love to hear good news even if it's a relatively small sample size. anecdotal, but i've heard that the antioxidants in fresh ground coffee is also very good!
> If allocated to caffeinated coffee consumption, patients were encouraged to drink at least 1 cup of caffeinated coffee (or at least 1 espresso shot) and other caffeine-containing products every day as per their usual lifestyle
I tried to skim to figure out how much caffeine/ml was actually in the drinks, but seems the researchers don't know themselves either? Wouldn't there be a huge difference depending on the beans, how it's made and so on? 1 espresso can be made very strong with packed coffee, or it can be made very weak, "1 cup of caffeinated coffee" basically says nothing at all, unless I'm missing the true definition elsewhere in the paper.
They were advised to drink at least one cup per day IIUC / maintain their current lifestyle. So there is no consistent amount, but it’s still meaningful vs being advised not to have any caffeine.
> "1 cup of caffeinated coffee" basically says nothing at all
Frankly, no. 1 cup of caffeinated coffee is on average significantly more caffeine than 0 cups, which is all you need for sufficient n. The only confounding variable to worry about here is whether caffeine is entering the diets of the two experimental groups at different rates via other channels (e.g., are the people who are forbidden to drink coffee drinking more tea to compensate?), though even this effect, if present, would likely tend to decrease the separation of the outcome distributions and is thus a low threat to validity.
People obsess over precision when it is often one of the least important aspects of an experiment. The outcomes of studies like this are in practice absolutely dependent on quality and rates of compliance. Choosing an uncomplicated treatment that is easy and natural for subjects to comply with is not merely acceptable but in fact a massively better design than complex protocols involving precisely measured quantities of lab-grown coffee in vials that can be misplaced, forgotten, deliberately shunned, etc. Also in this case the treatment corresponds closely to the real-world situation that the research is attempting to learn about.
Poor title. This is specific to patients who already underwent cardioversion (shocking the heart back into normal rhythm) AND were habitual coffee drinkers, who now have reduced coffee to 1 cup/day rather than sudden complete abstinence. Recurrence at 6 months was 47% instead of 64%. And this only applies to those who don't have clear caffeine-associated episodes.
I, too, have found that in the presence of a-fib, the optimal amount of caffeine is not zero; but I must think that every patient is different. Most people with diagnosed a-fib also take a beta blocker, and I (just only me) found that an excess of the beta blocker had paradoxical effects. So there is another potential interaction. Then, I also voted myself a small dose of OTC lithium, and subjectively derived obvious and substantial benefit from it, but there is (as yet) no science behind that, so I will not assert causation.
In the context of HN, the title is fairly misleading.
Suggestion: Got to the article, hit PgDn a few times, and look at the "Visual Abstract" graphic - which is both very short, and packed with important details.
The title does not match the conclusion. I would like to see lifetime abstainers from caffeine vs regular coffee drinkers. Remember caffeine is a form of a neurotoxin.
I've been doing my own personal experiments on myself trying to reduce caffeine intake to help with stress and anxiety. I've felt much better with just a small cutting back of my caffeine intake by taking my "main" cup of coffee (12oz cup) in the morning like I usually do and then just drinking 1/3 caffeinated, 2/3 decaf the rest of the day and going full decaf after 2pm if I have any at all.
I used to drink minimum 36oz (~150mg of caffeine per cup) of coffee per day and it was just turning me into an absolute wreck and just cutting back that little bit has made a huge difference. So instead of 450mg of caffeine, I'm getting ~270mg, so just a little above half the intake and it's made a huge difference.
A-fib just seemed like a natural consequence of the "caffeine peak" and reducing my consumption helped quite a bit.
The quick summary is that being advised to drink coffee (for habitual coffee drinkers with arrhythmia) leads to less arrhythmia, not more. This is surprising since caffeine is a stimulant and usually thought to be pro-arrhythmic.
I have afib and have been cardioverted once ~4 years ago. Own a kardia ekg and a regular blood pressure cuff. Coffee increases my pulse, but the waveform remains normal. Alcohol is the real killer, a very small amount like a beer will immediately show in ekg waveform abnormalities. Enough to get a buzz and it's a warzone let alone actually drunk. It's also surprising how long it lasts even into the hungover and no longer drunk zone. I'm not a doctor, but I would personally recommend to cut out all drinking with an occurrence of afib and yes, this is conjecture, but any sort of heart condition. I'm also not being sponsored by kardia and am creeped out by it storing my data presumably on the cloud.
15 comments
[ 3.9 ms ] story [ 36.8 ms ] threadI tried to skim to figure out how much caffeine/ml was actually in the drinks, but seems the researchers don't know themselves either? Wouldn't there be a huge difference depending on the beans, how it's made and so on? 1 espresso can be made very strong with packed coffee, or it can be made very weak, "1 cup of caffeinated coffee" basically says nothing at all, unless I'm missing the true definition elsewhere in the paper.
Frankly, no. 1 cup of caffeinated coffee is on average significantly more caffeine than 0 cups, which is all you need for sufficient n. The only confounding variable to worry about here is whether caffeine is entering the diets of the two experimental groups at different rates via other channels (e.g., are the people who are forbidden to drink coffee drinking more tea to compensate?), though even this effect, if present, would likely tend to decrease the separation of the outcome distributions and is thus a low threat to validity.
People obsess over precision when it is often one of the least important aspects of an experiment. The outcomes of studies like this are in practice absolutely dependent on quality and rates of compliance. Choosing an uncomplicated treatment that is easy and natural for subjects to comply with is not merely acceptable but in fact a massively better design than complex protocols involving precisely measured quantities of lab-grown coffee in vials that can be misplaced, forgotten, deliberately shunned, etc. Also in this case the treatment corresponds closely to the real-world situation that the research is attempting to learn about.
Suggestion: Got to the article, hit PgDn a few times, and look at the "Visual Abstract" graphic - which is both very short, and packed with important details.
> The DECAF (Does Eliminating Coffee Avoid Fibrillation?) trial...
Fantastic naming.
I used to drink minimum 36oz (~150mg of caffeine per cup) of coffee per day and it was just turning me into an absolute wreck and just cutting back that little bit has made a huge difference. So instead of 450mg of caffeine, I'm getting ~270mg, so just a little above half the intake and it's made a huge difference.
A-fib just seemed like a natural consequence of the "caffeine peak" and reducing my consumption helped quite a bit.