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I use both regularly. I never notice the "downslope" of caffeine, although maybe that's my tolerance. The neurology is totally different. Caffeine primarily affects the heart rate via adenosine (A1R) antagonism. Nicotine binds to the ion channel nAChR which is expressed all over the brain and the nervous system. Full agonists of nAChR cause convulsive seizures, while antagonists are paralytic, but nicotine is a partial agonist, producing a sort of stability. That's why nicotine is anxiolytic: it interferes with spikes and droughts of acetylcholine, smoothing the highs and lows of neural activation. The brain responds by "sensitizing", changing acetylcholine more dramatically in response to stimuli, and increasing the density of nACh receptors. That's why nicotine withdrawal is so awful: every mood is enhanced and you can't calm down. By contrast, caffeine, which primarily affects the A1 receptors that are expressed in cardiac neurons and smooth muscle tissue, is obviously never anxiolytic. A faster heartbeat does not produce calmness. The faster heartbeat increases the availability of energy in the brain and muscle, producing wakefulness. It has some other effects in the brain, particularly the basal forebrain, where inhibiting A1 also promotes wakefulness, but the cardiac effects of A1 dominate its practical effects to the extent that A1 agonists (opposite of caffeine) have never been implemented as sedatives because of their tendency to produce life-threatening drops in heart rate and blood pressure. You'd think, having studied this so much, I'd be more responsible, but humans are a funny animal. Anyway, there's no way a pure stimulant is going to substitute for an anxiolytic that takes effect in ten seconds. It makes sense in zero realities. |