The Tyramine Challenge Test as a Marker for Melancholia

Harrison, Wilma; Cooper, Thomas B.; Stewart, Jonathan W.; Quitkin, Frederic M.; McGrath, Patrick J.; Liebowitz, Michael R.; Rabkin, Judith R.; Markowitz, Jacqueline; Klein, Donald F.

doi:10.1001/archpsyc.1984.01790180051006

Cited by 53 publications

(9 citation statements)

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“…Recently, results from a large multicentre sib-pairs study gave further support to the existence of a separate atypical dimension (Korszun et al 2004); in a factor analysis of the familiality of symptom dimensions in depression, typical and reversed neurovegetative symptoms loaded on one factor, but gain of appetite and hypersomnia loaded negatively. A number of neuro-biological studies found differences between atypical and other forms of depression (Fotiou et al 2003;Bruder et al 2002Bruder et al , 1989Geracioti et al 1997;McGinn et al 1996; Asnis et al 1995;Quitkin et al 1985; Harrison et al 1984).…”

Section: Introductionmentioning

confidence: 99%

Atypical depressive syndromes in varying definitions

Angst

Gamma

Benazzi

et al. 2005

Eur Arch Psychiatry Clin Neurosci

107

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■ Abstract Background Atypical depression (AD) exhibits distinct patterns of gender, bipolar-II disorder, genetic, and neuro-biological measures. Using prospective data from a community sample, this paper identifies criteria (and correlates) for an AD syndrome that maximizes the association with female sex and bipolar-II. Methods The Zurich cohort study is composed of 591 subjects selected from a population-based cohort of young adults in the canton of Zurich in Switzerland, screened in 1978 and followed with six interviews through 1999. Seven definitions of atypical depression were tested, using varying combinations of vegetative symptoms and mood reactivity. Results The atypical definitions using 2 of 3 (fatigue, overeating, oversleeping) or 2 of 2 (overeating, oversleeping) vegetative symptoms showed the strongest association with gender, bipolarity, and family history of mania. The 2/3 definition was chosen for further analysis due to its high sensitivity for identifying these characteristics. This syndrome had cumulated weighted prevalence of 16.4 % (males 9.7 %, females 23 %); when associated with major depressive episodes, 8.2 % (males 3.2 %, females 15.1 %). AD patients were characterized by high treatment rates, severity, and work impairment, early age of onset and long illness. AD was comorbid with social phobia, binge eating, neurasthenia, migraine headache, and subjective cognitive impairment.■ Key words atypical depression · bipolar-II disorder · sex · prevalence

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Section: Introductionmentioning

confidence: 99%

Atypical depressive syndromes in varying definitions

Angst

Gamma

Benazzi

et al. 2005

Eur Arch Psychiatry Clin Neurosci

107

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“…However, consideration of the subtypes of depression which co-vary genetically with alcoholism and those which show tyramine conjugation abnormalities resolves this apparent contradiction. Tyramine abnormality has been demonstrated to occur in endogenous depressives and not in non-endogenous or neurotic depressives (Harrison et al, 1984;Hale et al, 1986). This latter group may be characterised as depression occurring in the context of personality problems or neurosis, in the presence of long-standing instability in interpersonal relationships, sexual, marital and work circumstances or neurotic symptoms (Winokur, 1987).…”

Section: Discussionmentioning

confidence: 99%

“…The abnormality was identified in depression (Sandler et al, 1975;Bonham Carter et al, 1978), migraine (Jarman et al, 1990) and some other pain syndromes sometimes seen as depressive equivalents (Aghabeigi et al, 1993). It is generally present in endogenous/ melancholic but not in non-endogenous depressed patients (Harrison et al, 1984;Hale et al, 1986), and in unipolar but not bipolar depressives (Hale et al, 1991). Half of a group of first degree relatives of depressives showed the abnormality (Hale et al, 1986).…”

Section: Introductionmentioning

confidence: 98%

“…Half of a group of first degree relatives of depressives showed the abnormality (Hale et al, 1986). This, together with the ability of the test to identify blind patients with a past history of depression from an at-risk group (Bonham Carter et al, 1980), the lack of relationship to severity of depression (Hale et al, 1986) and the persistence of the abnormality in drug-free recovered patients (Bonham Carter et al, 1978;Harrison et al, 1984), points to the abnormality being a trait marker for vulnerability to endogenous depression, perhaps genetically linked. For unipolar major depressives, tyramine sulphate conjugation seems able to predict acute treatment response to tricyclic antidepressants (Hale et al, 1989), but this is less clear with minor depressives (Hale, 1993).…”

Section: Introductionmentioning

confidence: 99%

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Detoxified alcoholics, major depressives and tyramine sulphate excretion

Hale

Hannah²,

Sandler³

et al. 1995

J Psychopharmacol

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The excretion of tyramine sulphate after challenge with an oral load of tyramine was assessed in recently detoxified, clinically depressed alcoholics and a matched group of major depressives. Tyramine excretion in the alcohol group (mean 5.95 ± 3.28 mg/3 h SD) was in the range previously observed in controls and was significantly higher than in the matched depressives (mean 3.43 ± 2.37 mg/3 h SD). Tyramine sulphate excretion has been suggested as a genetic vulnerability marker for major depression. This study suggests that depression associated with alcohol withdrawal is not characterised by decreased tyramine sulphate excretion after oral tyramine challenge, such decreased conjugation only being present, perhaps, in those patients with pre- existing endogenous depressive vulnerability. Although a genetic link between alcoholism and depression exists, these results support the absence of such a link to major depression.

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“…The only mood disorder subtype with some evidence of validity is atypical depression, which is discriminated from non-atypical depression on the basis of differential clinical features including an earlier onset, greater chronicity, and more severe symptoms than other depressive subtypes. Other discriminating factors include differential association with bipolar II disorder, compared to other depressive subtypes [135], differential treatment response [136,137], specific patterns of neuroendocrine challenge response [138], different patterns of comorbidity including stronger associations with social phobia and migraine, and some degree of specificity in twin [139] and family studies [140,141]. Although the validity of expression of atypical features in youth still is being investigated, studies of depression in children and adolescents confirm that atypical features also occur in youth [41].…”

Section: Lack Of Validity Of the Classification Systemmentioning

confidence: 99%

The epidemiology of mood disorders

Merikangas

Low²

2004

Curr Psychiatry Rep

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This review provides an overview of the epidemiology, risk factors, and genetic epidemiology of mood disorders in adults and children. The magnitude and impact of mood disorders in the community outweighs that of most other chronic diseases. Although there is substantial knowledge regarding the sociodemographic risk factors for mood disorders, our understanding of the pathogenesis and classification still is evolving. Comorbidity of mood disorders with anxiety disorders and substance abuse has been documented widely. Whereas substance abuse and mood disorders seem to be independent etiologically, anxiety and mood disorders result from partially common etiologic factors. The results of family, twin, and adoption studies reveal that a positive family history is the most potent risk factor for mood disorders, particularly bipolar disorder. However, the specific factors that are transmitted in families still are unknown. The two areas that will inform future genetic research include phenomenologic studies that refine the validity of the current phenotypic classification of mood disorders, and application of study designs to elucidate specific factors that may explain the familial transmission of these disorders.

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The Tyramine Challenge Test as a Marker for Melancholia

Cited by 53 publications

References 20 publications

Atypical depressive syndromes in varying definitions

Atypical depressive syndromes in varying definitions

Detoxified alcoholics, major depressives and tyramine sulphate excretion

The epidemiology of mood disorders

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