Endogenous Ethanol (EE) Production

Endogenous 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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