kyanite
Bluelighter
- Joined
- Oct 15, 2005
- Messages
- 248
Personally, I am mixed of asian and white decent, and like so many of my asian pals, we get really, really, really red when we drink. Not to boast, but how red I get isn't related to how well I can tolerate alcohol. I don't mind the redness, and can keep my liquor pretty well.
Anyways, the connection here is that redness is caused by a genetic handicap on our part: genetic polymorphism of the aldehyde dehydrogenase(ALDH) enzyme, coding for a dominant, less active allele. Supposedly about 50% of asians suffer from alcohol sensitivity. Citation1 Citation2.
What's supposed to happen is that alcohol is metabolized in the digestive tract and in the liver by alcohol dehydrogenase(ADH), and turned into acetaldehyde. Next, ALDH2E comes along and turns acetaldehyde into acetic acid, which is used in the body, excreted, etc and thats the end of the story. In people with the less active version, ALDH2K, this acetaldehyde isn't removed anywhere near as fast, acetaldehyde builds up, and so these people get the effects of red, flushed faces.
So why is this in ADD? Because I recently read of a way to get around this problem... and make better use of my money!
If you type "asian flush pepcid" in google(don't ask), the second link is to a forum where there is 37 pages of people swearing that if you take Pepcid AC or Zantac, which are both OTC, an hour before drinking then you will only get pink, and nowhere near a tomato. It's amazing what scientifically uninformed people can discover... 37 pages of anecdotal evidence can't be wrong, right? So anyways I tried it and it worked very well for me.
After some some looking around, it looks like both zantac and pepcid(ranitidine and famotidine) are H2 inverse agonists, like tagamet(cimetidine), and are also structurally fairly similar. Low and behold, tagamet is a known ADH inhibitor.
All three drugs are non-competitive inhibitors of ADH, but their potencies at inhibiting the general ADH enzymes in the digestive tract and the liver differ. Also there seems to be some funky absorption into specialized cells of the stomach, but thats besides the point. What these drugs seem to do is slow down the metabolism of alcohol into acetaldehyde, meaning slower build up of acetaldehyde and less facial flush. (Digestive Diseases and Sciences. Vol. 36, No. 12 (December 1991), pp. 1673-1679).
Similarly, since alcohol is being metabolized at a slower rate, there ends up being more alcohol in your blood for longer periods of time- I stayed drunk longer.
Clinical study into the relationship between Zantac and alcohol:
The American Journal of Gastroenterology
Volume 95 Issue 1 Page 208-213, January 2000
My personal experience backs this up. I took 20mg of Pepcid AC, waited an hour, and then sipped on 4 shots of vodka with ice. My usual tomato face became only a light pink, and I felt that the effects were definitely stronger, and that I wasn't sober until a good 2 hours longer than usual.
I'm not sure about the safety of taking these drugs regularly, but this was more of an informative post.
To complete this monster of a post here's an article calculating the potencies of each drug at inhibiting ADH in both the digestive tract and the liver. They come a conclusion that contradicts the clinical study, but IMO they got it wrong because the amount they assumed a person to drink was too low. What's important is the pretty graphs and tables =)
Digestive Diseases and Sciences. Vol. 36, No. 12 (December 1991), pp. 1673-1679 FULL TEXT
Structure of tagamet
Structure of zantac
Structure of pepcid
Anyways, the connection here is that redness is caused by a genetic handicap on our part: genetic polymorphism of the aldehyde dehydrogenase(ALDH) enzyme, coding for a dominant, less active allele. Supposedly about 50% of asians suffer from alcohol sensitivity. Citation1 Citation2.
What's supposed to happen is that alcohol is metabolized in the digestive tract and in the liver by alcohol dehydrogenase(ADH), and turned into acetaldehyde. Next, ALDH2E comes along and turns acetaldehyde into acetic acid, which is used in the body, excreted, etc and thats the end of the story. In people with the less active version, ALDH2K, this acetaldehyde isn't removed anywhere near as fast, acetaldehyde builds up, and so these people get the effects of red, flushed faces.
So why is this in ADD? Because I recently read of a way to get around this problem... and make better use of my money!
If you type "asian flush pepcid" in google(don't ask), the second link is to a forum where there is 37 pages of people swearing that if you take Pepcid AC or Zantac, which are both OTC, an hour before drinking then you will only get pink, and nowhere near a tomato. It's amazing what scientifically uninformed people can discover... 37 pages of anecdotal evidence can't be wrong, right? So anyways I tried it and it worked very well for me.
After some some looking around, it looks like both zantac and pepcid(ranitidine and famotidine) are H2 inverse agonists, like tagamet(cimetidine), and are also structurally fairly similar. Low and behold, tagamet is a known ADH inhibitor.
All three drugs are non-competitive inhibitors of ADH, but their potencies at inhibiting the general ADH enzymes in the digestive tract and the liver differ. Also there seems to be some funky absorption into specialized cells of the stomach, but thats besides the point. What these drugs seem to do is slow down the metabolism of alcohol into acetaldehyde, meaning slower build up of acetaldehyde and less facial flush. (Digestive Diseases and Sciences. Vol. 36, No. 12 (December 1991), pp. 1673-1679).
Similarly, since alcohol is being metabolized at a slower rate, there ends up being more alcohol in your blood for longer periods of time- I stayed drunk longer.
Clinical study into the relationship between Zantac and alcohol:
The American Journal of Gastroenterology
Volume 95 Issue 1 Page 208-213, January 2000
Alcohol levels are increased in social drinkers receiving ranitidine
* Satish Arora, M.D.aaAlcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, New York, New York, USA,
* Enrique Baraona, M.D.aaAlcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, New York, New York, USA,
* Charles S. Lieber, M.D.aaAlcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, New York, New York, USA
*
aAlcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, New York, New York, USA
Reprint requests and correspondence: Charles S. Lieber, M.D., Alcohol Research Center, Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468
Abstract
OBJECTIVE: Ranitidine increases blood alcohol concentrations by decreasing the first pass metabolism of ethanol. The effect of ranitidine on alcohol levels has been found to be variable when using large doses of alcohol or conditions in which its first pass metabolism is known to be minimal. Despite a consensus that the drug increases alcohol levels after small doses of ethanol, this effect has been considered inconsequential, because of the low alcohol levels. However, social drinking comprises repetitive consumption of small doses of alcohol and the ranitidine effect could thereby be potentiated.
METHODS: To study this factor, alcohol levels were determined by breath analysis in nine men (social drinkers), after four drinks of 0.15 g/kg ethanol given postprandially every 45 min, before and after ranitidine (150 mg b.i.d. for 7 days).
RESULTS: Their blood alcohol increased with repeated doses, reaching peak values of 24 ± 3 mg/dl before ranitidine and 33 ± 2 after ranitidine (p = 0.04). In seven of the nine subjects blood alcohol exceeded 25 mg/dl, a level at which impairment of judgment and of finely tuned skills occurs and which exceeds legal limits of driving in some European countries. Moreover, the high levels persisted for a longer time with than without the drug. These effects were associated with a 62% decrease in first pass metabolism.
CONCLUSION: Under conditions mimicking social drinking, ranitidine increases blood alcohol to levels known to impair psychomotor skills needed for driving.
My personal experience backs this up. I took 20mg of Pepcid AC, waited an hour, and then sipped on 4 shots of vodka with ice. My usual tomato face became only a light pink, and I felt that the effects were definitely stronger, and that I wasn't sober until a good 2 hours longer than usual.
I'm not sure about the safety of taking these drugs regularly, but this was more of an informative post.
To complete this monster of a post here's an article calculating the potencies of each drug at inhibiting ADH in both the digestive tract and the liver. They come a conclusion that contradicts the clinical study, but IMO they got it wrong because the amount they assumed a person to drink was too low. What's important is the pretty graphs and tables =)
Digestive Diseases and Sciences. Vol. 36, No. 12 (December 1991), pp. 1673-1679 FULL TEXT
Structure of tagamet
Structure of zantac
Structure of pepcid
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