I like a cup of coffee in the morning. Especially after I load it up with sugar and milk. But my routine is more hobby than habit; I’ve never come to rely on a daily caffeine jolt. In fact, if I didn’t have to stump off to work every morning, I could finish my coffee and immediately head back to bed.

But I know plenty of people who can’t get through the day without a steady supply of coffee, or tea, or soda, or chocolate. They need the buzz, and they don’t want the withdrawal headaches.

Now researchers from Carolina, Harvard, and five other institutions may have found out why some of us crave caffeine in great quantities while others get by on little or none.

Habitual caffeine consumption, says UNC epidemiologist Keri Monda, could be in your genes.

Monda and her colleagues analyzed the caffeine intake of some 47,000 people. Each person had filled out detailed questionnaires for years about the things they ate and drank, and each had given a DNA sample. The researchers looked at the entries for caffeinated coffee, tea, caffeinated sodas, and chocolate and compared the results with the participants’ genetic profiles.

Two genes jumped out at the researchers as having clear associations with habitual caffeine consumption. They’re called CYP1A2 and AHR. We all have them. One of their functions is to influence how our bodies metabolize caffeine and, possibly, the amounts each of us crave and consume.

People with certain variations of the genes tend to consume more caffeine, more often.

It could be that people who have the higher-caffeine-consumption genotype metabolize caffeine at a faster rate than others, Monda says, although their study didn’t extend to specific biologic functions. And that may mean some of us need more caffeine to get to or maintain the buzz, or even just to keep the withdrawal symptoms at bay.

Harvard’s Marilyn Cornelis, the lead researcher on the study, says her own father drinks at least ten cups of coffee a day.

“He’s not trying to achieve pleasurable effects,” she told WebMD. “Rather, he’s trying to maintain levels as a means to avoid the withdrawal symptoms. Without a cup he’d wake up in the middle of the night with a headache.” Cornelis thinks there’s a good chance her father’s genetic profile has something to do with it.

While studies over the years have shown that our social lives and demographics play a role in habitual caffeine consumption, scientists have long suspected a genetic component. There have been hints of it in studies of identical twins, including heritability estimates of 77 percent for heavy caffeine use.

But researchers have had a hard time pinning down specific genes that influence habitual use, dependency, and addiction. The exception is another popular stimulant: nicotine. Some studies have shown that habitual tobacco use is tied to certain gene variations. It’s likely that genes play a role in alcohol consumption and other behaviors, too, the study authors say.

The data Monda, Cornelis, and their colleagues analyzed was pooled from five epidemiological studies conducted between 1984 and 2001, including one based at UNC called ARIC (or the Atherosclerosis Risk in Communities Study). Vast amounts of data are now available from those studies and their 47,341 participants, including DNA samples from each. Now that more advanced genomic methods have come along, researchers are able to analyze the data in many different ways. The caffeine study is one small portion of the research possible with such a massive data set. 

Caffeine is the most widely consumed psychoactive substance in the world. Nearly 90 percent of us eat or drink it every day. Americans spend some $40 billion on coffee every year.

Even so, we’ve never been sure how caffeine affects our health. Some studies have associated it with all kinds of benefits—lower risk of diabetes, liver cancer, Parkinson’s disease. Others have hinted that too much could be bad for us—higher risk of heart palpitations, high blood pressure, or even miscarriage and stillbirth. It’s possible that our individual genetic profiles determine whether caffeine is good for us or not.

This study doesn’t answer our big questions about caffeine’s health effects, but it is a stepping stone on the road to health care’s Shangri-la, also known as personalized medicine.

The results will give scientists a better understanding of the genetic mechanisms behind caffeine consumption, and that understanding can inform future studies. Other researchers will be able to use the genetic factors as variables in their own studies and, eventually, maybe even come to some concrete conclusions about how caffeine affects our health.

Chances are it’s different for each of us. 

Keri Monda is an assistant professor in the Department of Epidemiology, and David Couper, another UNC study author, is a research associate professor in the Department of Biostatistics, both in the UNC Gillings School of Global Public Health. Marilyn Cornelis is a research associate in the Department of Nutrition at Harvard. Their study was published in PLoS Genetics on April 7, 2011. Funding came from the National Cancer Institute.