A genotype-controlled analysis of plasma dopamine beta-hydroxylase in healthy and alcoholic subjects: evidence for alcohol-related differences in noradrenergic function.

BACKGROUND: Norepinephrine and dopamine mediate important aspects of alcoholism and alcohol withdrawal. Dopamine-beta-hydroxylase (DbetaH) converts dopamine to norepinephrine. A recent study demonstrated a strong association between variance in plasma DbetaH activity and a novel polymorphism (DBH-1021C-->T) at the structural locus (DBH) encoding DbetaH protein. METHODS: Our study investigated whether the DBH-1021C-->T polymorphism and plasma DbetaH activity were associated with alcoholism or with delirium tremens (DT) during alcohol withdrawal by analyzing 207 German alcoholic and 102 healthy control subjects. We also examined the influence of the polymorphism on enzyme activity. RESULTS: Mean (+SD) plasma DbetaH activity measured in alcoholic subjects abstinent was significantly lower than that observed in control (27.7 + 16.7 vs. 35.6 + 18.8; p =.01). It did not differ between subjects with DT during withdrawal and subjects with mild withdrawal symptoms. The T allele of the DBH-1021C-->T polymorphism was significantly associated with lower plasma DbetaH activity. None of the alleles or genotypes were associated with alcoholism or DT. CONCLUSIONS: The data indicate that the alcoholism-related reduction in plasma DbetaH activity is independent of genotype at DBH-1021C-->T and replicate the finding that DBH-1021C-->T is strongly associated with plasma DbetaH activity in a native Western European population.     

Decreased dopamine beta-hydroxylase activity in unipolar geriatric delusional depression.

BACKGROUND: Decreased dopamine beta-hydroxylase (DBH) activity has been reported in unipolar psychotic depression. DBH comparisons between elderly delusional and nondelusional depressives and controls and determination of whether pretreatment group differences persist have not been reported. Our objective was to compare DBH activity in elderly delusional major depressives with that of nondelusional depressives and normal control subjects before and after hospital treatment. METHODS: Enzyme activity was assessed after hospital admission. A subsample had predischarge assessments. Treatment was not controlled but accounted for in analyses. Electroconvulsive therapy subjects were medication-free for posttreatment assays. RESULTS: Baseline and predischarge DBH assays were lower in subjects with delusional depression than in either comparison group. Despite high intraindividual correlation, treatment was associated with significant increases in activity in the clinical groups. CONCLUSIONS: Patients with late-life delusional depression have lower DBH activity before and after hospital treatment than age-matched nondelusional patients or normal controls.     

A functional dopamine-β-hydroxylase gene promoter polymorphism is associated with impulsive personality styles,but not with affective disorders

Dopamine-beta-hydroxylase (DbetaH) catalyzes the conversion of dopamine to norepinephrine in central noradrenergic and adrenergic neurons and thus is critically involved in the biosynthesis of catecholamines. There are equivocal findings concerning the question whether or not DssH activity levels are altered in affective disorders or in subtypes of affective disorders. Moreover, information about the role of dopamine beta-hydroxylase (DBH) genotype, which explains a large part of the variance of enzymatic activity, in affective disorders and personality dimensions is limited. To resolve these inconsistencies, association tests were performed using four independent samples, healthy volunteers (N = 387), patients with affective disorders (N = 182), adult attention deficit hyperactivity disorder (ADHD) patients (N = 407), and patients with personality disorders (N = 637). In the latter two samples, the revised NEO personality inventory (NEO-PI-R) was administered. All participants were genotyped for a putatively functional single nucleotide polymorphism (C-1021T, rs1611115). No differences in DBH C-1021T genotype distribution were observed between patients with affective disorders and healthy control subjects. Also when the patient sample was divided into uni- and bipolar patients versus controls, no significant differences emerged. Furthermore, no clear-cut association was detected between the TT genotype and personality disorder clusters while there was a significant association with adult ADHD. However, personality disorder patients carrying the DBH TT genotype exhibited higher neuroticism and novelty seeking scores as compared to individuals with the CC or CT genotype. Analyses on the level of the neuroticism and novelty seeking subscales revealed that the DBH TT genotype was primarily associated with personality features related to impulsiveness and aggressive hostility. Also adult ADHD patients carrying the homozygous TT genotypes displayed by significantly increased neuroticism scores; when both personality disorder and adult ADHD patient were analyzed together, TT carriers also displayed by significantly lower conscientiousness levels. Our results thus do not implicate the DBH C-1021T polymorphism in the pathophysiology of depressive disorders or personality disorders, yet homozygosity at this locus appears to increase the risk towards personality traits related to impulsiveness, aggression and related disease states, namely adult ADHD. These data argue for a dimensional rather than categorical effect of genetic variance in DBH activity; accordingly, the inconsistency of previous findings concerning DbetaH levels in affective disorders might be caused by the underlying association of the TT genotype at DBH-1021 with impulsive personality traits.     

A polymorphism in the dopamine β-hydroxylase gene is associated with “paranoid ideation” in patients with major depression

Background: Increased dopaminergic activity may play a primary role in psychotic depression. Dopamine β-hydroxylase (DβH) catalyses the key step in biosynthesis of the neurotransmitter noradrenaline from dopamine, and low DβH activity is a possible risk factor for developing psychotic depression. An exon 2 polymorphism (DBH∗444 g/a) of the DβH gene (DBH) is significantly associated with both serum and cerebrospinal fluid levels of DβH.Methods: We determined the genotype of the DBH∗444g/a polymorphism in a cohort of 164 patients with major depression and examined the association of this polymorphism with paranoid ideation, interpersonal sensitivity, and psychoticism on the Hopkins Symptom Checklist.Results: Patients who possessed the A allele were significantly more likely to have higher scores for interpersonal sensitivity and paranoia than patients without the A allele (p = .004 and p = .048, respectively), suggesting that this allele may predispose patients to paranoia in major depression. In addition, we found an association between prolactin levels in men and DBH∗444 g/a genotype such that homozygous G individuals displayed significantly higher levels than homozygous A or heterozygote individuals.Conclusions: Depressed patients with the GG genotype of DβH have lower scores for interpersonal sensitivity and paranoid ideation. The GG genotype may be protective against the development of psychosis in the presence of a major depressive episode.     

5-HTTLPR与卒中后抑郁及单相抑郁病因和疗效的关联分析

目的 探讨我国汉族人群卒中后抑郁（post-stroke depression,PSD）及单相抑郁（unipolar depression,UD）患者病因和疗效与5-羟色胺转运蛋白启动子区基因多态性（serotonin transporter gene-linked polymorphic,5-HTTLPR）之间的关系。方法 以4 5例P S D及41例U D患者作为研究对象,以149名正常人作对照,应用聚合酶链式反应（polymerase chain reaction,PCR）扩增技术测定所有研究对象的5-HTTLPR的基因型和等位基因,PSD和UD患者组患者使用氟西汀治疗12周,在基线及12周治疗末时使用汉密尔顿抑郁量表（Hamilton depressive scale,HAMD）-17项评定疾病严重程度及疗效。结果 5-HTTLPR的3种基因型（S/S、S/L和L/L）和等位基因（S和L）在PSD组、UD组和正常对照组之间的分布差异无统计学意义;PSD和UD组S/S纯合子与S/L杂合子及L/L纯合子的基线评分相比差异具有统计学意义;12周治疗后两组患者治愈组和未治愈组之间S/S与S/L和L/L基因型、S和L等位基因分布具有统计学差异。结论 5-HTTLPR与PSD及UD均无显著关联,S/S基因型患者可能抑郁症状较重,12周治疗后携带S/S基因型和S等位基因患者的临床痊愈率较低。     

A single nucleotide polymorphism at DBH, possibly associated with attention-deficit/hyperactivity disorder, associates with lower plasma dopamine beta-hydroxylase activity and is in linkage disequilibrium with two putative functional single nucleotide polymorphisms.

BACKGROUND: The DBH gene regulates plasma dopamine beta-hydroxylase activity (pDbetaH). Two single nucleotide polymorphisms (SNPs), -1021C-->T (rs1611115; SNP1) and +1603C-->T (rs6271; SNP3), independently influence pDbetaH. Another SNP, commonly known as DBH Taq1A (rs2519152; SNP2) is associated with attention-deficit/hyperactivity disorder (ADHD) in some (but not all) studies. We tested whether 1) SNP2 associates with pDbetaH; and 2) whether linkage disequilibrium (LD) between SNP2 and the other SNPs explains that association. METHODS: Plasma dopamine beta-hydroxylase activity and genotypes at the SNPs were determined in Caucasian subjects (n = 418). Associations to pDbetaH were examined using analyses of variance (ANOVAs) and LD among the SNPs using estimation maximization. RESULTS: 1) Each polymorphism analyzed alone associated with pDbetaH; 2) SNP2 was in strong LD with SNP1 and SNP3, respectively, but there was no significant LD between SNP1 and SNP3; and 3) analyzed jointly, each SNP contributed significantly and uniquely to plasma DbetaH activity. CONCLUSIONS: 1) SNP2 associates with pDbetaH; 2) SNP2 shows LD with SNP1 and SNP3; 3) most of the association between SNP2 and pDbetaH simply reflects that LD; however, 4) SNP2 also appears to exert a small independent effect on pDbetaH, suggesting that SNP2, or another variant in LD with it, uniquely influences pDbetaH.     

Evaluation of the sympathetic nervous system in trisomy-21 (Down's syndrome).

Dopamine-β-hydroxylase (DBH) is the enzyme which converts dopamine to norepinephrine (NE) and plasma DBH activity is diminished in patients with Down's syndrome. We have investigated sympathetic, noradrenergic neurotransmission in Down's patients by measuring plasma levels of NE and DBH in patients with trisomy-21 and their parents and comparing them to healthy volunteers of similar age. The Down's patients, like normal control subjects, responded to the stress of venipuncture and to standing with a significant increase in plasma levels of NE, indicating intact sympathetic nervous system responsivity. In fact the patients had significantly (p < 0·05) higher circulating levels of NE while supine and standing. Despite the higher NE levels systolic blood pressure was significantly lower in the patients (p = 0·005). Plasma DBH activity was significantly (p < 0·005) diminished in the Down's patients when compared to their parents, to age-matched controls or adult controls. While DBH does not appear to be an index of deficient sympathetic nervous activity in Down's syndrome, it may reflect the chromosome abnormality. Despite low levels of DBH, the synthetic enzyme for NE, Down's patients have normal or increased levels of NE.     

Cortisol hypersecretion in unipolar major depression with melancholic and psychotic features: dopaminergic, noradrenergic and thyroid correlates

Evidence supports that hyperactivity of the hypothalamic-pituitary-adrenal axis has a pivotal role in the psychobiology of severe depression. The present study aimed at assessing hypothalamic-pituitary dopaminergic, noradrenergic, and thyroid activity in unipolar depressed patients with melancholic and psychotic features and with concomitant hypercortisolemia. Hormonal responses to dexamethasone, apomorphine (a dopamine receptor agonist), clonidine (an alpha 2-adrenoreceptor agonist) and 0800 and 2300 h protirelin (TRH) were measured in 18 drug-free inpatients with a DSM-IV diagnosis of severe major depressive disorder with melancholic and psychotic features showing cortisol nonsuppression following dexamethasone and 23 matched hospitalized healthy controls. Compared with controls, patients showed (1) lower adrenocorticotropin and cortisol response to apomorphine (p<0.015 and <0.004, respectively), (2) lower growth hormone response to clonidine (p=0.001), and (3) lower responses to TRH: 2300 h maximum increment in serum thyrotropin (TSH) level (p=0.006) and the difference between 2300 and 0800 h maximum increment in serum TSH values (p=0.0001). Our findings, in a subgroup of unipolar depressed inpatients with psychotic and melancholic features, are compatible with the hypothesis that chronic elevation of cortisol may lead to dopaminergic, noradrenergic and thyroid dysfunction.     

单相与双相抑郁患者事件相关电位P50和P300比较

目的:比较单相与双相抑郁患者事件相关电位感觉门控P50及P300的电生理差异。方法:用配对听觉条件/测试刺激范式,对57例单相抑郁患者(单相组)、63例双相抑郁患者(双相组)进行事件相关电位P50,P300测定,测量其P50的波幅,P300的潜伏期及波幅。结果:双相组P50的S2波幅显著高于单相组,而且双相组P50的抑制率显著高于单相组。双相组N2,P3潜伏期长于单相组,同时N2,P3波幅低于单相组,差异均有统计学意义。结论:双相抑郁患者认知功能损害可能比抑郁症患者更严重,事件相关电位可以为鉴别单双相抑郁提供一种新的技术手段。     

Psychotic late-life depression: a 376-case study.

The aim of the report was to study clinical differences between psychotic late-life depression and psychotic depression in younger patients, to determine if differences were age-related or specific for psychotic late-life depression. Three hundred seventy-six consecutive outpatients, presenting for treatment of unipolar or bipolar depression (with or without psychotic features), were assessed by means of the Structured Clinical Interview for DSM-IV, the Montgomery and Asberg Depression Rating Scale, and the Global Assessment of Functioning Scale. Results showed that psychotic late-life (50 years or more) depression, versus psychotic depression in younger patients, was associated with significantly higher age at study entry/onset, longer duration, and lower comorbidity. Psychotic depression versus nonpsychotic late-life depression, in late-life and in younger patients, was associated with significantly greater severity, lower comorbidity, more patients with bipolar I disorder, and fewer patients with unipolar disorder. Findings were related to psychosis or to age, and not to specific features of psychotic late-life depression. These results support a unitary view of psychotic depression.     

Genetic marker of norepinephrine synthesis predicts individual differences in post-error slowing: A pilot study

When our brain detects the commission of an error, we slow down immediately thereafter: a phenomenon called post-error slowing (PES). Some researchers have speculated that slowing after unexpected errors or negative feedback is related to the activity of the neuromodulatory locus coeruleus–norepinephrine system. In the present pilot study, we tested whether individual differences in the size of PES are related to differences in genetic predisposition related to norepinephrine synthesis. In a sample of 100 healthy adults, we studied the dependency of an individual′s size of PES on the DBH5′-ins/del polymorphism—a variation in the DBH gene associated with the production of the enzyme dopamine β-hydroxylase, which catalyzes the conversion of dopamine to norepinephrine. DBH5′-ins/del heterozygotes, who have intermediate levels of plasma DβH activity, showed increased PES in a Simon task compared to del/del homozygotes and ins/ins homozygotes, who have low and high levels of plasma DβH activity, respectively. This outcome pattern presents preliminary evidence that the size of PES varies with DβH activity and, presumably, NE release according to an inverted U-shape: intermediate levels of DβH activity and NE release are associated with larger post-error adjustments.     

Psychotic (delusional) major depression: should it be included as a distinct syndrome in DSM-IV?

To review data supporting or not supporting the designation of unipolar psychotic major depression as a distinct syndrome in DSM-IV, the authors used computerized literature searches to identify reports of studies that have directly compared the characteristics, biology, familial transmission, course/outcome, and response to treatment of psychotic and nonpsychotic major depression. The review showed that statistically significant differences between the two types of depression have been found on each of these dimensions. There are greater guilt feelings and psychomotor disturbance, among other features, in psychotic depression. Studies have found significant differences between patients with psychotic and nonpsychotic depression in glucocorticoid activity, dopamine beta-hydroxylase activity, levels of dopamine and serotonin metabolites, sleep measures, and ventricle-to-brain ratios. Family studies show higher rates of bipolar disorder in first-degree relatives of probands with psychotic major depression than of probands with nonpsychotic major depression. Greater morbidity and residual impairment have also been reported in patients with psychotic major depression, and they respond more poorly to placebo and to tricyclic antidepressants. Differences between patients with psychotic and nonpsychotic major depression on many of these measures were not due to differences in severity or endogenicity. Since the data indicate that psychotic and nonpsychotic major depression can be separated, the frequency with which the diagnosis of psychotic major depression is missed and its unique course and response to treatment point to the practical importance of a separate diagnosis for this disorder. However, further studies are needed to resolve important methodological issues and to develop an optimal set of operational criteria.     

Neuropsychological dysfunction in antipsychotic-naive first-episode unipolar psychotic depression

OBJECTIVE: The profile of neuropsychological impairment associated with unipolar psychotic depression remains unclear. The authors used a neuropsychological test battery to characterize the neuropsychiatric profile of patients with unipolar psychotic depression, relative to that of patients with nonpsychotic unipolar depression, patients with schizophrenia, and healthy comparison subjects. METHOD: Study subjects included antipsychotic-naive patients with a first episode of psychotic unipolar depression (N=20), antipsychotic-naive and unmedicated patients with nonpsychotic unipolar depression (N=14), antipsychotic-naive patients with first-episode schizophrenia (N=86), and healthy volunteers (N=81). Groups were matched on age, sex, race, education, parental socioeconomic status, and estimated premorbid intelligence. Psychotic patients were followed clinically for 2 years to confirm diagnosis. All participants completed a standard neuropsychological battery, including tests of general intelligence, executive function, attention, verbal memory, motor skills, and visual-spatial perception. RESULTS: Patients with psychotic depression had a pattern of neuropsychological dysfunction that was similar to but less severe than that of patients with schizophrenia. In contrast, patients with nonpsychotic unipolar depression had a neuropsychological profile that was similar to that of healthy individuals but that included mild dysfunction on tests of attention. Neuropsychological test performance was generally independent of acute clinical symptoms, but some pairwise group differences were attenuated by covariation for symptom severity. CONCLUSIONS: The similar neuropsychological profiles for schizophrenia and psychotic depression suggest that these psychotic disorders may have common pathophysiological features. The dramatic differences in performance between the patients with psychotic depression and those with nonpsychotic depression point to a marked distinction in neurocognitive function associated with the expression of psychosis in depressed patients.     

cAMP signaling pathway in depressed patients with psychotic features

Abnormalities in protein kinase A (PKA) and Rap1 have recently been reported in depressed patients. The aim of the present study was to investigate the levels of these proteins in platelets from untreated unipolar and bipolar depressed patients with psychotic features. The levels PKA and Rap1 were assessed by Western blot analysis and immunostaining in 37 drug-free patients and 29 healthy subjects. Both unipolar and bipolar patients with psychotic depression have significantly lower levels of platelet regulatory type I and higher levels of catalytic subunits of PKA than controls, whereas the levels of regulatory type II were higher only in psychotic unipolar patients. No significant differences were found in the immunolabeling of both Rap1 and actin among groups. These findings support the idea that besides nonpsychotic depression, abnormalities of PKA could be linked, albeit in a somewhat different way, with psychotic depression.     

Pattern recognition analyses of brain activation elicited by happy and neutral faces in unipolar and bipolar depression

Mourão‐Miranda J, Almeida JRC, Hassel S, de Oliveira L, Versace A, Marquand AF, Sato JR, Brammer M, Phillips ML. Pattern recognition analyses of brain activation elicited by happy and neutral faces in unipolar and bipolar depression.
Bipolar Disord 2012: 14: 451–460. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. Objectives: Recently, pattern recognition approaches have been used to classify patterns of brain activity elicited by sensory or cognitive processes. In the clinical context, these approaches have been mainly applied to classify groups of individuals based on structural magnetic resonance imaging (MRI) data. Only a few studies have applied similar methods to functional MRI (fMRI) data. Methods: We used a novel analytic framework to examine the extent to which unipolar and bipolar depressed individuals differed on discrimination between patterns of neural activity for happy and neutral faces. We used data from 18 currently depressed individuals with bipolar I disorder (BD) and 18 currently depressed individuals with recurrent unipolar depression (UD), matched on depression severity, age, and illness duration, and 18 age‐ and gender ratio‐matched healthy comparison subjects (HC). fMRI data were analyzed using a general linear model and Gaussian process classifiers. Results: The accuracy for discriminating between patterns of neural activity for happy versus neutral faces overall was lower in both patient groups relative to HC. The predictive probabilities for intense and mild happy faces were higher in HC than in BD, and for mild happy faces were higher in HC than UD (all p < 0.001). Interestingly, the predictive probability for intense happy faces was significantly higher in UD than BD (p = 0.03). Conclusions: These results indicate that patterns of whole‐brain neural activity to intense happy faces were significantly less distinct from those for neutral faces in BD than in either HC or UD. These findings indicate that pattern recognition approaches can be used to identify abnormal brain activity patterns in patient populations and have promising clinical utility as techniques that can help to discriminate between patients with different psychiatric illnesses.     

Impaired temporal resolution of visual attention and dopamine beta hydroxylase genotype in attention-deficit/hyperactivity disorder.

BACKGROUND: Dopamine beta hydroxylase (DbetaH) catalyzes the conversion of dopamine to noradrenaline. Attention-deficit/hyperactivity disorder (ADHD) has been associated with the A2 allele of a Taq I polymorphism of the DBH gene. Since catecholamines regulate visual attention, we examined whether participants with ADHD were impaired on a task requiring temporal attention and how DBH genotype influenced temporal attention in ADHD. METHODS: Thirty-seven children and adolescents with ADHD and 52 matched, normal control subjects participated. Participants were presented with two visual stimuli, separated in time by either 50, 100, or 200 milliseconds, and were asked to judge the temporal order of their onset. Genotypes for the Taq 1 polymorphism were available for 33 of the ADHD participants. RESULTS: Attention-deficit/hyperactivity disorder participants were more error prone than control subjects, particularly when stimuli were presented close together in time (i.e., at the 50 milliseconds asynchrony). Moreover, ADHD individuals homozygous for the A2 allele performed more poorly than those without this allele, and this difference was accentuated at the 50 milliseconds asynchrony. CONCLUSIONS: Attention-deficit/hyperactivity disorder participants have an impaired rate of perceptual processing for rapidly presented visual events. Deficits in the temporal resolution of visual attention in ADHD are associated with the A2 allele of the Taq I DBH polymorphism or another variant with which it is in linkage disequilibrium.     

Exaggerated orthostatic responsivity of plasma norepinephrine in depression

An orthostatic challenge paradigm was used to assess noradrenergic regulation in depressive disorders. Plasma norepinephrine (NE) concentrations and concurrent blood pressure and pulse were measured at rest and after five minutes of standing in groups of bipolar (N = 22) and unipolar (N = 19) depressives and in 12 partially age-matched healthy female volunteers. Supine plasma NE levels were significantly lower in bipolar patients than in either unipolar depressives or normal volunteers. Following the orthostatic challenge, the fractional NE increase in both patient groups--particularly the bipolar group--was greatly exaggerated, exceeding that in the controls by approximately 100%. Nonetheless, the postural cardiovascular changes--elevations of diastolic blood pressure and heart rate--failed to distinguish the three subject groups. Noradrenergic dysregulation in depression thus is characterized by inefficient hyperreactivity to physiologic stress.     

Lithium: effects of short-term and chronic treatments in rats on the activity of dopamine-beta-hydroxylase (DBH) in the central versus peripheral nervous system

The therapeutic usefulness of lithium in mania is now well-established. However, the precise neurochemical mechanisms by which lithium brings about its effects remain poorly understood. This report describes the effects of lithium on the central and peripheral levels of activity of dopamine-β-hydroxylase (DBH), the enzyme that catalyzes the final step in the biosynthetic pathway to the formation of norepinephrine (NE) from dopamine. Since the neurotransmitter NE has been implicated in the mediation of lithium's action, what effects lithium may have on the activity of DBH was deemed worth investigating. Lithium chloride was administered intraperitoneally in rats on a short-term and chronic basis and the effects on DBH activities in the hypothalamus and serum were evaluated. A significant reduction in DBH activity occurred in the hypothalamus after short-term lithium butthere was no change following chronic treatment. In contrast, serum DBH activity remained unchanged after both acute and chronic lithium injection. Since increased noradrenergic activity in the brain has been implicated in the etiology of mania, the lithium-induced decrease in hypothalamic DBH is suggestive of a neurochemical mechanism by which lithium may act in psychotic patients.     

Serum dopamine-beta-hydroxylase in diagnostic subgroups of depressed patients and in relation to their personality characteristics

Serum dopamine-beta-hydroxylase (DBH) levels were assessed in 150 depressed patients of both sexes, with a mean age of 44.0 +/- 12.3 (SD) years. Patients were divided into unipolars (n = 46), bipolars (n = 25), neurotic-reactive (n = 46) and unspecified (n = 38) i.e., those who did not fit into any of the previous categories. According to their status 38 patients were psychotic and 104 clearly nonpsychotic at the time of the DBH assessment. Personality characteristics were assessed for the same patients when they had markedly improved from their depression. In line with previous findings bipolar patients were found to have slightly lower serum DBH values than unipolars, and psychotic patients slightly lower values than nonpsychotic. However, none of the differences among diagnostic groups or between psychotic and nonpsychotic patients was statistically significant. Weak negative correlations were found between serum DBH and the personality variables social desirability and indirect aggression, but an earlier finding of a positive correlation with the personality trait monotony avoidance, could not be confirmed. Owing to the large interindividual variations in serum DBH it is concluded that correlations between serum DBH and personality characteristics might be spurious and due to chance. This study does not support the assumption that significant differences in serum DBH might occur among subgroups of depressed patients.