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The Miserable Effects of Too Much Caffeine

March 11, 2020 7 min read

miserable effects of too much caffeine

Coffee, terror, and the push towards caffeinism

You’ve just had your fifth double espresso. Things are getting weird: you can’t focus, your chest is tight, and for whatever reason you keep twitching your toes. These are just a few of the myriad ways in which caffeine can make life difficult. They’re each less fun than the last.

Many of us safely avoid this point on the caffeine-consumption spectrum; we have an iced latte or whatever and call it good. Moderate amounts like this can help us focus, study, and — most importantly — do productive things in the morning. But most of us aren’t satisfied with just moderate amounts.

In an attempt to maximise the good effects of caffeine, many of us push too far. We underestimate how much we’ve had, drink more, then enter that world of Great Regret. This transition moves us from a place of productivity, where we actually enjoy our lives, to one in which we’re nervous, paranoid, and skittish. This is a story of how we make that transition.

When it comes to caffeine, the amount we drink varies. In the United States, the average is a surprisingly paltry 100 to 200 mg. In places like Norway and Sweden, it’s an unconscionable 800 mg. For reference, a sixteen fluid ounce Pike Roast from Starbucks is 310 mg. A venti is 410 mg.

Undesirable doses linger around the 400 mg area. If you actually finish a venti drip — which, regrettably, I have — you put yourself squarely in this space. This is the point at which most of us turn from happy and productive to, well, everything bad.

In an attempt to maximise the good effects of caffeine, many of us push too far.

The curse of excess caffeine isn’t just about quantity, though — it’s about the timeframe in which you drink it. Caffeine takes roughly fifteen minutes to begin its digestion in the liver, and another thirty to finish. Then, it has a half-life of around four hours. This means that to cross from the good to the bad, you have to drink too much too quickly.

This experience is made worse by the fact that for the first fifteen minutes, we’re essentially flying blind — we don’t know how much we’ve had. This creates a terrible window in which, while searching for the desirable effects, we can drink too much.

You’ll notice my explanation so far has focused on coffee. There’s a reason for this: coffee has more milligrams of caffeine per fluid ounce than tea, chocolate, soda pop, or energy drinks. It is, in other words, a more likely progenitor of over-caffeination than the others. If you feel awful after eating chocolate or drinking a bunch of energy drinks, it’s probably not because of caffeine.

For caffeine to exert its effects on us, it has to undergo a process of conversion in the liver. This process cuts it down from its original shape into methylxanthine, the molecule responsible for all of its effects. Once converted, this modified version will enter the blood and get shipped to the brain.

When methylxanthine enters the brain, it blocks our receptors for adenosine. Adenosine is a molecule that decreases arousal and shuts down the body for sleep. It accumulates throughout the day as a byproduct of cellular metabolism, and the more it accumulates, the more it organises our body for sleep. People sometimes call it the “brakes” of the body: the more there is, the more it slows us down.

Caffeine takes roughly fifteen minutes to begin its digestion in the liver, and another thirty to finish.

Adenosine receptors are ubiquitous throughout the brain. The place most responsible for our sleep-wake cycles, though, is the basal forebrain. This frontal lobe structure is like a biological “on switch” for the brain: it helps coordinate the activity of our arousal networks (called the ascending activating systems) to alter our brain’s general level of alertness and arousal.

Our arousal networks are what give us the desirable effects of caffeine. They secrete neurotransmitters like dopamine and norepinephrine to make us more alert, motivated, attentive, and functional. Since adenosine is prevented from pressing these systems’ brakes, they get clicked into overdrive. The result is the stimulation and joy most of us get from those morning iced lattes.

These arousal networks are also the explanation for caffeine’s miserable effects. In an attempt to maximise these pleasant feelings, many of us drink beyond our limit. We grow impatient waiting for the buzz, have another shot or two, and only later realise the error of our ways. This is when our experience takes a turn for the worse.

The experience of too much caffeine is called caffeinism. Some of the more common symptoms include nervousness, irritability, tachycardia (a fast heart rate), “gastrointestinal malfunctioning,” and an all-around bad time. These symptoms arise in part from the over activation of the brain’s arousal systems, but also in part from something else.

In the field of behavioural ecology, there’s this idea called the “predatory imminence continuum,” which suggests that our brain’s neural activity changes in distinct ways the closer we get to a predator. These changes exist in three stages:

  1. Pre-encounter. This is life before you meet the beast. You relax, hang out, eat, and engage in other cognitively complex tasks. Maybe you do math or something.
  2. Post-encounter. This is life after you meet the beast. You panic, freeze, look for an escape. Math becomes a little more difficult.
  3. Circa-strike. This is when the beast spots you and charges. You run. You fight. Maybe you escape. Maybe you don’t. Either way you’re freaked. Definitely no more math.

The closer in proximity we get to this predator, the more “midbrain” parts of our brain take over. These regions are often responsible for survival functions, like fight or flight. As the midbrain increases its activity, our “higher” brain — that thing responsible for thinking, planning, decision-making, and math — shuts down.

We grow impatient waiting for the buzz, have another shot or two, and only later realise the error of our ways.

While several parts of the brain are involved in this process, three stand out: the amygdala, the brain’s so-called “fear center”; the periaqueductal grey, a pair of nuclei involved in pain inhibition; and the medial prefrontal cortex, an area responsible for inhibiting the former two regions. As the amygdala and periaqueductal grey increase their activity, the prefrontal cortex shuts down.

What’s striking about this continuum is that too much caffeine can provoke a similar shift in neural activity. When we approach our limit — i.e., when we finish that venti drip — we move closer to the post-encounter stage: our amygdala and periaqueductal grey get more active while the prefrontal cortex shuts down. Too much caffeine, then, invokes an experience similar to having just seen a lion.

Now, you may be thinking to yourself, “Wow, I’ve never had that experience before. It must not actually exist.” If so, I assure you this is merely luck. There are individual differences in the way our bodies process caffeine, so some of us will inevitably digest it more quickly, have shorter half-lives, etc. These differences lower the chances of accumulating an undesirable concentration. But there’s another reason we might be different.

The experience of caffeinism is more likely to occur in those with predispositions toward anxiety. In people like this, smaller amounts are more likely to trigger paranoia and nervousness — profiles similar to the post-encounter stage. Not everyone shares such proclivities, so not everyone will feel the same effects.

Those of us with predispositions toward anxiety, then, are more likely to interpret the abundant arousal from too much caffeine as fear and panic, not joy and fun.

Such dispositions matter because of the way emotion works in our bodies. The “appraisal theory of emotion,” for instance, states that emotion has both a physiological and cognitive component. This means that we can have the same physiological experience — the tight chest, fidgety legs, increased heart rate — but interpret it in different ways. It’s the difference between skydiving and running for your life.

Those of us with predispositions toward anxiety, then, are more likely to interpret the abundant arousal from too much caffeine as fear and panic, not joy and fun. For us, the experience initiates movement along the predatory continuum: fight or flight parts of the brain take over, other parts shut down. The result is that nasty breed of nervousness, agitation, and vigilance we feel toward everything around us.

For those of us who do experience caffeinism, it’s decidedly the worst feeling ever. Every benefit we initially sought from caffeine withers into nothingness — we can’t concentrate, our legs get fidgety, we can’t do much of anything. It’s like we’ve just spotted a lion lurking behind some nearby bushes. Perhaps this is good information to keep in mind before downing that fifth espresso.

At Ārepa we have spent years trying to find a good and responsible alternative to coffee. Together with neuroscientists and food technologists we have created a Nootropic Smart Drink and on the go Nootropic Capsules (some call it nuggets of purple goodness) that will get and keep you sharp during the day. Many costumers have dialed down or completely cut off their coffee intake, and we would love for you to jump on our nootropics bandwagon!


  1. This paper describes the various caffeinated items we consume along with their corresponding levels of caffeine.
  2. These three papers (herehere, and here) enumerate caffeine’s uglier side as well as how it’s digested and processed in the body.
  3. This review summarizes caffeine’s interactions with our different adenosine receptors.
  4. This paper describes everything you could ever want to know about the ascending arousal systems and their interaction with caffeine.
  5. These three papers (herehere, and here) can teach you more about the predatory imminence continuum and its manifestation in the brain.
  6. This article speaks to the anxiogenic effects of caffeine, and how their origin might lie in adenosine receptor mutations.


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