CSF Monoamine Metabolites in Alcoholism: A Comparative Study With Depression

Takahashi, Saburo; Yamane, Hideo; Kondo, Hisao; Tani, Naoki; Kato, Nobukatsu

doi:10.1111/j.1440-1819.1974.tb02312.x

Cited by 33 publications

(20 citation statements)

References 19 publications

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“…Our findings are consistent with previous reports that alcoholism affects CSF HVA levels (Roos and Silfverskiöld, 1973;Kato et al, 1979;Goldman et al, 1992;Takahashi et al, 1974;Major et al, 1977;Fujimoto et al, 1983;Roy et al, 1991a;Virkkunen et al, 1996;Fils-Aime et al, 1996;Petrakis et al, 1999). Roy et al (1991a) reported that depressed subjects with alcoholism had significantly lower concentrations of HVA than never depressed subjects with alcoholism.…”

Section: Biological Findingssupporting

confidence: 83%

“…Low CSF HVA may have more to do with psychopathology related to alcoholism as opposed to mood disorder biology. Our finding is consistent with studies that suggest that dopaminergic mechanisms play a part in the biology of alcohol use disorders, including mechanisms of alcohol dependence and withdrawal (Diana et al, 1993;Weiss et al, 1996;Weiss and Koob, 1991;Koob, 1992;Noble, 1996;Wiesbeck et al, 2000;Fromme and D'Amico, 1999;Nevo and Hamon, 1995;Roos and Silfverskiöld, 1973;Kato et al, 1979;Goldman et al, 1992;Takahashi et al, 1974;Major et al, 1977;Fujimoto et al, 1983;Roy et al, 1991a;Virkkunen et al, 1996;Fils-Aime et al, 1996;Petrakis et al, 1999;Samson et al, 1990;Valenzuela and Harris, 1997;Robinson and Berridge, 1993;VavrousekJakuba et al, 1992;Quarfordt et al, 1991;Modell et al, 1993;Grace, 2000).…”

Section: Biological Findingssupporting

confidence: 79%

“…The CSF HVA levels in our control group are consistent with values reported in healthy volunteers (Takahashi et al, 1974;Kato et al, 1979;Roos and Silfverskiöld, 1973;Roy et al, 1990;Hibbeln et al, 1998;Westenberg and Verhoeven, 1988;Koslow et al, 1983;Kanemaru et al, 1998;Engstrom et al, 1999). Some studies have found lower CSF HVA level in subjects with depression (for reviews, see Kapur and Mann, 1992;Brown and Gershon, 1993;Nemeroff et al, 1997).…”

Section: Biological Findingssupporting

confidence: 79%

“…Some studies have found lower CSF HVA level in subjects with depression (for reviews, see Kapur and Mann, 1992;Brown and Gershon, 1993;Nemeroff et al, 1997). However, the mean CSF HVA level of depressed subjects without a history of alcoholism in our study is higher than reported by other researchers who studied depressed subjects (Takahashi et al, 1974;Kato et al, 1979;Placidi et al, 2001;Å sberg et al, 1984;Reddy et al, 1992;Westenberg and Verhoeven, 1988;Koslow et al, 1983). This difference may be related to the fact that we used a sample of depressed subjects without a history of alcoholism.…”

Section: Biological Findingscontrasting

confidence: 56%

“…Roy et al (1991a) found lower CSF levels of the dopamine metabolite HVA in depressed compared with never depressed subjects with alcohol dependence. Although multiple studies have shown changes in CSF monoamine metabolites in subjects with alcoholism (Roos and Silfverskiöld, 1973;Kato et al, 1979;Goldman et al, 1992;Takahashi et al, 1974;Major et al, 1977;Fujimoto et al, 1983;Virkkunen et al, 1996;Fils-Aime et al, 1996;Petrakis et al, 1999;Adinoff et al, 1996Adinoff et al, , 1995Adinoff et al, , 1991Geracioti et al, 1994Geracioti et al, , 1993Virkkunen et al, 1994;Kaakkola et al, 1993;Roy et al, 1990;Roy and Linnoila, 1989;Hawley et al, 1988;Borg et al, 1982;Geracioti, 1997), the study by Roy et al (1991a), to our knowledge, is the only study that measured CSF HVA in depressed individuals with alcoholism. Most studies do not distinguish possible biological effects of related psychopathology such as depression, psychosis, suicidal behavior, or smoking.…”

Section: Introductionmentioning

confidence: 99%

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Lower CSF Homovanillic Acid Levels in Depressed Patients with a History of Alcoholism

Sher

Oquendo

et al. 2003

Neuropsychopharmacol

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Major depression and alcoholism are often comorbid, resulting in more impairment and more suicidal behavior compared with either diagnosis alone. This study compared clinical features and cerebrospinal fluid (CSF) monoamine metabolites in depressed subjects with and without a history of alcoholism and healthy volunteers. We hypothesized that depressed subjects with a history of alcoholism would be more aggressive, impulsive, and suicidal than depressed subjects without a history of alcoholism, and would have lower CSF monoamine metabolite levels. We compared 63 subjects with a current major depressive episode (MDE) and a history of alcoholism, 72 subjects with a current MDE but without a history of alcoholism, and 22 healthy volunteers. Participants with a history of alcoholism were in remission for at least 6 months. All subjects were free from prescribed medications known to affect brain serotonin, dopamine, or norepinephrine systems for a minimum of 14 days. Depressive symptoms, lifetime aggression, impulsivity, Axis II disorders, and suicidal behavior were assessed. CSF was sampled and homovanillic acid (HVA), 5-hydroxyindolacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were assayed by high-performance lipid chromatography with electrochemical detection. Depressed subjects with a history of alcoholism did not differ from depressed subjects without a history of alcoholism in current severity of depressive symptoms, or in past suicidal behavior. Depressed subjects with a history of alcoholism had lower CSF HVA levels, and higher lifetime aggression and current suicide ideation scale scores and were more likely to be tobacco smokers compared with depressed subjects without a history of alcoholism. Low HVA was present after adjustment for sex, aggression and depression scores, cigarette smoking, antisocial and borderline personality disorders, psychomotor retardation, and delusions. Controls had CSF HVA levels intermediate between the two depressed groups. We found no group difference in CSF 5-HIAA and MHPG levels. In individuals with current MDE, those with a history of comorbid alcoholism had lower CSF HVA levels compared with those without a history of alcoholism. Low CSF HVA suggests that impaired dopaminergic activity is associated with a history of alcoholism in persons with current MDE.

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