Caffeine’s an adenosine antagonist. Now, let’s figure out what that means.
Neurons have proteins embedded in their membranes called receptors. Chemicals (e.g. neurotransmitters) can bind to these receptors, which causes stuff to happen. For instance, adenosine is a chemical, and it can bind to receptors in your brain cells, resulting in sleepy behavior.
(Here seems to be the place to mention that this is a vastly oversimplified explanation. Those interested in a technical explanation would do well to check out the appropriate textbook, because I literally just condensed over three chapters of my psychopharmacology textbook in as many sentences.)
Caffeine is an antagonist. Antagonists are able to bind to receptors without causing the stuff to happen. Since the receptors are already bound, the adenosine can’t bind to them, meaning the stuff (in this case, sleepy behavior) happens less.
This leads nicely into tolerance. Your body reacts to not-enough-working-adenosine-receptors by adding adenosine receptors. Thus, when your not hopped up on caffeine, you have too many adenosine receptors (and therefore too much sleepy behavior), and even when you are on caffeine, the effects are muted.
Fortunately, it’s pretty straightforward to reduce the number of adenosine receptors: you just stop ingesting caffeine, your body notices there’s too many adenosine receptors, and removes them. This doesn’t happen immediately, so you get withdrawal. Checking wikipedia, this should last 2–9 days at nuisance level. (Relative to the other drugs in my textbook, this is positively innocuous).
Also, it’s worth mentioning caffeine’s pharmacokinetics. The rate at which caffeine is metabolized is proportional to how much is in your system. Solving the differential equation gives you something like $A e^{-kt}$; the important thing to know is it has a half-life of about 6 hours.
Out of every course I took in college, psychopharmacology had by far the highest [actual IRL use] : [expected IRL use] ratio. Drugs are ubiquitous and having a solid understanding constantly pays small dividends.
Is there any research on why caffeine seems to affect some people more/differently than others? Anecdotally, I’ve noticed over the years that I get the “jitters” after two cups and have to stop because I can’t stand the feeling, whereas others can drink half a pot and barely notice the effects.
I initially thought that these others had just ‘pushed through the jitters’ and built up a tolerance, but some of them have told me they’ve never experienced the jittery feeling I’m talking about. Or maybe it just didn’t make them as uncomfortable as it makes me?
The answer, as with most questions like ‘why does X seem to work well for some people and not others’ is going to be complex. For example, one of the recent links in my newsletter touches on this topic:
Aside from finding some hits, caffeine consumption has long had meaningful heritability estimates (some are cited in that paper, others can be found in Google Scholar with the obvious query ‘caffeine heritability’). So that seems to be part of it: genetics.
Thanks for the paper (that’s a lot of authors!). The complexity you mention makes it difficult to determine whether substance X (caffeine, alcohol, eggs, etc.) has a net positive or negative for any given person when it comes to health benefits. Coffee has been linked to some positive health effects, but maybe only for those people who don’t get the jitters....that’s the sort of thing that would be cool to know. Until then, I’m just going to listen to my body and minimize consumption.
Let’s talk about drugs!
Caffeine’s an adenosine antagonist. Now, let’s figure out what that means.
Neurons have proteins embedded in their membranes called receptors. Chemicals (e.g. neurotransmitters) can bind to these receptors, which causes stuff to happen. For instance, adenosine is a chemical, and it can bind to receptors in your brain cells, resulting in sleepy behavior.
(Here seems to be the place to mention that this is a vastly oversimplified explanation. Those interested in a technical explanation would do well to check out the appropriate textbook, because I literally just condensed over three chapters of my psychopharmacology textbook in as many sentences.)
Caffeine is an antagonist. Antagonists are able to bind to receptors without causing the stuff to happen. Since the receptors are already bound, the adenosine can’t bind to them, meaning the stuff (in this case, sleepy behavior) happens less.
This leads nicely into tolerance. Your body reacts to not-enough-working-adenosine-receptors by adding adenosine receptors. Thus, when your not hopped up on caffeine, you have too many adenosine receptors (and therefore too much sleepy behavior), and even when you are on caffeine, the effects are muted.
Fortunately, it’s pretty straightforward to reduce the number of adenosine receptors: you just stop ingesting caffeine, your body notices there’s too many adenosine receptors, and removes them. This doesn’t happen immediately, so you get withdrawal. Checking wikipedia, this should last 2–9 days at nuisance level. (Relative to the other drugs in my textbook, this is positively innocuous).
Also, it’s worth mentioning caffeine’s pharmacokinetics. The rate at which caffeine is metabolized is proportional to how much is in your system. Solving the differential equation gives you something like $A e^{-kt}$; the important thing to know is it has a half-life of about 6 hours.
Out of every course I took in college, psychopharmacology had by far the highest [actual IRL use] : [expected IRL use] ratio. Drugs are ubiquitous and having a solid understanding constantly pays small dividends.
Is there any research on why caffeine seems to affect some people more/differently than others? Anecdotally, I’ve noticed over the years that I get the “jitters” after two cups and have to stop because I can’t stand the feeling, whereas others can drink half a pot and barely notice the effects.
I initially thought that these others had just ‘pushed through the jitters’ and built up a tolerance, but some of them have told me they’ve never experienced the jittery feeling I’m talking about. Or maybe it just didn’t make them as uncomfortable as it makes me?
The answer, as with most questions like ‘why does X seem to work well for some people and not others’ is going to be complex. For example, one of the recent links in my newsletter touches on this topic:
“Genome-wide meta-analysis identifies six novel loci associated with habitual coffee consumption”, The Coffee and Caffeine Genetics Consortium et al 2014 (excerpts)
Aside from finding some hits, caffeine consumption has long had meaningful heritability estimates (some are cited in that paper, others can be found in Google Scholar with the obvious query ‘caffeine heritability’). So that seems to be part of it: genetics.
Thanks for the paper (that’s a lot of authors!). The complexity you mention makes it difficult to determine whether substance X (caffeine, alcohol, eggs, etc.) has a net positive or negative for any given person when it comes to health benefits. Coffee has been linked to some positive health effects, but maybe only for those people who don’t get the jitters....that’s the sort of thing that would be cool to know. Until then, I’m just going to listen to my body and minimize consumption.
Fantastic explanation, and now I have another book to read eventually. Thanks!