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Editor,—We read with great interest the paper by Gorard et al (Gut 1996;39: 551–5) on intestinal transit in patients with anxiety and depression. The authors used the lactulose hydrogen breath test to evaluate 21 consecutive outpatients attending a general psychiatry clinic who fulfilled DSM III R criteria for major depression or generalised anxiety disorders, or both. They reported a significantly prolonged orocaecal transit time (OCTT) in depressed patients compared with anxious patients, and a significant correlation between whole gut transit time and the score of the psychometric tests used to assess depression, showing evidence for an association between severity of depression and colon inertia. The authors conclude that depressed patients tend to be constipated and that mood has an effect on intestinal motor function, although mechanisms by which mood can alter colonic motility remain unknown.
Recently, we found a significantly prolonged OCTT in patients with chronic alcoholism without severe liver disease compared with social drinkers and teetotal subjects.1 Thirty one alcoholic patients without diseases which could affect OCTT were enrolled in the study on the basis of DSM III R criteria. Mean alcohol consumption was 191.1 g/day (range 90–360) and the mean duration of addiction was 15.9 years (range 1–36). Thirty one healthy, social drinkers and 24 teetotal subjects matched for sex and age were studied as controls. OCTT was assessed using the hydrogen breath test after administration of 10 g lactulose. The test was performed in the morning after a 12 hour fast. The concentration of expired H2 evaluated in parts per million (ppm) was measured before and at 10 minute intervals for four hours after administration of lactulose. An increase in the concentration of H2 > 10 ppm in at least three measurements with respect to the baseline values was considered indicative of the arrival of the lactulose in the caecum. In one alcoholic, four social drinkers and two teetotal subjects no increase in hydrogen excretion of at least 10 ppm was detected for 300 minutes after lactulose ingestion. These subjects were excluded from statistical analysis as the OCTT could not be evaluated. Three alcoholic patients had small intestinal bacterial overgrowth (two with diarrhoea) indicated by a rapid rise in breath hydrogen concentration during the first 45 minutes after ingestion of lactulose, and were excluded from statistical analysis. The OCTT in alcoholic patients (mean (SD) 156.3 (29.7) minutes, range 90–200) was significantly delayed compared with social drinkers (94.1 (11.3) minutes, range 70–120) and healthy teetotal subjects (85.5 (15.67) minutes, range 60–120) (fig 1). In alcoholic subjects there was no significant correlation between the OCTT and daily alcohol intake or years of alcohol addiction respectively. Our findings support the hypothesis that the toxic effect of ethanol on the smooth muscle contractile proteins of the small intestine and on vagal functions may be a causal factor of the dyspeptic symptoms in alcoholic patients.
Depression and alcohol abuse frequently co-exist with a co-occurrence that varies from 16% to 68%2; the co-morbidity between alcohol disorders and major depression has frequently been reported in alcoholic and psychiatric patient samples.3 The relation between depression and alcohol abuse has been difficult to define. Some authors have suggested that depressed mood is largely associated with the episode of drinking and may be due to the effect of chronic alcohol intoxication,2 whereas others have shown a consistent and significant association between depression and alcohol disorders providing persuasive evidence that major depression is a critical component of alcohol abuse and dependence.3 4
In the study by Gorard et al it is not reported whether alcohol abuse was investigated and considered as an exclusion criterion. If alcoholic patients were not excluded, this factor could be partly responsible for the prolonged OCTT in their depressed patients. Conversely, if the alcohol disorders were considered as exclusion criteria and only depressed patients were evaluated, Gorardet al’s data could provide a further valid explanation for prolonged OCTT in alcoholic patients with major depression.
Editor,—We appreciate the interest that Addoloratoet al have shown in our paper. We can verify that in our study none of the subjects drank alcohol excessively nor had a history of alcoholism. Therefore, the longer transit times in our depressed subjects cannot be attributed to increased alcohol use.
In the study by Addolorato et al showing prolonged OCTT in patients with chronic alcoholism, it is therefore possible that associated depression in their patients may have contributed to this result. These authors also postulate a possible toxic effect of ethanol on intestinal smooth muscle as the explanation for their findings, but other neurohumoral factors may be important. For example, alcoholic patients have high cortisol concentrations, as to a lesser extent do depressed patients, and corticotrophin releasing hormone is known to have inhibitory effects on upper gastrointestinal motor function.1-1 Furthermore, if their alcoholic patients were withdrawing from alcohol while participating in the study, then the stress of withdrawal with increased adrenergic tone could have contributed to prolonged OCTT.1-2
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