Nightsong
Senior Member (Voting Rights)
I would like to see more research on alcohol-induced symptoms & intolerance, both mechanistic and epidemiological; the latter to determine how common it is in well-characterised ME/CFS cohorts, the precise nature of the symptoms experienced and their time-course, and to determine whether those who report it also report intolerance to other medications that act on the central nervous system in differing ways.
Bansal (BMC Family Practice (2016) 17:81) suggested that this was an unusual symptom that "may be used to confirm the diagnosis", stating that from his clinical experience "nearly all patients. . . have reduced their intake of alcohol and I have not seen a single patient who had increased his/her alcohol intake".
There are very few conditions that result in unusual alcohol-induced symptoms or significant alcohol intolerance. There are many reports of alcohol-associated pain in Hodgkin's disease which seems to have been first described in 1950 (Amer J Roentgenol 64:613) followed by a number of case reports in the 1950s and 1960s; the first systematic investigation of it seems to have been in 1960 (Quart Journ Med XXIX:113). There was a suggestion in a letter to the Lancet in the 1970s that alcohol intolerance in Hodgkin's was not as commonly found as implied by the initial reports. Nonetheless, case reports of the same phenomenon continue; there was one in 2019 (BMJ Case Rep 2019;12:e228440) in which it was a presenting symptom.
Alcohol intolerance also occurs in the hypereosinophilic syndrome: in 1988 two cases where alcohol intolerance was a presenting feature were reported (Alcohol Clin Exp Res 12(1):147-8). There is also the well-known "alcohol flush" syndrome reported to result from a variant in ALDH2 causing deficiency of aldehyde dehydrogenase II. Alcohol intolerance can also be deliberately induced by medication as treatment for alcoholism: disulfiram (Antabuse) acts by inhibiting aldehyde dehydrogenase resulting in the accumulation of acetaldehyde from which a number of unpleasant symptoms flow. There was a broader discussion of alcohol intolerance syndromes in "Alcohol: intolerance syndromes, urticarial and anaphylactoid reactions" (Clin Dermatol 17(4):417-422). Flushing associated with alcohol has also been reported in carcinoid syndrome.
Alcohol intolerance in ME/CFS has only very rarely been studied. One of the few publications of significance is "Alcohol use in chronic fatigue syndrome" (J Psychosom Res 56(2004):203-206) where it was reported that in a study of 114 CFS patients 2/3rds self-reported a reduction in alcohol use and the most common reasons for this were exacerbations of physical symptoms.
In "Onset Patterns and Course of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome" (Front Paediatr 7:2019) there is a small table showing the prevalence of alcohol intolerance in ME/CFS in various studies.
Interestingly there are also occasional references to it in the historical neurasthenia literature, some of which may have been cases of ME/CFS.
Bansal (BMC Family Practice (2016) 17:81) suggested that this was an unusual symptom that "may be used to confirm the diagnosis", stating that from his clinical experience "nearly all patients. . . have reduced their intake of alcohol and I have not seen a single patient who had increased his/her alcohol intake".
There are very few conditions that result in unusual alcohol-induced symptoms or significant alcohol intolerance. There are many reports of alcohol-associated pain in Hodgkin's disease which seems to have been first described in 1950 (Amer J Roentgenol 64:613) followed by a number of case reports in the 1950s and 1960s; the first systematic investigation of it seems to have been in 1960 (Quart Journ Med XXIX:113). There was a suggestion in a letter to the Lancet in the 1970s that alcohol intolerance in Hodgkin's was not as commonly found as implied by the initial reports. Nonetheless, case reports of the same phenomenon continue; there was one in 2019 (BMJ Case Rep 2019;12:e228440) in which it was a presenting symptom.
Alcohol intolerance also occurs in the hypereosinophilic syndrome: in 1988 two cases where alcohol intolerance was a presenting feature were reported (Alcohol Clin Exp Res 12(1):147-8). There is also the well-known "alcohol flush" syndrome reported to result from a variant in ALDH2 causing deficiency of aldehyde dehydrogenase II. Alcohol intolerance can also be deliberately induced by medication as treatment for alcoholism: disulfiram (Antabuse) acts by inhibiting aldehyde dehydrogenase resulting in the accumulation of acetaldehyde from which a number of unpleasant symptoms flow. There was a broader discussion of alcohol intolerance syndromes in "Alcohol: intolerance syndromes, urticarial and anaphylactoid reactions" (Clin Dermatol 17(4):417-422). Flushing associated with alcohol has also been reported in carcinoid syndrome.
Alcohol intolerance in ME/CFS has only very rarely been studied. One of the few publications of significance is "Alcohol use in chronic fatigue syndrome" (J Psychosom Res 56(2004):203-206) where it was reported that in a study of 114 CFS patients 2/3rds self-reported a reduction in alcohol use and the most common reasons for this were exacerbations of physical symptoms.
In "Onset Patterns and Course of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome" (Front Paediatr 7:2019) there is a small table showing the prevalence of alcohol intolerance in ME/CFS in various studies.
Interestingly there are also occasional references to it in the historical neurasthenia literature, some of which may have been cases of ME/CFS.
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