Last week I came down with strep throat! – first time since I was a kid, lo these many years ago. (They finally removed my tonsils after I had it about a zillion times.)
A few days later, I had a really gargantuan anxiety attack commingled with a crippling daylong depression. I get anxiety attacks every couple of years, but nothing like that one; and nihilistic bleak depression is pretty much antithetical to my nature. I was perplexed as hell until someone told me about the (causal?) connection between immunological crises and resultant adverse mood states. My Google-fu turned up only some vague overview of this topic, and a lot of stuff about the reverse, i.e., how your mood affects your immune system.
I want to understand how this works specifically. I am extrapolating something like depression=seratonin depletion; seratonin is depleted because… perhaps it’s dismantled by the immune system to assemble something else? Or is there such thing as a seratonin reuptake enhancer that is produced for some reason? Are tryptamines a basic building block that can be chemically recombined by the body into many other things we need, or are they a fairly complicated specialty item that is more or less irreducible? (I hope I am making sense here.)
Also, is it possible (theoretically, of course) that such a situation with the immune system would modulate the effect of other tryptamines added from outside the system, such that their function or effect might be nullified?
(Like, for instance, sumatriptan wouldn’t work for a migraine. Or the only thing you got from toad-licking was a lot of warty stalkers.)
To further complicate things, I have long suspected for various reasons that my body produces a higher quantity of melatonin than is average. Could that account in part for my optimistic default mood state? Is melatonin also depleted by a stressed immune system? (assuming otherwise optimum conditions for melatonin production, i.e., I sleep in a dark and quiet room and have healthy REM cycles)
I hope these aren’t really goofy questions! Thanks for sharing your insight with me.
Brief answer while I have time: serotonin and melatonin are both closely-related indolamines. Serotonin is the depression one but both may be implicated in Seasonal Affective Disorder.
Not sure I understand the third paragraph completely, but any drug that does the opposite of SSRIs would be a serotonin antagonist. Tryptophan is ingested and enzymes turn it into 5-HTP, which is then changed into serotonin. I don’t think we know the exact mechanisms of serotonin depletion but they could arise from a combination of reduced receptors, less efficient receptors, smaller terminal buttons, etc.
I actually think the change in anxiety and depression from illness isn’t neurochemical, or, at least, isn’t serotonin related.
What I notice is that my heart rate goes up and my blood pressure soars whenever my immune system is fighting off a bug. Both of these are common anxiety producers.
I also notice that I feel more tired, as my body is doing more work at rest than usual, and is probably not giving as much energy to non-immune system based tasks. There is a definite link between tiredness and depression.
Granted, both of these processes involve neurochemicals, but not in the simplified form of just having less serotonin. The blood pressure increase involves norepinephrine and possibly adrenaline, and being tired involves a ton of hormones (of which neurochemicals are of one kind.)
BTW, melatonin is often thought of as a sleep hormone, but that’s incorrect. It’s a night time/darkness hormone that happens to help the sleep cycle in humans. Not only can other animals use it differently, but humans can train themselves to respond differently to melatonin.
One more thing: the effects I mentioned above are worse in people who already have a little depression/anxiety. And that’s not even getting into how pain also is linked with depression. (That’s why some people feel like they want to die when they have the flu.)
So the question is how do infectious illnesses set off psychiatric ones?
There are several possible mechanisms.
The first group are variants of what you’ve thought of: the stress of an infectious illness alters the neuroendocrine milieu. Cortisol levels increase and change their normal diurnal cycles and so on. The neuroendocrine system being all interrelated it would be very difficult indeed to dissect out which single step of the consequent dance was etiologic.
The second is a bit more interesting. It seems that some infectious agents trigger off an autoimmune response that effects portions of the brain in susceptible individuals. The best described example, albeit not completely uncontroversial, is Pediatric Autoimmune Neuropsychiatric Associated Syndrome (PANDAS) in which bouts of strep thought appear to trigger off OCD and tic disorders. By definition PANDAS is a pediatric condition but speculation includes that similar exacerbations occur in some adults as well.
