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I think at that point what I’ve found in doing a lot of consulting work in this area over the years one of the great secrets of success in consulting practice is to catch people at a time when they, many if you’re lucky, will be willing to listen to something. You tell them very grandmotherly basic things but maybe they’ll listen and what you’ll often find a list of twenty things that have been tried and augmenting with antipsychotic and a thyroid problem and blah, blah, blah and they’re still not doing well they tell you that the fact is that the fish in Boston are being poisoned because most of the stuff went down the toilet because they couldn’t tolerate the agent’s side effects. So what we basically need to do is to make sure the patients are actually getting the pill in the mouth and taking this and you can monitor blood levels for drugs about which we know something about the blood levels and do basic things.
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I think if you’re in category A has been tried, let’s say you’ve done a bunch of SSRI therapies and you’re not getting anywhere, don’t forget that we still have the golden oldies like nortriptyline, desipramine and even, God forbid, an MAO inhibitor if other things don’t work. Rather than going through every conceivable modern drug before you give up and go to an alternate drug I think that doesn’t make a lot of sense.
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Adding lithium really matters and I don’t know whether this is because of the subtle, occult bipolarity overload sometimes. In fact, the older I get the more I’m beginning to appreciate and manage so-called treatment resistant patients who are probably bipolar II’s in disguise. Some of them are people in sort of mixed agitated states of bipolar disorder. Some of them are rapidly cycling because you’re pushing antidepressant through the rest of it. Anyway, for that and other reasons we don’t understand, lithium really matters and there’s real double blind placebo control data to back that up.
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A little bit of neuroleptic may help some people. Recently, little bits of risperidone or clozapine have become quite fashionable. You don’t necessarily need to be highly agitated or psychotic. MAO inhibitors probably really matter. At least that’s what the data are even though most of us are uneasy about using these drugs. When other things are failing don’t forget aggressive use of Nardil and Parnate has rescued maybe 60% of treatment failures with standard medicine. Finally, if nothing else is working, ECT for various severely ill psychotic suicidal melancholy patients and especially older people who often have very tough depressions may be a very important thing to do.

If you are a severe but nonpsychotic, you’re a little bit better but not great. If you are moderately ill and classic, that’s the optimal group and then in the less severe group, the variance is huge because there are all sorts of illnesses that are being kind of swept together. There have been a lot of attempts to use various techie biologic measures – endocrine tests like the dexamethasone suppression test, the TSH stimulation test, sleep/eating machine measurements, REM suppression, that sort of thing, measured in mystical metabolites in the body fluids known as the MAPG up down or sideways. That kind of stuff. It’s bunk. I mean, it’s nice to write papers about and do research on but please don’t take it seriously because those kinds of measurements, while they may be statistically helpful predicting treatment response and that sort of thing, really doesn’t hold up all that well and the group of indications on the left, that is, the clinical form of the illness, severity of the illness, psychotic/nonpsychotic. These things are really much more powerful in predicting clinical response.
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Certainly one is not going to deprive a patient of a trial even if let’s say they flunk the DST and their cortisol suppression is perfectly normal and they have a classic melancholy textbook depression I would think that most clinicians would say let’s invariably treat.
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Then there’s the whole question about let’s say you do everything wisely and well and you work the doses up gradually and they’re maximally tolerated levels and you’ve tried a couple of classic antidepressants aggressively and you’re not getting anywhere, what do you do next? Well, that’s another complicated story but I think things that really matter are to go back your state of mind and assume that you don’t know what’s going on in this picture. If you can’t do that, send the patient down the hall to a friend with fresh eyeballs. It doesn’t matter if it’s the world’s expert, just fresh eyeballs who’ll ask innocent questions, “What’s wrong with this patient? Let me take the history. Let me get an internist to check out his medical neurological endocrine status as well.” Just go back to the basic bread and butter things that we were taught many years ago rather than just banging away on our tenth SSRI, you know, at six months. Just get off that kind of allopathic compulsion and try to sit back and think for a minute or two and reevaluate what you’re dealing with.
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I think that really matters and you’ll sometimes dig up things that you missed. The person may be drinking too much. They may be using cocaine. They may have liver disease. They may have a brain tumor. They may have thyroidism. They may have a really severe problem. They may have horrendous marital diff… I mean there are all sorts of things that could be important that you may have overlooked.

Nefazodone is another important antidepressant drug that can inhibit 3A and can produce some potentially dangerous drug/drug interactions, again, you need to match this list to the proceeding list and go back and forth and you can make your own guesses about which one is doing what to whom.
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I think I want to move onto the clinical aspects of antidepressant drugs. The first probably most important thing to tell you about is that the effectiveness of the antidepressant drugs is one of the best kept scandals in our industry. The antidepressant drugs are good. I’m glad we’ve got them. They do wonderful things. I wouldn’t dare try practice trying to treat patients without them but to be quite honest about them they’re superiority to placebo is sometimes rather iffy. On average, if you want a kind of a rough number to keep in mind, about a third of people who meet the DSM-IV criteria for major depression will respond to a placebo within one to two months and about two-thirds, if you’re lucky, three-quarters will respond to an active drug. So the difference of drug and placebo is about a third of the action.
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Now some of that placebo response may include spontaneous remissions. One of the most important effects of major depression is that it is an episodic illness and if you can keep somebody alive and hopeful for nine months or a year, most people will recover spontaneously. It may well be that some of the variants of the placebo response is people coming in to treatment late in the illness and about to undergo a spontaneous remission. Anyway, the numbers that you see here show, again, this famous two-thirds/one-third rule and the difference is roughly 30% and this is what you’re betting on when you give any antidepressant.
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With ECT, the numbers are much better – a 90% ECT response, 10-20% placebo response. It’s better but it’s not perfect. With all these drugs – with the tricyclics, the SSRIs, MAO inhibitors, atypical drugs – the story is very similar and this kind of one_third/two-third rule sometimes, for example, with mirtazapine, it can be even less impressive but that’s the general rule of thumb in this field.
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So that leads to the quest for who’s the ideal candidate. That’s a very complicated story but rather quickly the story is if you have a classic endogenous melancholy, no-doubt- about-it depression is more likely to respond than a neurotic, questionable dysphoric kind of illness. If the severity is somewhere in the middle range, that is, people who have very mild but classic illnesses tend to respond questionably. People with very, very severe classic illnesses don’t respond as well so you have this kind of biphasic response versus severity relationship. So you have this two-dimensional story. There’s the type of illness – melancholy/non-melancholy is one dimension and then severity is another dimension.

Yet a third dimension is psychotic/nonpsychotic. Psychotic usually implies greater severity and one needs to tease apart the contributions of each and that has been done recently particularly by Jim Cosas at Cornell. The finding is that if you’re severe and psychotic you do rather poorly with any antidepressant, maybe better with ETC. Maybe a little bit better if you add a neuroleptic to an antidepressant.

Most of the other SSRIs have much more benign half lives, on the order of a day or less and they tend to wash out in five or six half lives. So a week later you should be able to use other interacting drugs safely including MAO inhibitors – Demerol – and so on.
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If you mix an SSRI with a tricyclic the danger there is that the blood level of the tricyclic will end up being much higher than you might guess with the drug given by itself. So for example there’s been a popular mixing of SSRIs with small doses with desipramine as a way to get a kind of an SNRI combination going and using that as a way of trying to rescue treatment resistant patients. It’s potentially dangerous and tricky means you’ve have to back off on the dosing of the tricyclics because the blood levels will be higher on the SSRI than you might have predicted.
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As far as blood levels, monitoring and using these things to guide clinical practice to predict response and side effectors, that whole exercise over the past 20 years or so has yielded not very much. I know that clinical and commercial laboratories will assay anything that you send them blood and money for but the information has limited clinical value with a few exceptions. With almost any antidepressant a blood level can be used at least as a litmus test that allows you to say, “Yes, this patient has taken some medicine in the recent past.” Period. End of statement.
With a few drugs, notably nortriptyline, they are pretty good and pretty good data for amitriptyline and imipramine. We have pretty good correlations of blood levels running up usually in the 100-200 nanograms are probably optimal for most patients in terms of the balance between efficacy and safety and tolerability. Tricyclic, the SSRIs, blood levels are virtually meaningless. It really doesn’t help much other than to say yes the patient has taken some drug.
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The 2C system substrates include the drugs ketoconazole, Nizoral. The 2D6 system is very important to psychotropic drugs because many tricyclics go through that system and other drugs that are of psychiatric interest.

The 3A system is a place where serotonin reuptake inhibitors, tricyclic antidepressants and other drugs tend to go and when you block this enzyme, for example, with fluvoxamine. Antihistamines like terfenadine can build up and kill cardiac induction and kill patients. Cisapride is another one that has the same potential to build up low levels and inhibit cardiac induction and there have been some deaths from these kinds of interactions. Again, this is an enormously complicated topic and would take an entire hour just to even begin to get into it but I just need to remind you that it’s something that you need to be aware of and try to learn about from the literature and the handout.

Drugs that interact in these systems include, I think this first line is the group that you really need to memorize since these are the most likely interactions, but fluvoxamine actually turns up in several categories at the 1A and 2C and the 3A system. Alpha 2B6 Prozac and Taxol are the two leading candidates and then there are other drugs that may interact with much less likely importance.

Now, there are very similar analogous phenomena that are not as well worked out that seem to occur in the serotonin system whereby making more serotonin available by blocking its uptake. Autoreceptors for serotonin, again, desensitize and the serotonin system revs up and makes more transmitter available and some of the postsynaptic serotonin receptors analogous to alpha-1 in the adrenergic system remain available and do what has to be done.
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I’ve covered all this stuff and I think it’s time we cut to the chase and give you, again, kind of a bird’s eye summary. The story, again, is you can translate this, just change the name of the players but let’s say with the tricyclic antidepressants you block norepinephrine uptake and it stays knocked out indefinitely. As best as we know that makes more epinephrine available per unit time and per impulse and release and if mores available, does more. Paradoxically the system is designed to defeat the best efforts of the neuropharmacologist so what this really does is the presynaptic machinery turns itself off very quickly and you stop firing and you stop producing and you stop releasing norepinephrine and may actually get some sedative effects, hypertensive effects early on.
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But if you hold on for a week, two weeks, three weeks, the presynaptic alpha-2 autoreceptors become locked out, desensitized and the presynaptic machinery revs up and actually can go above baseline. So that by the time the drug is working out here at three or four weeks you still block the uptake, you’ve restored the presynaptic machinery to normal or more and you have retained sensitivity in the alpha-1 system postsynaptically to mediate the effects of the transmission.
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Beta fades out and that’s too bad. Some people used to speculate that loss of beta was the mechanism of action of antidepressant drugs. You ought to be aware of that because it may come up at a board exam but you could quote me and say, “If that were the case, then propranolol would be an excellent antidepressant” and just the opposite is the case. So I think this is a concomitant price of doing business probably. I don’t think that losing beta is necessarily the effect.

Just a word on drug disposition and pharmacokinetics and things of that kind and in the interest of time I really want to move onto more clinical topics. We know a good deal about the pharmacological half lives of these drugs. They vary considerably. Among the short acting are prazidone and bupropion. It’s one of the reasons that bupropion’s been reformulated into a sustained release. The same has happened with fexor, fentathizine has a short life of five hours and it too has been made into a long acting product.

Among the longest half life drugs are the secondary amine tricyclics and that would include drugs like, for example, protriptyline is very long acting. Probably the champion of longevity is the active byproduct of  Prozac, the demethylated Norflex which has a half life that’s not accurately known but it’s probably on the order of a week or more. So it means that that activity, and it’s biologically active, that drug will hang around for some weeks and if you start switching from Prozac to, God forbid, an MAO inhibitor or even a tricyclic antidepressant you can expect tricky problems to occur even a week or more after you stop the Prozac because of this long wash out time.

In both systems, there is substantial storage of the transmitter in presynaptic membrane, enclosed vesicles. The vesicles fuse with the cell membrane when a depolarized stimulus comes down the pike and calcium is present, these membranes fuse and the goodie gets out into the synaptic arena by a process called exocytosis that works for many, in fact, most neurotransmitter and many endocrine systems that require an active molecule to get outside of the cell in which its made. That process, again, involves fusion of the vesicle and the cell membrane.
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The receptive cells in the environment contain a number of receptors that include notably the alpha receptors and the beta receptors. To make a long story short, facilitating transmission through alpha-1 and beta would be a good thing for mood elevation. But drugs that stimulate those receptors tend to have an up-effect on activity, mood, arousal and so on and it would be nice if we could jazz up those steps in neurotransmission by giving an antidepressant. But it’s more complicated than that and I will get back to that point in a minute.

This whole process is inactivated by actively pumping the amine back into the presynaptic nerve terminal by a process called transport that works by very specific large proteins sitting on the membrane that work in concert with the sodium pumping mechanism to energetically pull the amine back into the presynaptic cell where it can be recycled into vesicles and go around again or swept up by the janitor neuroterminal sitting in the membranes of the mitochondria of which there are many in the nerve terminal.

Obviously if you block MAO in the nerve terminal, you’ll make more serotonin, norepinephrine and even dopamine available and indirectly enhance their transmission. But the reuptake process is critically important physiologically and this process is selectively blocked by various antidepressant drugs. The tricyclics, especially the secondary amine tricyclics for the adrenergic system and the serotonin reuptake inhibitors for the serotonin system but they’re very similar in both systems.
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The other thing that happens at least with the tricyclic antidepressants is that they have variable affinity for adrenergic receptors and that leads to the more complete story of how these drugs work. It turns out that most antidepressant drugs and especially the tricyclics have very low affinity at beta receptors, very low affinity at alpha-2 receptors and it means that those two receptors lie naked to the increased availability of the transmitter when you block its inactivation by blocking the uptake process.
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What happens over several days to weeks is that alpha-2 and beta down-regulate, desensitize, get out of the way and stop working. Now that’s bad news for loss of the potentially useful mood elevating effect through beta but that’s part of the price of this business. It’s good news that you knock out the alpha-2 system because the alpha-2 receptors are autoreceptors. One of the first things that happens after you block the reuptake is that complicated feedback processes including local alpha-2 feedback shuts down the adrenergic system. So you get this paradoxical reaction of shutting down and then gradually over two or three weeks as the drug begins to work clinically these alpha_2 autoreceptors are knocked out of commission. So the presynaptic machinery revs up again.