All you need to know about Asian Glow

“Asian Glow”, also known as “Asian Flush” or more accurately, “alcohol flushing reaction” is typified by skin-reddening and sometimes other uncomfortable reactions to alcoholic beverages. This article is intended to help those who are affected and those who care for the affected to make more informed decisions. Disclaimer: This information is not intended as medical advice.

Who is affected?

The alcohol flushing reaction is most often caused by genetic variation(s) known to affect people of East and Southeast Asian, Ashkenazi Jew, and Inuit descent. It can also be caused by a handful of medications.

What’s the root cause?

The typical metabolic pathway for alcohol (ethyl alcohol, ethanol) is:

Ethanol (CH3CH2OH) is oxidized into acetaldehyde (CH3CHO), pronounced “asset tal duh hide”. Most of the ethanol in the body is broken down in the liver by an enzyme called alcohol dehydrogenase (ADH), which transforms ethanol into a toxic compound called acetaldehyde (CH3CHO), a powerful toxin and known carcinogen. This process normally takes roughly one hour per “standard” drink, which in the USA is defined as ~14 grams of pure alcohol. For context, there are 14 grams of pure alcohol in:

12 ounces of beer (5% alcohol content by volume, ABV)
8 ounces of malt liquor (7% ABV)
5 ounces of wine (12% ABV)
1.5 ounces or a “shot” of 80-proof (40% ABV) distilled spirits or liquor

Toxic acetaldehyde is normally short-lived; with a metabolic half-life of a mere 90 seconds, it is quickly oxidized into a less toxic compound called acetate (CH3COO-) and NADH by another enzyme called aldehyde dehydrogenase mitochondrial (ALDH).
The NADH is oxidized by a series of chemical reactions in the mitochondria (the mitochondrial electron transport system, or respiratory chain), eventually resulting in the transfer of electrons to molecular oxygen (O2), which then binds protons (H+) to generate water (H2O).
Most of the acetate resulting from acetaldehyde metabolism escapes the liver to the blood and is eventually metabolized to CO2 and water (H2O) in heart, skeletal muscle, and brain cells.

Studies have shown that:

80% of East Asian populations convert ethanol to acetaldehyde faster than normal, due to a mutation of the ADH1C gene (the ADH1C*1 variant) .
30% to 50% of East Asians can't break down acetaldehyde normally, because the aldehyde dehydrogenase mitochondrial (ALDH) encoded by their ALDH2 gene is formed incorrectly - making it only 1/40th (or, 2.5%) as effective as the typical enzyme. This mutation is called the ALDH2*2 gene mutation.

#1 was the more recent finding hence why most literature only refers to effect #2.

The benefit of these mutations is that alcoholism is much less likely, because of the substantial increase both in speed and severity of negative effects of ingesting recreational quantities of alcohol. The drug disulfiram (Antabuse) inhibits acetaldehyde dehydrogenase, similar to the ALDH2*2 mutation. As such, disulfiram is sometimes used as a deterrent in clinical settings for alcoholics wishing to achieve sobriety.

Unfortunately, neither mutation has been found to be associated with any other positive biological side-effects; unlike another common East Asian-affecting mutation, the recessive ABCC11 gene which reduces body odor in exchange for drier & flakier earwax.

So what?

Acetaldehyde is a much stronger poison than ethyl alcohol but is (normally) metabolized super fast unless one actually overwhelms their supply of the enzyme. Hence it is rare for people unaffected by the ALDH2*2 variant to have a hangover or other acute consequences from 1-2 standard drinks (besides, of course, catching a buzz).

Acetaldehyde toxicity stems from its capacity to bind to proteins including enzymes, microsomal proteins, and microtubules.

Acetaldehyde is an irritant of the skin, eyes, mucous membranes, throat, and respiratory tract.

Acetaldehyde is a known carcinogen in humans, and it is damaging to DNA via the particularly heinous “interstrand crosslinks”, a type of damage that is likely to produce mutations when your body attempts to repair it.

Acetaldehyde causes abnormal muscle development as it binds to proteins.

Acetaldehyde is also responsible for alcohol-related memory loss (blacking out) and is associated with liver disease for chronic alcohol abusers.

A lethal concentration of Acetaldehyde is one-third (⅓) that of ethanol. It is generally accepted that a blood alcohol content (BAC) of 0.31-0.40% has potentially lethal consequences for humans. Hence, while a lethal dose of alcohol for a 170 lb male (as assigned at birth) would entail 11 standard drinks, someone unable to quickly metabolize acetaldehyde may suffer the same lethal risks at as few as 3.75 standard drinks (or, two long island iced teas; less than a single 40 oz bottle of Olde English). For a 130 lb female (as assigned at birth), these figures are reduced to 7.5 drinks and 2.5 drinks, respectively.

What can I do to prevent or reduce the alcohol flushing reaction?

Unfortunately, not a lot.

Someone suffering from mutation #1 (faster metabolism of alcohol to acetaldehyde) but not mutation #2 (that is, they can still metabolize acetaldehyde quickly) can simply drink alcohol more slowly in the first place, thereby regulating the buildup of acetaldehyde.

Similarly, eating high fat foods within 30 minutes prior to partaking in alcohol can help to slow absorption of the alcohol. Fries with aioli, pork belly sliders, heavily buttered bread, or just about any dish with full fat sour cream would do the trick nicely.

Anyone suffering mutation #2 needs to be very careful to not over ingest alcohol altogether. On the plus side, controlling your intake is likely to result in financial savings - both in immediate reductions in your bar tab, and in terms of the long term medical benefits associated with living a low-alcohol lifestyle.

Reducing loads on your liver may be helpful as well. The liver faces a heavy load when needing to process high protein foods, high fructose corn syrup (contained in large quantities in many soda products and many cocktail mixers), as well as some medicines including retinoids such as Accutane.

There is no approved medication to treat alcohol flush reaction, and this author did not identify any medication or supplement which would solve the root causes of the reaction.

Cosmetically, green makeup can offset the redness caused by alcohol flushing syndrome. Select foundation or concealer with a green tint to minimize the appearance of redness.

USE CAUTION TREATING SYMPTOMS:

Acetaldehyde increases histamine release. This is the main cause of the facial flushing that happens with the reaction. Allergy medications which block histamine could help prevent this from happening. But blocking histamine doesn’t stop acetaldehyde from building up — and that’s where the real damage comes from.

Several antihistamines, such as cetirizine (Zyrtec) and diphenhydramine (Benadryl), can raise your risk of dizziness and drowsiness when they’re combined with alcohol.

Cimetidine (Tagamet) is a heartburn medication called an H2 blocker. These medications also block histamine, but that’s not why people use them for alcohol flush syndrome. Cimetidine blocks ADH in the stomach. The idea is that blocking ADH prevents alcohol from being turned into acetaldehyde. If acetaldehyde isn’t formed, the alcohol flush reaction doesn’t take place. But most alcohol isn’t processed in the stomach… it is processed in the liver. Hence blocking ADH in the stomach has little effect on the alcohol flush reaction.

Other H2 blockers, such as famotidine (Pepcid AC), are often suggested as alcohol flush reaction treatments, even though they don’t seem to affect ADH the same way as cimetidine.

Using medications to hide flushing can lead to drinking more. By preventing your body’s natural response to alcohol, those affected may miss out on a helpful warning sign that their acetaldehyde levels are too high.

How can I know which mutation(s) I have?

Hypothetically, one could drink a little, quickly… perhaps ½ to 1 standard drink of liquor, and observe two important variables:

How much time passes between when you began drinking and when you began feeling the effects of the alcohol flush reaction (i.e., redness)? If the alcohol flush reaction occurs within 5 minutes, it is likely that you are affected by variation #1 (the ADH1C*1 allele), meaning you break down alcohol into acetaldehyde rapidly.
Measuring from the time the alcohol flush reaction began - how long does the alcohol flush reaction last? With a halflife of 90 seconds and a small amount of alcohol, the alcohol flush reaction should easily be gone within 20 minutes. If it lingers for an hour or longer despite the small quantity of alcohol ingested, it is likely that you are affected by variation #2 (the ALDH2*2 allele), meaning your ability to metabolize acetaldehyde is 1/40th that of those unaffected by this genetic variation.

How are these genes inherited? Will my children also have Asian Glow?

Most likely, yes. Alcohol flush reaction is hereditary.

ALDH2*2 is a dominant gene, and hence it is likely to be passed on if even one parent has the gene prominently in their ancestry.

This author couldn’t confirm it, however, ADH1C*1 is most likely a dominant gene as well, given it affects an even larger population than ALDH2*2.

What else causes alcohol flushing reaction-like symptoms?

Tannins and sulfates present in some wines and other beverages can cause histamine release and hangovers for those sensitive to them.

–

References & Citations:

https://en.m.wikipedia.org/wiki/Acetaldehyde

https://hmdb.ca/system/metabolites/msds/000/000/889/original/HMDB00990.pdf?1358893258

https://en.wikipedia.org/wiki/Ethanol

https://www.niaaa.nih.gov/publications/alcohol-metabolism