Monday, September 23, 2013

Auto-brewery Syndrome - Free Beer

A personal brewery could fit in there.

A recent 'news' story caught my attention as it was about a man with a bizarre affliction. The subject was apparently drunk to varying degrees for five years straight. Of course this isn't that unusual, except that he was not drinking alcohol, the flora in his gut was fermenting dietary carbohydrates into ethanol. After years of being a suspected 'closet drinker' he was treated with antifungal medication and is now free of his involuntary inebriation.

According to the linked news article the condition is very rare, however upon searching for this syndrome on pubmed I am given a different impression. The only article I found that examined frequency of endogenous ethanol production examined patients blood for a glucose tolerance test. Baseline measurements in 2.7% of patients demonstrated the presence of some ethanol after receiving capsules of glucose. Most surprisingly, over 60% of the patients had an increase in ethanol one hour after receiving oral glucose. Those who had a baseline ethanol measurement also had the greatest increase in blood ethanol levels. Sixty percent is not a rare occurrence and it makes one wonder if endogenous ethanol production is clinically relevant in the context of some health conditions. This has been proposed before but I haven't seen anything convincing.

For context, an 80kg male drinking three drinks in two hours will have a blood ethanol concentration of 33mg/dL, while the measured increases in this study averaged under 3mg/dL and the highest measured increase was 7mg/dL. Clearly, none of the patients would notice the effects of ethanol from dietary carbohydrate ingestion. Additionally, it has already been argued that the possibility of having this syndrome is not a credible defence against a drunk driving charge.

Unfortunately the most 'beneficial' effects of ethanol are achieved, most often, at levels requiring an exogenous source. Fortunately beer is tasty.



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Wednesday, September 11, 2013

Sarin Gas

If you haven't checked out SciShow on Youtube yet, please do yourself this favour. Consisting of quick science related videos it is accessible, entertaining and surprisingly informative. The SciShow team have a pretty good time with the material, probably best evidenced by the recent "Is SHARKNADO Possible?"
A recent SciShow describes some basic facts about Sarin gas, the nerve agent that recently killed hundreds of Syrian civilians. The video describes Sarin as an inhibitor of acetylcholinesterase. Sarin's inhibition of this enzyme prevents removal of actylecholine from neuromuscular junctions resulting in continuously contracting muscles and death from asphyxia due to the inability to control the muscles involved in breathing function.
Interestingly there are antidotes for sarin gas exposure and the resulting irreversible inhibition of acetylcholinesterase. Some antidotes simply inhibit acetylcholine receptors preventing the action of the accumulated acetylcholine and are themselves a poison. However pralidoxime (2-pyridine aldoxime methyl chloride,) or 2-PAM actually restores function to the irreversibly inhibited enzyme. It reacts with organophosphorus nerve agents such as sarin and reverses the covalent bond to the serine in the active site of acetylcholinesterase resulting in a reactivated enzyme. I have never heard of such an antidote or reaction. While I guess it is comforting to think there are antidotes to these weapons they are largely impractical due to the time frame in which they must be administered.
Are there any other examples of molecules that can reverse the irreversible inhibition of an enzyme?


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