DUIEndogenous Ethanol (EE) Production
Where does EE come from? While there’s some evidence that small amounts are formed inside cells as metabolic intermediaries or products, mostly it’s manufactured in the mobile fermentation vat known as your gut. Some of the tiny things that live in there, especially yeasts, are constantly munching ingested carbs and churning out booze. The body absorbs this normally modest volume of EE and it goes straight to the liver, where it’s metabolized. Barring unusual circumstances, very little EE makes it to the rest of the body.
To get a significant BAC from EE alone would require increased fermentation, diminished ability to metabolize alcohol, or (probably) both. In Japan since the 1950s there have been dozens of published case reports of people feeling drunk after eating carbohydrates such as rice, a condition called meitei-sho or, in English, auto-brewery syndrome. You’re thinking: great—free sake. Not quite. It comes with a price.
In almost every case in one review, intestinal overgrowth of candida or other yeasts was identified as the cause. Most patients had undergone some sort of gastrointestinal surgery—such procedures sometimes result in increased fermentation thanks to blind loops left in the intestine, where microbes can eat and multiply undisturbed. In most cases not involving prior surgery, some other abnormality was noted, such as low stomach acidity.
Auto-brewery syndrome has never been convincingly reported outside Japan. Why? It’s all about enzymes. When the liver processes ethanol, the enzyme alcohol dehydrogenase first converts it to acetaldehyde. In most people a second enzyme, aldehyde dehydrogenase (ALDH), quickly converts the acetaldehyde to harmless acetate. But roughly 50 percent of Japanese and other east Asians and some American Indians (but practically no Europeans or Africans) have a mutated gene that impairs ALDH activity. In these people, even a modest dose of alcohol, imbibed or endogenous, leads to acetaldehyde buildup and unpleasant symptoms: facial flushing, palpitations, dizziness, nausea, headache and confusion. As acetaldehyde builds up, some is converted back to ethanol, retarding BAC decline. Eventually various enzymes slowly clear the acetaldehyde and the symptoms dissipate. People on drugs such as Antabuse that inhibit ALDH activity might also be subject to meitei-sho, but so far that hasn’t been documented.
What’s likely happening in the Japanese cases is a combination of high carb intake (which the Japanese diet is famous for), yeast infection and a limited ability to metabolize the alcohol produced—any of these alone probably won’t do the trick. My guess is that even without considering their BAC, auto-brewery sufferers might be in no condition to drive, since they’d be under the influence of acetaldehyde.
The legal implications of all this vary. Generally, driving while impaired for any reason (including tiredness or taking legal medications) is against the law. Ignorance that you’re impaired, which arguably might apply in the case of auto-brewery syndrome, isn’t necessarily a defense—impaired-driving laws in many states don’t require the element of intent. As a practical matter, the potential consequences of EE are of greatest concern to those subject to so-called zero-tolerance laws—mainly drivers under 21, who may face sanctions for driving with a BAC greater than zero, .01, or .02 percent, depending on the state. Those with candidiasis and low ALDH activity (for genetic or pharmaceutical reasons) can exceed those levels. If that describes you, maybe you should think seriously about that skateboard. If not, disregard the wacky factlets and remember that only knuckleheads drink and drive.
Comments, questions? Take it up with Cecil on the Straight Dope Message Board, StraightDope.com, or write him at the Chicago Reader, 11 E. Illinois, Chicago 60611.
Source: http://www.slweekly.com/
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