Early-onset alcoholics have lower cerebrospinal fluid 5-hydroxyindoleacetic acid levels than late-onset alcoholics.
BACKGROUND
We investigated the interrelationships of age at onset of excessive alcohol consumption, family history of alcoholism, psychiatric comorbidity, and cerebrospinal fluid monoamine metabolite concentrations in abstinent, treatment-seeking alcoholics.


METHODS
We studied 131 recently abstinent alcoholics. Supervised abstinence was maintained on a research ward at the National Institutes of Health Clinical Center for a minimum of 3 weeks. All alcoholics received a low-monoamine diet for a minimum of 3 days before lumbar puncture. Lumbar punctures were performed in the morning after an overnight fast. Monamine metabolites and tryptophan in cerebrospinal fluid were quantified with liquid chromatography by means of electrochemical detection. Psychiatric diagnoses were established from blind-rated Schedule for Affective Disorders and Schizophrenia-Lifetime version interviews administered by a research social worker. Severity and age at onset of excessive alcohol consumption were documented with a structured lifetime drinking history questionnaire and with selected alcoholism screening questionnaires (CAGE and Michigan Alcoholism Screening Test). Family history of alcoholism was obtained from the probands.


RESULTS
A majority of the treatment-seeking, primarily white male alcoholics had a lifetime history of psychiatric disorders other than alcoholism. None fulfilled criteria for antisocial personality disorder. Early-onset alcoholics (onset of excessive consumption before 25 years of age) had a more severe course of alcoholism and lower mean cerebrospinal fluid 5-hydroxyindoleacetic acid concentration than late-onset alcoholics. Patients who reported both parents to be alcoholics had particularly low mean cerebrospinal fluid 5-hydroxyindoleacetic acid, homovanillic acid, and tryptophan concentrations.


CONCLUSIONS
Among treatment-seeking alcoholics, early age at onset is generally associated with a more severe course of alcoholism and lower cerebrospinal fluid 5-hydroxyindoleacetic acid concentration.
Fils-Aime
M L
ML
Laboratory of Clinical Studies, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md. USA.
Eckardt
M J
MJ
George
D T
DT
Brown
G L
GL
Mefford
I
I
Linnoila
M
M
D000328:Adult; D017668:Age of Onset; D000428:Alcohol Drinking / Q000134:cerebrospinal fluid; D000437:Alcoholism / Q000134:cerebrospinal fluid* / Q000175:diagnosis / Q000453:epidemiology; D015897:Comorbidity; D005190:Family; D005260:Female; D006719:Homovanillic Acid / Q000134:cerebrospinal fluid; D006801:Humans; D006897:Hydroxyindoleacetic Acid / Q000134:cerebrospinal fluid*; D008297:Male; D001523:Mental Disorders / Q000453:epidemiology; D008734:Methoxyhydroxyphenylglycol / Q000134:cerebrospinal fluid; D015995:Prevalence; D011569:Psychiatric Status Rating Scales; D012720:Severity of Illness Index; D014364:Tryptophan / Q000134:cerebrospinal fluid
D008734:Methoxyhydroxyphenylglycol; D006897:Hydroxyindoleacetic Acid; D014364:Tryptophan; D006719:Homovanillic Acid