Effects of Sex, Drinking History, and Omega-3 and Omega-6 Fatty Acids Dysregulation on the Onset of Liver Injury in Very Heavy Drinking Alcohol-Dependent Patients.
Study Goal
The researchers aimed to evaluate the association of heavy alcohol consumption with changes in Omega-6 and Omega-3 fatty acid levels and their inflammatory effects in alcohol-dependent patients without clinical liver injury.
Results Summary
The study found a pro-inflammatory shift in the Omega-6:Omega-3 ratio, particularly in females with mild liver injury, and noted sex-based differences in fatty acid responses to heavy drinking. Males showed increased DHA and EPA levels, while females had lower DHA and no comparable rise in EPA.
Population
114 heavy-drinking alcohol-dependent patients (aged 21-65) without clinical liver injury, grouped by ALT levels.
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
heavy alcohol consumption | increase | liver inflammation/injury | - | - | causes | #1 |
heavy alcohol consumption | increase | elevated ALT and aspartate aminotransferase (AST) | alcohol-dependent (AD) patients without clinical manifestations of liver injury | - | showed close association with | #2 |
heavy alcohol consumption | increase | AST level | females with mild biochemical liver injury (GR.2) | - | showed significantly higher | #3 |
heavy alcohol consumption | increase | AST and total drinks in past 90 days (TD90) | females | - | showed significant association of | #4 |
heavy alcohol consumption | increase | AST and heavy drinking days in past 90 days (HDD90) | males | - | showed significant association of | #5 |
heavy alcohol consumption | increase | ω-6:ω-3 ratio | females with mild liver injury (GR.2) | - | showed a significant pro-inflammatory response | #6 |
heavy alcohol consumption | increase | Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) | males with liver injury | - | were increased | #7 |
heavy alcohol consumption | no change | EPA | females | - | did not show any comparable rise | #8 |
heavy alcohol consumption | decrease | DHA levels | females | - | were lower | #9 |
heavy alcohol consumption | increase | liver injury | - | - | predicted changes in | #10 |
heavy alcohol consumption | increase | ω-3 and ω-6 FA levels and the ω-6:ω-3 ratio | patients with biochemical liver injury | - | showed a pro-inflammatory shift | #11 |
heavy alcohol consumption | increase | liver inflammation/injury | - | - | may represent one mechanism for | #12 |
BACKGROUND: Heavy alcohol consumption frequently causes liver inflammation/injury, and certain fatty acids (FAs) may be involved in this liver pathology. In this study, we evaluated the association of heavy drinking and the changes in the FA levels involved in the ω-6 (pro-inflammatory) and ω-3 (anti-inflammatory) state in alcohol-dependent (AD) patients who had no clinical manifestations of liver injury. We aimed to identify sex-based differences in patients with mild or no biochemical evidence of liver injury induced by heavy drinking. METHODS: A total of 114 heavy drinking AD female and male patients aged 21 to 65 years without clinical manifestations of liver injury, who were admitted to an alcohol dependence treatment program, were grouped by the alanine aminotransferase (ALT) levels: ≤40 IU/l, as no liver injury (GR.1), and >40 IU/l, as mild liver injury (GR.2). Patients were actively drinking until the day of admission. Comprehensive metabolic panel, comprehensive FA panel, and drinking history data were evaluated. RESULTS: Elevated ALT and aspartate aminotransferase (AST) showed close association with markers of heavy alcohol intake. In the patients with mild biochemical liver injury (GR.2), females showed significantly higher AST level than males. Significant association of AST and total drinks in past 90 days (TD90) in females, and AST and heavy drinking days in past 90 days (HDD90) in males was observed. The ω-6:ω-3 ratio showed a significant pro-inflammatory response only in females with mild liver injury (GR.2) when adjusted by drinking history marker, TD90. Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were increased in males with liver injury, while females did not show any comparable rise in EPA; and DHA levels were lower. CONCLUSIONS: Measures of heavy drinking, TD90 and HDD90, predicted changes in liver injury. Changes in the ω-3 and ω-6 FA levels and the ω-6:ω-3 ratio showed a pro-inflammatory shift in patients with biochemical liver injury with a significant effect in females. Changes in FAs involved in the inflammatory state may represent one mechanism for liver inflammation/injury in response to heavy alcohol drinking.