Exacerbation of Hangover Symptomology Significantly Corresponds with Heavy and Chronic Alcohol Drinking: A Pilot Study

Vatsalya, Vatsalya; Hassan, Hamza; Kong, Maiying; Stangl, B; Schwandt, Melanie L.; Schmidt-Teron, Veronica Y; Verster, Joris C.; Ramchandani, Vijay A.; McClain, Craig J.

doi:10.3390/jcm8111943

Cited by 10 publications

(10 citation statements)

References 32 publications

(36 reference statements)

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“…Heavy alcohol drinking has been well characterized by the recent drinking history using Timeline Followback (TLFB) for past 90 days in AUD patients in recent research on AUD. 18 , 19 These markers have also been tested on AUD patient cohorts who also exhibited other forms of addiction such as cocaine, pathophysiological or behavioral symptomology including depression. 20 - 22 Heavy drinking markers derived from TLFB do not only characterize the drinking behavior, consequences, and pathological course but are also highly useful as therapeutic targets of treatment efficacy.…”

Section: Introductionmentioning

confidence: 99%

Interaction of Heavy Drinking Patterns and Depression Severity Predicts Efficacy of Quetiapine Fumarate XR in Lowering Alcohol Intake in Alcohol Use Disorder Patients

et al. 2020

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Background: Shared etiological pathways of dopamine and serotonin neurotransmission play a central role in heavy alcohol intake and exacerbation in the symptoms of depression. We investigated the treatment efficacy of Quetiapine fumarate extended release (XR) in lowering alcohol intake in alcohol use disorder (AUD) patients indicated by the shared alleviation of depression ratings and patterns of heavy drinking. Methods: Hundred and eight male and female heavy drinking AUD patients in the age range of 18 to 64 years. participated in a randomized clinical trial (RCT) to receive 12 weeks of quetiapine XR or placebo (N = 115). Participants were sub-grouped by the severity grading of depression using Montgomery-Asberg Depression Rating Scale (MADRS) (clinically relevant ⩾8 [CR], clinically non-relevant ⩽7 [CNR]) at baseline in both the groups. Drinking history and depression ratings were assessed at the patients’ visits. Results: Heavy drinking days (HDD) and total drinks (TD) were significantly fewer in CR patients at the treatment end. A true positive response in AUROC analysis supported the lowering of TD in CR patients. The number of drinking days (NDD) and average drinks per drinking day (AvgD) were lower in the CNR patients at treatment-end. Significant associations with increasing effect sizes were observed for all the heavy drinking measures (HDD, TD, NDD, and AvgD) and MADRS scores by the end of the treatment course. Conclusions: Baseline elevated depressive symptoms could likely predict the course of heavy alcohol drinking during the treatment, and efficacy outcome of a treatment. AUD patients with baseline clinically significant depression had a progressive lowering in heavy drinking markers significantly corresponding to the lowering of depression symptoms by the end of treatment with Quetiapine fumarate XR. ClinicalTrials.gov: NCT#0049862 ( https://clinicaltrials.gov/ct2/show/NCT00498628?term=litten&draw=2&rank=3 )

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Section: Introductionmentioning

confidence: 99%

Interaction of Heavy Drinking Patterns and Depression Severity Predicts Efficacy of Quetiapine Fumarate XR in Lowering Alcohol Intake in Alcohol Use Disorder Patients

et al. 2020

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“…Its role was also significant in the association analyses for deficient ω3 PUFAs and low zinc. e connection of specific markers of heavy drinking with the exacerbation of metabolic dysregulation in liver injury has been recently highlighted [35].…”

Section: Discussionmentioning

confidence: 99%

Dysregulation in Plasma ω3 Fatty Acids Concentration and Serum Zinc in Heavy Alcohol-Drinking HCV Patients

Vatsalya

Agrawal

Frimodig

et al. 2020

Advances in Virology

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Alcohol use disorder (AUD) patients comorbid with hepatitis C virus (HCV) infection (HCV + AUD) could have progressively severe clinical sequels of liver injury and inflammation. Serum zinc and several polyunsaturated fatty acids (PUFAs) get dysregulated in AUD as well as HCV. However, the extent of dysregulation of PUFAs and zinc deficiency and their interaction in HCV + AUD as a comorbid pathology has not been studied. We examined the role of dysregulation of FAs and low zinc in HCV + AUD patients. 138 male and female participants aged 21–67 years were grouped as HCV-only (Gr. 1; n = 13), HCV + AUD (Gr. 2; n = 25), AUD without liver injury (Gr. 3; n = 37), AUD with liver injury (Gr. 4; n = 51), and healthy volunteers (Gr. 5 or HV; n = 12). Drinking history, individual demographic measures, fasting fatty acids, liver function, and zinc were measured and analyzed. HCV + AUD patients showed the highest ALT level compared to the rest of the groups. Serum zinc concentrations were the lowest, and the proinflammatory shift was the highest (characterized by ω6 : ω3 ratio) in the HCV + AUD patients. Total ω3, eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) were the lowest in HCV + AUD patients. Total ω3, α-linoleic acid (α-LA) along with covariable number of drinking days past 90 days (NDD90), eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) independently showed significant association with low zinc in the HCV + AUD patients. Heavy drinking pattern showed that NDD90 has a significant mediating role in the representation of the relationship between candidate ω3 PUFAs and zinc uniquely in the HCV + AUD patients. Low serum zinc showed a distinctively stronger association with total and candidate ω3s in the HCV + AUD patients compared to the patients with HCV or AUD alone, supporting dual mechanism involved in the exacerbation of the proinflammatory response in this comorbid cohort. This trial is registered with NCT#00001673.

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“…Thus, understanding the gut-brain axis in the pathology of AUD and its therapy is important. Chronic and heavy drinking, [17][18][19] as well as frequent episodes of relapse [20][21][22] observed in AUD, limit the efficacy of treatment 23,24 . Alcohol withdrawal is an essential feature of AUD that could predict the rate and frequency of relapse 25 .…”

Section: Introductionmentioning

confidence: 99%

Illustration of a Novel Gut-Brain Axis of Alcohol Withdrawal, Withdrawal-Associated Depression, Craving and Alcohol-Severity Index in Alcohol Use Disorder Patients

Vatsalya

Ranganathan

Verster

et al. 2022

Preprint

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Pathways underlying the gut-brain axis and pro-inflammatory cytokine production influence brain functions and behavior. Alcohol use disorder (AUD) patients exhibit domains such as alcohol withdrawal, depression, and craving; and the gut-immune response may play a significant role in these domains of AUD. This study examined the role of intestinal permeability, pro-inflammatory cytokines, and hormones levels on the domains of AUD.Forty-eight AUD patients [male (n=34) and female (n=14)] aged 23-63 yrs. were grouped categorically using the Clinical Institute Withdrawal Assessment of alcohol scale (CIWA) as either clinically significant CIWA group (CS-CIWA [score>10] Gr.1 [n=22]), and clinically not-significant group (NCS-CIWA [score≤10] Gr.2 [n=26]). A sub-set of 13 AUD patient were also tested for reward response for drug-seeking using Penn-Alcohol Craving Score (PACS). Clinical data and blood samples were collected upon enrollment. Blood samples were analyzed for pro-inflammatory cytokines, and hormones, and markers of intestinal permeability. CIWA, 90-day timeline followback (TLFB90), and lifetime drinking history (LTDH) were also collected for comparison.As expected, recent and chronic heavy drinking were significantly higher in Gr.1: HDD90 (heavy drinking days), NDD90 (number of drinking days), as was LTDH, especially in Gr.1 females. Further, in Gr.1, adiponectin (associated with withdrawal) was significantly higher; and numerically higher levels of lipopolysaccharide (LPS) and LPS-binding protein (LBP) were also reported. Gr.1 patients exhibited higher effects of association on the withdrawal-associated depression domain for the parameters of LPS, sCD14, IL-6 and IL-8. Leptin also showed a significantly high effect of association with HDD90 in those AUD patients with craving. The craving domain (assessed by PACS, Penn-Alcohol Craving Scale) could be described as a gut-immune-brain model by the gut-dysregulation (LBP and Leptin) markers, and specific pro-inflammatory activity (IL-1β and TNF-α). Such pathway model describes the heavy drinking phenotype, HDD90 with even higher effects (R2=0.955, p=0.006) in the AUD patients who had higher ratings for craving (PACS>5).Interaction of gut-dysfunction, cytokines involved in both inflammation and in mediating-chemotactic activity constitute a novel pathophysiological gut-brain axis for withdrawal, and alcohol-associated depression and craving domains of AUD. AUD patient with higher craving show higher reinforcing effects of the gut-brain axis response for heavy drinking.

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Exacerbation of Hangover Symptomology Significantly Corresponds with Heavy and Chronic Alcohol Drinking: A Pilot Study

Cited by 10 publications

References 32 publications

Interaction of Heavy Drinking Patterns and Depression Severity Predicts Efficacy of Quetiapine Fumarate XR in Lowering Alcohol Intake in Alcohol Use Disorder Patients

Interaction of Heavy Drinking Patterns and Depression Severity Predicts Efficacy of Quetiapine Fumarate XR in Lowering Alcohol Intake in Alcohol Use Disorder Patients

Dysregulation in Plasma ω3 Fatty Acids Concentration and Serum Zinc in Heavy Alcohol-Drinking HCV Patients

Illustration of a Novel Gut-Brain Axis of Alcohol Withdrawal, Withdrawal-Associated Depression, Craving and Alcohol-Severity Index in Alcohol Use Disorder Patients

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