I was 8 years old, sitting at dinner with my grandparents, watching Gong Gong’s face turn bright red after a few sips of yellow wine. He loved making me laugh, and though he enjoyed his drinks, I think he liked my reaction even more.

Over a decade later, I would recognize the same alcohol flush reaction at parties and happy hours in some of my East Asian friends, and in myself. A few of these friends took histamine blockers like Pepcid AC before going out, hoping to hide the anticipated redness. Once, I watched someone keep drinking through the flush to prove they had a higher tolerance than what their body was communicating.

Most of us knew the reaction by its colloquial name: “Asian glow.” The phrase makes the phenomenon sound harmless, even playful.

It was not until I started medical school and attended an Asian American and Pacific Islander Heritage Month event that I understood the science behind the reaction. After taking an ethanol patch test that turned positive, I learned that flushing is a common marker of reduced activity in mitochondrial aldehyde dehydrogenase 2, or ALDH2, an enzyme involved in breaking down alcohol. This inherited deficiency affects an estimated one-third of people of East Asian descent and is exceedingly rare in other ethnicities. (Its associated redness may be mistaken for rosacea, which some studies suggest that drinking can raise the risk of developing, but rosacea is a separate condition involving chronic inflammation that affects all skin tones and types.)

There is no safe or healthy level of alcohol consumption for any given person. However, people with ALDH2 deficiency face both immediate discomfort and long-term cell damage and susceptibility to developing cancers of the upper digestive tract. Every clinician with East Asian patients should dedicate time to explaining the biological consequence behind what has long been dismissed as an aesthetic quirk.

When ALDH2 activity is reduced, acetaldehyde, a toxic intermediate in alcohol metabolism, accumulates in the body, dilating blood vessels, promoting histamine release, and causing facial redness, nausea, and rapid heartbeat. Acetaldehyde is also a DNA-damaging mutagen with implications in cell death pathways.

Not every person with deficiency presents the same way. People heterozygous for the most common ALDH2 reduced-function mutation, or ALDH2*2, have one active copy of the gene inherited from one parent and one variant copy inherited from the other. Their symptoms are not severe enough to discourage continued drinking, so they often keep going, even though their alcohol consumption is associated with a greater risk of cardiovascular disease, brain disorders, pancreatitis, and malignancies, particularly esophageal cancer. Homozygotes, who inherit two inactive copies of the gene, are less likely to develop cancer because they get such severe reactions to drinking that they avoid alcohol.

Although many East Asians recognize that they flush after drinking, they might not understand the associated risks. Health care providers should identify patients who experience alcohol flushing and counsel them on what it means for their health. Simple questionnaires about past flushing reactions, and in some settings ethanol patch testing like the one I took in medical school, have been shown to reveal ALDH2 deficiency with relatively high sensitivity and specificity. These tools can be incorporated into routine social history taking, alongside questions about alcohol use and family history.

For some groups of people, alcohol may hold special social and cultural meaning. For them, education should be widespread and, importantly, tailored and considerate.

Teenagers and young adults like me, for example, navigate significant peer pressure around drinking. My East Asian college friends deserved to know that taking antihistamines to hide flushing might reduce visible redness, but it would not lower acetaldehyde levels in their blood. They deserved to know that masking their body’s warning signals can make it easier to drink more than they otherwise would.

Recently, Nectar, a canned hard seltzer and cocktail brand, launched an AAPI Heritage Month campaign urging people to reframe the alcohol flush reaction as an “Asian Glow Up.” Though the intention may have been to turn a source of embarrassment into a viral beauty moment, the company’s failure to include a disclaimer mentioning the health indications pushes a narrative that encourages more drinking within an already vulnerable, under-informed population. An Instagram caption for the promo said: “Sharing drinks with friends before so you can share your glow with everyone after.”

Of course, young people, the target audience for ads like these, deserve to receive information about the reality behind “Asian glow” not as a reprimand, but as knowledge that preserves their agency and could help them make more informed choices.

On my medical school campus, many of the events promoting alcohol intolerance awareness are small focus groups led by my own peers, where attendees are more willing to trust and ask questions. A 2010 randomized study found that personalized ALDH2 genetic feedback reduced 30-day drinking frequency and quantity among Asian American young adults with one inactive ALDH2 allele; future studies may want to consider seeing what the results are if such feedback were given by peers.

A similar principle applies to counseling older adults and immigrant families. Telling an entire subset of the population simply to stop drinking risks being dismissive of the worlds that patients hail from. Alcohol serves as a social lubricant in certain East Asian cultures. To ignore that reality may deepen mistrust and gaps in culturally responsive care for Asians.

Providers can bridge this gap by partnering with trusted community centers and leaning on hospital advisory boards to host events that reinforce clinical counseling within familiar spaces. This year, I plan to host a service event inviting a Stanford physician to speak on ALDH2 deficiency after service one day at a nearby Chinese Baptist church.

When immigrant families like mine moved to the United States, they had to decide what to carry with them and what to leave behind. Some things were obvious: loved ones, places, languages. Others were quieter: recipes, rituals, and everyday habits, including drinks poured at mealtime, for guests, or before making a business deal. I grew up at the crossroads of their world and my American one, where blame or exclusion rarely led anywhere useful.

When I first learned about ALDH2 deficiency, I itched to call family and friends back home, some of whom do not have access to health insurance or a regular primary care provider, to tell them about it. But I had to approach it carefully: I’m not a doctor yet.

My father ended up having an ethanol patch test performed at a free clinic visit, while I was on FaceTime with him. Since hearing about ALDH2 deficiency, he has been drinking significantly less. He probably would not have responded as well to an order for him to abstain completely from alcohol or a lecture about acetaldehyde-induced DNA adducts and cross-linking in white blood cells.

My mother, too, may not need to know every molecular pathway by which acetaldehyde-induced oxidative stress impacts bone formation. But she deserves to know, in language that is accessible to her, that ALDH2 deficiency increases the risk of osteoporosis that she may already be more vulnerable to as a post-menopausal East Asian woman.

In my family, roles reverse as I grow older. Gong Gong, now 91, is the one I try to make laugh. Medicine, I am learning, is not only what I know. It is how gently and truthfully I offer what I know to the people I love, and to the strangers who one day trust me with their care.

Brian Zhang is a second-year M.D. student at the Stanford University School of Medicine, where he currently serves as student body president.