Discussion in 'Hypersensitivity and Intolerance' started by Cort, Oct 7, 2010.
I like it!
I enjoyed alchohol a great deal before CFIDS. After sudden flu-like onset 20 years ago I can't drink even small amounts without sufffering immediate sickness and a hangover. I read an explanation once but it was biochemistry and I can't find it now.
I've always had a very high tolerance to alcohol but when I first became sick, I didn't drink because I was sick and didn't want to. After my health improved, I started drinking a glass of wine to help with my sleep problems and over the years drank a couple (or more) glasses of wine daily and this went on for many years. My CFS started flaring badly again a couple of years ago and suddenly I could not drink at all. The alcohol didn't affect me while I was drinking it but afterwards, I had a hangover that went on for days. After about a year of mostly being abstinent, I've had a couple glasses of wine on occasion and seem to be tolerating it again, although I always feel like I'm taking a risk. Sometimes it's worth it.
i'm the opposite. i can't do hard liquor or wine now, but can only stomach 1-2 beers before being dealthy sick or PEM.
Definitely varies throughout the illness...tolerable at the beginning and not at the end...wine never tolerable
I used to be able to drink a ton, no problem. Then all of a sudden when I was 20 I could no longer drink it. Made me feel really sick and poisoned. I tried to stomach it up to keep up with friends for about 8 months. But now I can't even have a few drops or it makes me really sick.
One of my first symptoms was that a small glass of wine made me wasted as if I had half a bottle. After a few months a spoon of herbal tincture with alcohol would make me to sit down. Now a glass is ok with food. It could be vasodilation-related.
I can't tolerate any alcohol whatsoever, not even in tinctures. I ticked the wrong box on the poll though , didn't read all the choices properly first!
Should add that I was not able to tolerate alcohol at all for the first 15 years or so of sickness, when my health was at its worst. But as I have slowly learned to better manage being sick, my alcohol tolerance has also improved slowly. Though it is still low compared to the average healthy person.
Certainly not suggesting that alcohol intolerance can be fixed by simply switching to vodka.
I noticed a decrease in alcohol tolerance prior to developing MCS and CFS that continued with its occurence. It felt like poison to me then, so I tend to stay away from it.
Alcohol quite often brings on pain in my legs, and/or a restless, agitated feeling, not entirely dissimilar to a mild opiate withdrawal.
My alcohol tolerance is now officially zero. I stupidly had two smallish glasses of white wine the other night and was soooooooooo sick the next day. My stomach couldn't digest anything. I eventually brought up everything I had consumed that day, in the evening. Even all the water I had been drinking all day!
I definitely feel as though I have been poisoned. My body thinks so too, which is why it can't digest anything.
Worst bit is that I didn't even enjoy it when I was drinking it.
take care, ness
I've always been pretty cadbury (glass & a half), but cant really tolerate it these days. I think more so due to the severity of my POTS
I used to (until a few months ago) be able to drink a glass of wine or a weak drink before feeling pretty tipsy. After being sick for a month I took one sip of a weak drink (exactly the same I'd had before) and felt horrible immediately. With so many of us being alcohol intolerant, I find the videos at http://webcasts.prous.com/Chronic_Fatigue/program.asp to be quite hilarious. The sample patient is a student with a job, who drinks a fair amount. How atypical could they get?
Effects of Ethanol in ME/CFS and the GD-MCB hypothesis
As has been suggested a couple of times on this thread, the toxic effect of ethanol in most PWCs is explained very well by the Glutathione Depletion--Methylation Cycle Block hypothesis. In fact, ethanol intolerance could contribute to diagnosis of ME/CFS for most cases, in my opinion, because it directly interrogates what I believe is the hallmark mechanism in the pathophysiology of ME/CFS.
Ethanol hits PWCs right where it hurts. Specifically, ethanol is metabolized by the liver. The liver is normally the main producer of glutathione in the body, and as other tissues become depleted in glutathione, the liver is the main bulwark that keeps PWCs from going into multiple organ failure and death. It has first access to amino acids coming from food in the gut, from which to make glutathione, and it has a complete transsulfuration pathway to make cysteine from methionine, as well as the alternative BHMT pathway for its methylation cycle, upstream of glutathione synthesis. In short, it is in the best position to hold the line when glutathione becomes depleted bodywide, and thus keep PWCs alive.
Unfortunately (see abstract below) ethanol causes oxidative stress particularly in the liver, and depletes glutathione there, worsening the scarcity that already exists.
However, in agreement with the present results of this poll and a few of the posts in this thread, I have also encountered a small number of PWCs who are able to tolerate ethanol. In cases in which they have shared their pre-onset history with me, I have found that they had a fairly high ethanol consumption before becoming ill with ME/CFS, and I have therefore hypothesized that their livers were able to develop a greater capacity for metabolizing ethanol before they became ill, and this greater capacity remains. At least one of the pathways for metabolizing ethanol in the liver is inducible, meaning that it can be expanded to greater capacity with greater chronic exposure to ethanol.
On the "bright" side (not really all that bright, I realize), if it were not for the toxicity of ethanol in CFS, I think it would be very likely that many would become alcoholics and succumb from cirrhosis of the liver, in an attempt to counter the pain and secondary depression. Sadly, it's sort of a case of the devil and the deep blue sea. But, as I continue to emphasize here, there is hope for lifting the partial methylation cycle block and restoring glutathione by the methylation-type treatments, and I encourage people to consider them, if they have not already done so.
Semin Liver Dis. 2009 May;29(2):141-54. Epub 2009 Apr 22.
Oxidative stress and alcoholic liver disease.
Wu D, Cederbaum AI.
Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, New York 10029, USA.
Reactive oxygen species (ROS) are highly reactive molecules that are naturally generated in small amounts during the body's metabolic reactions and can react with and damage complex cellular molecules such as lipids, proteins, or DNA. This review describes pathways involved in ROS formation, why ROS are toxic to cells, and how the liver protects itself against ROS. Acute and chronic ethanol treatment increases the production of ROS, lowers cellular antioxidant levels, and enhances oxidative stress in many tissues, especially the liver. Ethanol-induced oxidative stress plays a major role in the mechanisms by which ethanol produces liver injury. Many pathways play a key role in how ethanol induces oxidative stress. This review summarizes some of the leading pathways and discusses the evidence for their contribution to alcohol-induced liver injury.
I voted for the first two, because in the first 2-3 months my capacity was reduced maybe 20%. At that time, my symptoms were mainly vascular, plus the tiredness and some SOB. Then following that, I went back to the same capacity, same as it ever was.
I suspect it has to do with acetaldehyde dehydrogenase. In any event, I'd suggest taking vit C regularly during and after any imbibing to try and quench the acetaldehyde, say every 2-3 hours with C's short half-life.
AFAIK, acetaldehyde creates more harmful effects than the alcohol does anyway.
I also do recall one night, after having had no alcohol for a month or two, when I did drink and got a very powerful vasodilation, together with the reflex tachycardia and pounding heart. But that happened only once. I think I'm in a different phase now.
I remember this article from 1996 on such topics:
It is impossible for me to get a hangover. Maybe I naturally generate a lot of cysteine/glutathione, or maybe and/or the dehydrogenases. If the latter, then I might be the opposite of Asian Flush Syndrome. My PEM only ever lasted 1-2 days.
AFAIK, substances to counter or prevent liver damage are mainly vit C, milk thistle, lecithin and then maybe vit E.
BTW and IIRC, the congeners (flavor molecules) in whiskey, et al, are related to acetaldehyde.
I suspect also that the acetaldehyde dehydrogenase and possibly the alcohol dehydrogenase ties in with histamine. At the moment I don't quite recall but it has to with with breakdown processes.
[edit June 15 2011] Here's the tie-in: alcohol breaks down to acetaldehyde, which is further broken down by acetaldehyde dehygrogenase. Meanwhile, histamine, when broken down by DAO, produces imidazole acetaldehyde, which in turn is broken down by acetaldehyde dehygrogenase. (Another metabolite of DAO is hydrogen peroxide, so there's a contribution to ROS overload.)[/edit]
One last thing to mention, jaw pain that comes immediately after alcohol is associated with lymphoma, especially Hodgkin's Disease... but it is not necessarily a surefire sign of HD.
Am I right in thinking there are at least two different effects mixed in here?
1) the same amount of alcohol as before produces more intoxication
2) alcohol makes a person sick with hangover type symptoms, in which case I'd wonder how that effect compares to what happens with people who take Antabuse (if that's still sold/prescribed anymore). AFAIK, Antabuse essentially blocks acetaldehyde dehydrogenase, so that the buildup of acetaldehyde makes the user sick from alcohol.
I think there are several things going on when a PWME/PWC drinks alcohol, and I think the two you mentioned are part of them. The acetaldehyde dehydrogenase reaction in the liver requires NAD, which can be in short supply in ME/CFS. If there isn't enough, acetaldehyde can build up. This can also block the process of gluconeogenesis in the liver, which is an important part of the Cori cycle. PWMEs/PWCs depend on the Cori cycle more than healthy normals, because it is used to convert lactic acid back to glucose for reuse by the glycolysis pathway in the cells. Lactic acid is produced at higher than normal rates by PWMEs/PWcs because their mitochondria are dysfunctional. So if gluconeogenesis is partially blocked, it can produce the combination of lactic acidosis and hypoglycemia.
On top of all this, alcohol produces oxidative stress in the liver. In a lot of ways, the liver is what is keeping PWMEs/PWCs alive. That's why I say that alcohole really hits where it hurts in this population.
I may be another who fits this picture, for the most part I can tolerate alcohol fairly well since becoming sick - so not much change. And I suppose I had a fair amount of "practice" before becoming ill (more regularity than quantity), coupled with a pretty strong hereditary predilection for the stuff. Alcohol seems to serve as an easy quick energy source for my body, and I've found that when I crave a drink, usually my blood sugar is low and I feel exhausted.
But I don't drink much since becoming sick, I just can't imagine it's good for me. Though my health doesn't seem to change between periods of zero or moderate (glass of wine/bourbon a night) consumption.
Side note: I did have complete intolerance (immediate hangover, no pleasant feeling, general ick) for a few weeks. I believe it was a little while after taking the abx rifaximin for gut stuff.
I put After ME/CFS I dont do well with even small amounts of alcohol.
Actually, after I did a liver detox I was/am back to my pre-ME/CFS alcohol tolerance of 2 drinks. I drink so seldom that I am not sure whether that is still true.
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