This a lay hypothesis based on a weak, simplistic understanding of the human brain, but I shall propose it anyway, because thinking about it is absolutely driving me nuts.
The brain has a certain range of normal function, and resists drastic change to this. If there’s significantly less stimulation from a certain neurotransmitter for a period, for example, the brain may upregulate the number of receptors for the substance in order to achieve it’s “normal” level of stimulation. With the use of certain antidepressants, intended to increase stimulation from certain neurotransmitters, we see the opposite response; more stimulation, brain resists it, serotonin/norepinephrine/whatever receptors are down-regulated (usually not to the point of the original depression, though, obviously). Hence, certain seratonin-related drugs like LSD tend to be observably less efficacious a few weeks into antidepressant therapy.
Now, take a drug like marijuana. It’s a partial dopamine antagonist and a CB1 agonist. Dopamine, which plays a big role in the brain’s “reward” system and reinforces “favorable” and addictive behavior, is partially blocked-out by the pot, working counter how many “hard” drugs work; coke and crack, for example, cause explosive dopamine rushes, making the user feel great about pretty much everything and anxious to re-administer the drug. Taken on its own, this effect isn’t really of much interest to the recreational pot-smoker. I’ve seen many a toker, even myself on occasion, run for a cigarette immediately after a cypher to counter the “fuzziness” of the “head high” or suppress “the munchies” (conceiveably effects of low dopamine?) while leaving the “body high” (cannabinoid agonism?) intact. However, taken with all the other effects of marijuana, the resultant high is generally considered quite enjoyable.
When treating depression, there’s an obvious danger in dropping already deficient neurotransmitters to an even lower point in an effort to upregulate receptors and increase stimulation in the long run. I can’t imagine any doctor would feel comfortable telling a patient seeking treatment for major depression that the drugs they are taking will make them feel even worse for a few weeks while their body adapts, and that their mood is probably going to take at least a minor hit every time they take more. But consider psychological dysfunction that’s tied to low dopamine–certain anxiety disorders, schizophrenia and related conditions, and probably a whole bunch more I haven’t read up on. Here we have a drug that generally produces a positive change in mood for most users, has no appreciably toxicity, and, if administered regularly, could cause an upregulation of dopamine receptors due to its antagonistic properties, potentially relieving schizophrenic/anxiety/whatever symptoms. Patients could smoke it in their free time or before going to bed and consequently see a lessening of their symptoms while sober without an appreciable worsening of their symptoms during the drug therapy. Perhaps the “laziness” generally associated with pot smokers even while sober could be at least somewhat explained by an increased sense of self-worth and accomplishment from performing simple, everyday tasks that most people don’t recieve much of a dopamine boost from doing.
Alright, so that’s a stretch, but I think it’s pretty apparent I’m coming from a somewhat biased point of view, here–sorry, guys.
Anyway, this is largely wishful thinking, but I can’t think of anything blatantly wrong with the hypothesis besides the very simplistic model of brain function it’s based on. Anyone wanna help me out? Any personal experience that supports/refutes this? Any medical theory to share?