Caffeine Consumption & Genetics

How it works

When it’s time to hit the sack (or just take a nap) our bodies let us know by firing off a molecule called adenosine. Caffeine helps perk us back up by blocking adenosine’s signals.

The genetic link

Scientists have identified genetic variants that influence how your body handles caffeine. These variants are located near two genes: CYP1A2 and AHR. Variants in these genes may affect how quickly the body breaks down and clears away caffeine.

caffeine and adenosine

Did you know?

Caffeine interferes with the brain system that causes sleepiness. A molecule called adenosine acts as a signal between brain cells to bring on sleepiness. Caffeine blocks adenosine’s signals, making you feel more alert. This is also why caffeine can make it hard to fall asleep and interfere with deep sleep.

Explore more

Have you ever wondered why you drink more or less caffeine than your friends? 23andMe’s Health + Ancestry Service can help you learn about genetic factors that may be involved. Order a kit, send us your spit, and find out what your genetics predict about your caffeine consumption level.

Health + Ancestry Service Kit

Health + Ancestry Service

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References

Coffee and Caffeine Genetics Consortium et al. (2015). “Genome-wide meta-analysis identifies six novel loci associated with habitual coffee consumption.” Mol Psychiatry. 20(5):647-56.

Cornelis MC et al. (2016). “Genome-wide association study of caffeine metabolites provides new insights to caffeine metabolism and dietary caffeine-consumption behavior.” Hum Mol Genet. doi: 10.1093/hmg/ddw334.

Fredholm BB. (2011). “Notes on the history of caffeine use.” Handb Exp Pharmacol. (200):1-9.

HHS and USDA. “Scientific Report of the 2015 Dietary Guidelines Advisory Committee: Part D. Chapter 5: Food Sustainability and Safety – Continued.”

Huang ZL et al. (2005). “Adenosine A2A, but not A1, receptors mediate the arousal effect of caffeine.” Nat Neurosci. 8(7):858-9.

James JE and Rogers PJ. (2005). “Effects of caffeine on performance and mood: withdrawal reversal is the most plausible explanation.” Psychopharmacology (Berl). 182(1):1-8.

Zhou SF et al. (2009). “Insights into the substrate specificity, inhibitors, regulation, and polymorphisms and the clinical impact of human cytochrome P450 1A2.” AAPS J. 11(3):481-94.


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