Like for many young adults, college was an opportunity to “find” myself and, in particular, connect with my Asian Americanness. In fact, one of the first college courses I enrolled in was Asian American Literature in which one of the prevailing themes in the class was how history and media depicted Asian men as passive, subservient, effeminate or asexual individuals. These emasculated stereotypes would set the stage for my own experience in college, where I learned that masculinity is often measured by how much alcohol you can drink.
It was in this light that I found my own “manhood” challenged because, like many Asians, when I drink my face betrays me. I flush and turn red, often after having just one drink. But while the spectacle of an Asian flushing is not uncommon, in my experience it almost always solicited comments that were variations on one stereotype: Asians can’t drink.
“Cut that Asian kid off.”
“What? You’re already drunk? After one drink? Oh right he’s Asian.”
“He can’t handle drinking. He’s Asian. Look, he’s already red.”
Dismissive and disparaging comments like these accomplished two things: they labelled me as “other” and marked me as less than by some arbitary and artificial measure of masculinity. Worse, though, was that inevitably someone would add insult to injury by trying to explain the biology underlying my deficits…incorrectly.
“It’s because you don’t have the alcohol dehydrogenase gene.”
“Your alcohol dehydrogenase doesn’t work.”
To set the record straight, the “Asian Glow” results from buildup of acetaldehyde, an intermediate of alcohol metabolism. The first step in metabolizing ethanol is its conversion into acetaldehyde by the alcohol dehydrogenase enzyme (ADH1B). Acetaldehyde is, in turn, converted into acetic acid, a reaction catalyzed by the aldehyde dehydrogenase enzyme (ALDH2). Sufferers of alcohol flush syndrome have either a mutation in ADH1B that supercharges the enzyme and dramatically increases the rate that it churns out acetaldehyde from ethanol or a mutation that renders ALDH2 defective in converting acetaldehyde into acetic acid. The consequence of either mutation is the same: a traffic jam of acetaldehyde. The accumulation of acetaldehyde in the system leads to the dilation of capillaries in the face, causing the stereotypical flush. This is followed by early symptoms of hangover such as lightheadedness, nausea, and palpitations– signs indicating that you should probably stop drinking. Carriers of either mutation often feel the effects sooner and more severely.
These undesireable effects might explain the lower incidence of alcoholism amongst East Asian men. After all, why would you keep subjecting yourself to such torture? In fact, these effects mimic to a lesser extent reactions to disulfiram, an inhibitor of ALDH2 activity that is used to treat alcoholism. These mutations in ADH1B and ALDH2 could, therefore, serve as built-in anti-alcoholism mechanisms. Humiliating effects of flushing aside, acetaldehyde also carries with it a significant health risk as it is a known carcinogen. Consistent with this, these mutations in ADH1B and ALDH2 correlate with a higher incidence of esophageal cancer. Furthermore, the mutation in ALDH2 in particular may reduce both the effectiveness of nitroglycerin in treating angina and survival after a heart attack, while increasing the risk for neurodegenerative diseases such as Alzheimer’s.
With these health risks in mind, why would these mutations be so prevalent Asians? From an evolutionary standpoint, the high frequency of these mutations in people of East Asian descent (>59% carry the ADH1B∗47His variant, while approximately 40% carry the ALDH2∗487Lys variant) suggests that these mutations in ADH1B and ALDH2 were positively selected for in recent human history. Why would evolution select for mutations that increase levels of the toxin acetaldehyde? Under what conditions would these mutations provide an evolutionary advantage? And, more importantly, is there an evolutionary basis for drinking wussiness in Asians? While these questions remain unanswered, scientists have proposed several hypotheses. One explanation proposes that the higher concentrations of acetaldehyde resulting from these mutations may act as a defense against infections by parasites that are unable to metabolize acetaldehyde. Alternatively, the adverse reactions to alcohol in individuals with these mutations may have provided greater protection against alcoholism or risks associated with alcohol consumption. For instance, given that alcohol consumption and Hepatitis B virus (HBV) infection can synergistically increase the risk for liver cancer and considering that the geographic distribution of the mutation in ALDH2 overlaps with areas endemic for HBV, the mutation in ALDH2 may have mitigated the effects of HBV infection. Similarly, it has been proposed that sensitivity to alcohol could be a defense mechanism that limits consumption of alcoholic or fermented foods containing toxic or disease-related compounds. All of these hypotheses, however, remain speculative.
While this version of the emasculated Asian male stereotype bothers me on a visceral and instinctual level, I don’t subscribe to this view of masculinity defined by alcohol consumption. There are countless things I’d rather do than trying to prove myself by drinking to oblivion and end up hugging cold, hard porcelain at the end of the night. But I can’t say the same is true for all Asian Americans (women included). Regardless of whether we come to a concrete evolutionary explanation for the prevalence of these mutations, the biology indicates that for a significant number of Asians drinking poses potentially more severe health problems than just alcohol flush, low tolerance, or hangovers alone. These are health concerns that we must keep in mind as Asian Americans conform to a culture that places significant emphasis on drinking, especially in cases where they are pressured into trying to break the stereotype that “Asians can’t drink” because for many of them, they’ll be fighting biology also.
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