regards to your association that “Non-temporary worsening of symptoms doesn’t sound like a common side effect.”: Sertraline (zoloft): depression is a “common” side effect affecting more than 1 in 100 people Citalopram: more than 1 in 100 people experience anxiousness, nervousness, apathy (which can be a symptom of depression for some) while (uncommon) more than 1 in 1000 experience aggressive behvaiour or mania (i.e. the medication could trigger a manic episode in a bipolar patient diagnosed purely with depression, highlighting my point about a diagnosis being based on behaviour)
My point is not, as you seem to think “we don’t understand depression properly so we can’t medicate”. I am rather highlighting the difficulties in medicating patients with mental health problems, particularly depression and bipolar disorder, as there is a complexity not found with such regularity in cases of fatigue and pain as you gave examples. How often is a patient given a pain medication only to find their senses heightened to the pain, rather than dulled? What is the frequency with which a patient given a medication to reduce blood pressure finds it rising? Not nearly as often as those with depression can have their symptoms worsened with medication, or, as I pointed out, a manic episode triggered in a bipolar patient who has not been diagnosed as such.
We should medicate, by all means—but in reference to the original post, we are looking at odds for some medications of more than 1 in 100, or 1 in 1000, and each individual response varies much more than if we were using morphine or aspirin or warfarin. Anecdotally speaking, to highlight the point that this may be used to our benefit in understanding depression, is the fact that my response to every SSRI I have been on (quite a few) I experience several days to a week of hypomania before having my depression drop suicidally low. If we could understand brain chemistry more, perhaps scientists could identify why me (and perhaps others) have this routine response to a certain type of depression medication, and not to others. Understanding nuances would help us better medicate.
As you see, I am not suggesting we stop medicating because we don’t understand, simply that we aim to learn more to reduce the variance in responses that currently occurs with depressive medications that does not occur with most other areas (i.e. the medication provokes a response counter to the response that was intended)