The Relationship of Alcohol Use Disorders and Depressive Symptoms to Tryptophan Metabolism: Cross-Sectional Data from a Nepalese Alcohol Treatment Sample
Background Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a reduction in tryptophan availability for serotonin synthesis. As alcohol consumption affects tryptophan metabolism and disposition, we de...
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| Published in | Alcoholism, clinical and experimental research Vol. 39; no. 3; pp. 514 - 521 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Blackwell Publishing Ltd
01.03.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0145-6008 1530-0277 1530-0277 |
| DOI | 10.1111/acer.12651 |
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| Abstract | Background
Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a reduction in tryptophan availability for serotonin synthesis. As alcohol consumption affects tryptophan metabolism and disposition, we determined serum levels of tryptophan, kynurenine, and an index of tryptophan degradation (kynurenine/tryptophan ratio) in patients with alcohol‐use disorder (AUD) and compared their levels considering abstinence duration, AUD severity, and comorbid depression.
Methods
The study sample included 169 AUD inpatients from 8 alcohol treatment facilities in Kathmandu, Nepal. The Composite International Diagnostic Interview was administered to generate the AUD diagnosis. The Alcohol Use Disorder Identification Test (AUDIT) captured AUD severity and patterns of alcohol use. The Hopkins Symptom Checklist‐25 was used to reveal current depressive symptoms. Serum kynurenine and tryptophan levels were determined by high‐performance liquid chromatography, and tryptophan degradation was measured by KT ratio (kynurenine/tryptophan × 103).
Results
Patients with above average AUDIT scores had higher mean serum levels of kynurenine (2.1 μM ± 0.7 vs. 1.8 μM ± 0.6, p = 0.006) and KT ratios (48.6 ± 17.6 vs. 40.4 ± 14.3, p = 0.002) than those with below average scores. Patients with current depressive symptoms had higher mean tryptophan concentrations (49.9 μM ± 13 vs. 45.7 μM ± 14.1, p = 0.047) and lower KT ratios (41.4 ± 14 vs. 47.5 ± 17.6, p = 0.028) compared to patients whose reported depressive symptoms were below the standard cutoff. Higher tryptophan levels and lower KT ratios in the depressed group were specific to patients with longer abstinence and higher AUD severity.
Conclusions
Depression‐related deregulation in tryptophan metabolism was found to depend on length of abstinence and on AUD severity. Together, results suggest that in AUD populations, peripheral tryptophan metabolism is subject to interactions between AUD severity and depressive symptoms. |
|---|---|
| AbstractList | Background
Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a reduction in tryptophan availability for serotonin synthesis. As alcohol consumption affects tryptophan metabolism and disposition, we determined serum levels of tryptophan, kynurenine, and an index of tryptophan degradation (kynurenine/tryptophan ratio) in patients with alcohol‐use disorder (AUD) and compared their levels considering abstinence duration, AUD severity, and comorbid depression.
Methods
The study sample included 169 AUD inpatients from 8 alcohol treatment facilities in Kathmandu, Nepal. The Composite International Diagnostic Interview was administered to generate the AUD diagnosis. The Alcohol Use Disorder Identification Test (AUDIT) captured AUD severity and patterns of alcohol use. The Hopkins Symptom Checklist‐25 was used to reveal current depressive symptoms. Serum kynurenine and tryptophan levels were determined by high‐performance liquid chromatography, and tryptophan degradation was measured by KT ratio (kynurenine/tryptophan × 103).
Results
Patients with above average AUDIT scores had higher mean serum levels of kynurenine (2.1 μM ± 0.7 vs. 1.8 μM ± 0.6, p = 0.006) and KT ratios (48.6 ± 17.6 vs. 40.4 ± 14.3, p = 0.002) than those with below average scores. Patients with current depressive symptoms had higher mean tryptophan concentrations (49.9 μM ± 13 vs. 45.7 μM ± 14.1, p = 0.047) and lower KT ratios (41.4 ± 14 vs. 47.5 ± 17.6, p = 0.028) compared to patients whose reported depressive symptoms were below the standard cutoff. Higher tryptophan levels and lower KT ratios in the depressed group were specific to patients with longer abstinence and higher AUD severity.
Conclusions
Depression‐related deregulation in tryptophan metabolism was found to depend on length of abstinence and on AUD severity. Together, results suggest that in AUD populations, peripheral tryptophan metabolism is subject to interactions between AUD severity and depressive symptoms. Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a reduction in tryptophan availability for serotonin synthesis. As alcohol consumption affects tryptophan metabolism and disposition, we determined serum levels of tryptophan, kynurenine, and an index of tryptophan degradation (kynurenine/tryptophan ratio) in patients with alcohol-use disorder (AUD) and compared their levels considering abstinence duration, AUD severity, and comorbid depression. The study sample included 169 AUD inpatients from 8 alcohol treatment facilities in Kathmandu, Nepal. The Composite International Diagnostic Interview was administered to generate the AUD diagnosis. The Alcohol Use Disorder Identification Test (AUDIT) captured AUD severity and patterns of alcohol use. The Hopkins Symptom Checklist-25 was used to reveal current depressive symptoms. Serum kynurenine and tryptophan levels were determined by high-performance liquid chromatography, and tryptophan degradation was measured by KT ratio (kynurenine/tryptophan 103). Patients with above average AUDIT scores had higher mean serum levels of kynurenine (2.1 mu M plus or minus 0.7 vs. 1.8 mu M plus or minus 0.6, p = 0.006) and KT ratios (48.6 plus or minus 17.6 vs. 40.4 plus or minus 14.3, p = 0.002) than those with below average scores. Patients with current depressive symptoms had higher mean tryptophan concentrations (49.9 mu M plus or minus 13 vs. 45.7 mu M plus or minus 14.1, p = 0.047) and lower KT ratios (41.4 plus or minus 14 vs. 47.5 plus or minus 17.6, p = 0.028) compared to patients whose reported depressive symptoms were below the standard cutoff. Higher tryptophan levels and lower KT ratios in the depressed group were specific to patients with longer abstinence and higher AUD severity. Depression-related deregulation in tryptophan metabolism was found to depend on length of abstinence and on AUD severity. Together, results suggest that in AUD populations, peripheral tryptophan metabolism is subject to interactions between AUD severity and depressive symptoms. Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a reduction in tryptophan availability for serotonin synthesis. As alcohol consumption affects tryptophan metabolism and disposition, we determined serum levels of tryptophan, kynurenine, and an index of tryptophan degradation (kynurenine/tryptophan ratio) in patients with alcohol-use disorder (AUD) and compared their levels considering abstinence duration, AUD severity, and comorbid depression.BACKGROUNDActivation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a reduction in tryptophan availability for serotonin synthesis. As alcohol consumption affects tryptophan metabolism and disposition, we determined serum levels of tryptophan, kynurenine, and an index of tryptophan degradation (kynurenine/tryptophan ratio) in patients with alcohol-use disorder (AUD) and compared their levels considering abstinence duration, AUD severity, and comorbid depression.The study sample included 169 AUD inpatients from 8 alcohol treatment facilities in Kathmandu, Nepal. The Composite International Diagnostic Interview was administered to generate the AUD diagnosis. The Alcohol Use Disorder Identification Test (AUDIT) captured AUD severity and patterns of alcohol use. The Hopkins Symptom Checklist-25 was used to reveal current depressive symptoms. Serum kynurenine and tryptophan levels were determined by high-performance liquid chromatography, and tryptophan degradation was measured by KT ratio (kynurenine/tryptophan × 10(3)).METHODSThe study sample included 169 AUD inpatients from 8 alcohol treatment facilities in Kathmandu, Nepal. The Composite International Diagnostic Interview was administered to generate the AUD diagnosis. The Alcohol Use Disorder Identification Test (AUDIT) captured AUD severity and patterns of alcohol use. The Hopkins Symptom Checklist-25 was used to reveal current depressive symptoms. Serum kynurenine and tryptophan levels were determined by high-performance liquid chromatography, and tryptophan degradation was measured by KT ratio (kynurenine/tryptophan × 10(3)).Patients with above average AUDIT scores had higher mean serum levels of kynurenine (2.1 μM ± 0.7 vs. 1.8 μM ± 0.6, p = 0.006) and KT ratios (48.6 ± 17.6 vs. 40.4 ± 14.3, p = 0.002) than those with below average scores. Patients with current depressive symptoms had higher mean tryptophan concentrations (49.9 μM ± 13 vs. 45.7 μM ± 14.1, p = 0.047) and lower KT ratios (41.4 ± 14 vs. 47.5 ± 17.6, p = 0.028) compared to patients whose reported depressive symptoms were below the standard cutoff. Higher tryptophan levels and lower KT ratios in the depressed group were specific to patients with longer abstinence and higher AUD severity.RESULTSPatients with above average AUDIT scores had higher mean serum levels of kynurenine (2.1 μM ± 0.7 vs. 1.8 μM ± 0.6, p = 0.006) and KT ratios (48.6 ± 17.6 vs. 40.4 ± 14.3, p = 0.002) than those with below average scores. Patients with current depressive symptoms had higher mean tryptophan concentrations (49.9 μM ± 13 vs. 45.7 μM ± 14.1, p = 0.047) and lower KT ratios (41.4 ± 14 vs. 47.5 ± 17.6, p = 0.028) compared to patients whose reported depressive symptoms were below the standard cutoff. Higher tryptophan levels and lower KT ratios in the depressed group were specific to patients with longer abstinence and higher AUD severity.Depression-related deregulation in tryptophan metabolism was found to depend on length of abstinence and on AUD severity. Together, results suggest that in AUD populations, peripheral tryptophan metabolism is subject to interactions between AUD severity and depressive symptoms.CONCLUSIONSDepression-related deregulation in tryptophan metabolism was found to depend on length of abstinence and on AUD severity. Together, results suggest that in AUD populations, peripheral tryptophan metabolism is subject to interactions between AUD severity and depressive symptoms. Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a reduction in tryptophan availability for serotonin synthesis. As alcohol consumption affects tryptophan metabolism and disposition, we determined serum levels of tryptophan, kynurenine, and an index of tryptophan degradation (kynurenine/tryptophan ratio) in patients with alcohol-use disorder (AUD) and compared their levels considering abstinence duration, AUD severity, and comorbid depression. The study sample included 169 AUD inpatients from 8 alcohol treatment facilities in Kathmandu, Nepal. The Composite International Diagnostic Interview was administered to generate the AUD diagnosis. The Alcohol Use Disorder Identification Test (AUDIT) captured AUD severity and patterns of alcohol use. The Hopkins Symptom Checklist-25 was used to reveal current depressive symptoms. Serum kynurenine and tryptophan levels were determined by high-performance liquid chromatography, and tryptophan degradation was measured by KT ratio (kynurenine/tryptophan × 10(3)). Patients with above average AUDIT scores had higher mean serum levels of kynurenine (2.1 μM ± 0.7 vs. 1.8 μM ± 0.6, p = 0.006) and KT ratios (48.6 ± 17.6 vs. 40.4 ± 14.3, p = 0.002) than those with below average scores. Patients with current depressive symptoms had higher mean tryptophan concentrations (49.9 μM ± 13 vs. 45.7 μM ± 14.1, p = 0.047) and lower KT ratios (41.4 ± 14 vs. 47.5 ± 17.6, p = 0.028) compared to patients whose reported depressive symptoms were below the standard cutoff. Higher tryptophan levels and lower KT ratios in the depressed group were specific to patients with longer abstinence and higher AUD severity. Depression-related deregulation in tryptophan metabolism was found to depend on length of abstinence and on AUD severity. Together, results suggest that in AUD populations, peripheral tryptophan metabolism is subject to interactions between AUD severity and depressive symptoms. |
| Author | Hestad, Knut Neupane, Sudan Prasad Martinez, Priscilla Bramness, Jørgen G. Lien, Lars |
| AuthorAffiliation | 2 Innlandet Hospital Trust, Hamar, Norway 3 Department of Public Health, Hedmark University College Elverum, Norway 5 Department of Psychology, The Norwegian University of Science and Technology, Trondheim, Norway 1 SERAF-Norwegian Centre for Addiction Research, University of Oslo, Norway 4 Alcohol Research Group, University of California, Berkeley, USA |
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| Author_xml | – sequence: 1 givenname: Sudan Prasad surname: Neupane fullname: Neupane, Sudan Prasad email: s.p.neupane@medisin.uio.no organization: SERAF-Norwegian Centre for Addiction Research, University of Oslo, Oslo, Norway – sequence: 2 givenname: Lars surname: Lien fullname: Lien, Lars organization: SERAF-Norwegian Centre for Addiction Research, University of Oslo, Oslo, Norway – sequence: 3 givenname: Priscilla surname: Martinez fullname: Martinez, Priscilla organization: Alcohol Research Group, University of California, California, Berkeley – sequence: 4 givenname: Knut surname: Hestad fullname: Hestad, Knut organization: Innlandet Hospital Trust, Hamar, Norway – sequence: 5 givenname: Jørgen G. surname: Bramness fullname: Bramness, Jørgen G. organization: SERAF-Norwegian Centre for Addiction Research, University of Oslo, Oslo, Norway |
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| Keywords | Kynurenine Pathway Alcohol Depression Comorbidity Tryptophan Metabolism |
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Neupane SP, Bramness JG (2014) Who seeks treatment for alcohol problems? Demography and alcohol-use characteristics of patients in taboo and non-taboo drinking groups attending professional alcohol services in Nepal. Asian J Psychiatr 12: 82-87. Raison CL, Dantzer R, Kelley KW, Lawson MA, Woolwine BJ, Vogt G, Spivey JR, Saito K, Miller AH (2010) CSF concentrations of brain tryptophan and kynurenines during immune stimulation with IFN-alpha: relationship to CNS immune responses and depression. Mol Psychiatry 15:393-403. Badawy AA, Doughrty DM, Marsh-Richard DM, Steptoe A (2009) Activation of liver tryptophan pyrrolase mediates the decrease in tryptophan availability to the brain after acute alcohol consumption by normal subjects. Alcohol Alcohol 44:267-271. Sullivan LE, Fiellin DA, O'Connor PG (2005) The prevalence and impact of alcohol problems in major depression: a systematic review. Am J Med 118:330-341. Shrestha NM, Sharma B, van Ommeren M, Regmi S, Makaju R, Komproe I, Shrestha GB, De Jong JT (1998) Impact of torture on refugees displaced within the developing world: symptomatology among Bhutanese refugees in Nepal. JAMA 280:443-448. Maes M, Mihaylova I, Ruyter MD, Kubera M, Bosmans E (2007) The immune effects of TRYCATs (tryptophan catabolites along the IDO pathway): relevance for depression - and other conditions characterized by tryptophan depletion induced by inflammation. Neuro Endocrinol Lett 28:826-831. Capuron L, Neurauter G, Musselman DL, Lawson DH, Nemeroff CB, Fuchs D, Miller AH (2003) Interferon-alpha-induced changes in tryptophan metabolism relationship to depression and paroxetine treatment. Biol Psychiatry 54:906-914. Wittchen HU (1994) Reliability and validity studies of the WHO Composite International Diagnostic Interview (CIDI): a critical review. J Psychiatr Res 28:57-84. Branchey L, Branchey M, Shaw S, Lieber CS (1984a) Depression, suicide, and aggression in alcoholics and their relationship to plasma amino acids. Psychiatry Res 12:219-226. Stone TW, Forrest CM, Darlington LG (2012) Kynurenine pathway inhibition as a therapeutic strategy for neuroprotection. FEBS J 279:1386-1397. Quak J, Doornbos B, Roest AM, Duivis HE, Vogelzangs N, Nolen WA, Penninx BW, Kema IP, de Jonge P (2014) Does tryptophan degradation along the kynurenine pathway mediate the association between pro-inflammatory immune activity and depressive symptoms? Psychoneuroendocrinology 45:202-210. Saunders JB, Aasland OG, Babor TF, de la Fuente JR, Grant M (1993) Development of the alcohol use disorders identification test (AUDIT): WHO collaborative project on early detection of persons with harmful alcohol consumption-II. Addiction 88:791-804. Coppen A (1967) The biochemistry of affective disorders. Br J Psychiatry 113:1237-1264. Sinha R, Fox HC, Hong KA, Bergquist K, Bhagwagar Z, Siedlarz KM (2009) Enhanced negative emotion and alcohol craving, and altered physiological responses following stress and cue exposure in alcohol dependent individuals. Neuropsychopharmacology 34: 1198-1208. Van Ommeren M, Sharma B, Thapa S, Makaju R, Prasain D, Bhattarai R, de Jong J (1999) Preparing instruments for transcultural research: use of the translation monitoring form with Nepali-speaking Bhutanese refugees. Transcult Psychiatry 36:285-301. Dunjic-Kostic B, Ivkovic M, Radonjic NV, Petronijevic ND, Pantovic M, Damjanovic A, Poznanovic ST, Jovanovic A, Nikolic T, Jasovic-Gasic M (2013) Melancholic and atypical major depression-connection between cytokines, psychopathology and treatment. Prog Neuropsychopharmacol Biol Psychiatry 43:1-6. O'Connor JC, Andre C, Wang Y, Lawson MA, Szegedi SS, Lestage J, Castanon N, Kelley KW, Dantzer R (2009) Interferon-gamma and tumor necrosis factor-alpha mediate the upregulation of indoleamine 2,3-dioxygenase and the induction of depressive-like behavior in mice in response to bacillus Calmette-Guerin. J Neurosci 29:4200-4209. Maes M, Meltzer H (1995) The serotonin hypothesis of major depression. Psychopharmacology 10: 933-934. Dantzer R, O'Connor JC, Lawson MA, Kelley KW (2011) Inflammation-associated depression: from serotonin to kynurenine. Psychoneuroendocrinology 36:426-436. LeMarquand D, Pihl RO, Benkelfat C (1994) Serotonin and alcohol intake, abuse, and dependence: clinical evidence. Biol Psychiatry 36:326-337. DeMyer MK, Shea PA, Hendrie HC, Yoshimura NN (1981) Plasma tryptophan and five other amino acids in depressed and normal subjects. Arch Gen Psychiatry 38:642-646. Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshleman S, Wittchen HU, Kendler KS (1994) Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry 51:8-19. Neupane SP, Lien L, Hilberg T, Bramness JG (2013) Vitamin D deficiency in alcohol-use disorders and its relationship to comorbid major depression: a cross-sectional study of inpatients in Nepal. Drug Alcohol Depend 133:480-485. Badawy AA (2002) Tryptophan metabolism in alcoholism. Nutr Res Rev 15:123-152. Lynskey MT (1998) The comorbidity of alcohol dependence and affective disorders: treatment implications. Drug Alcohol Depend 52:201-209. Fernstrom JD (1983) Role of precursor availability in control of monoamine biosynthesis in brain. Physiol Rev 63:484-546. 2009; 44 2002; 15 1998; 280 2010; 15 2013; 43 1997; 43 1993; 88 1995; 10 1967; 113 2014; 49 2011a; 32 2005; 118 1984b; 141 1997 2008; 10 2011; 36 1994; 28 2007; 98 2007; 12 2014; 45 2003; 54 1974; 19 2014; 65 2009; 29 2014; 20 2007; 28 2009; 34 1984a; 12 2010; 47 2000 2004; 37 2011b; 35 1999; 36 2013; 133 1981; 38 1988; 23 1994; 36 1983; 63 2012; 26 1998; 52 2012; 279 1989; 16 1973; 6 2014; 12 1994; 51 2006; 364 Sinha (10.1111/acer.12651-BIB0039|acer12651-cit-0039) 2009; 34 Sullivan (10.1111/acer.12651-BIB0041|acer12651-cit-0041) 2005; 118 American Psychiatric Association (10.1111/acer.12651-BIB0501|acer12651-cit-0501) 2000 Schrocksnadel (10.1111/acer.12651-BIB0037|acer12651-cit-0037) 2006; 364 Saunders (10.1111/acer.12651-BIB0036|acer12651-cit-0036) 1993; 88 Derogatis (10.1111/acer.12651-BIB0010|acer12651-cit-0010) 1974; 19 Muller (10.1111/acer.12651-BIB0027|acer12651-cit-0027) 2007; 12 Ommeren (10.1111/acer.12651-BIB0042|acer12651-cit-0042) 1999; 36 Quak (10.1111/acer.12651-BIB0034|acer12651-cit-0034) 2014; 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Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites... Activation of the kynurenine pathway of tryptophan metabolism results in increased production of potentially depressogenic tryptophan catabolites and a... |
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| SubjectTerms | Adult Alcohol Alcohol-Related Disorders - blood Alcohol-Related Disorders - diagnosis Alcohol-Related Disorders - epidemiology Biomarkers - blood Comorbidity Cross-Sectional Studies Depression Depression - blood Depression - diagnosis Depression - epidemiology Female Humans Kynurenine - blood Kynurenine Pathway Male Middle Aged Nepal - epidemiology Treatment Outcome Tryptophan - blood Tryptophan - metabolism Young Adult |
| Title | The Relationship of Alcohol Use Disorders and Depressive Symptoms to Tryptophan Metabolism: Cross-Sectional Data from a Nepalese Alcohol Treatment Sample |
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