Nutritional and Lifestyle Therapy for NAFLD in People with HIV
Nutrients · 5 authors, 5 centres
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This narrative review examines nutritional and lifestyle therapies for nonalcoholic fatty liver disease (NAFLD) in people with HIV (PWH), finding that NAFLD affects 13–65% of PWH and is often more severe than in the general population. Key findings include that fatty acid imbalances are linked to hepatic steatosis in PWH, vitamin E shows efficacy for NASH in this population, and coffee consumption is associated with reduced liver fibrosis in HIV/HCV coinfection. With no FDA-approved pharmacotherapies for NAFLD in PWH and most drug trials excluding this group, lifestyle intervention—including a 7–10% weight loss target for overweight/obese patients and 3–5% for lean individuals—remains the cornerstone of treatment.
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**Background:** NAFLD is the leading cause of liver disease worldwide, affecting 25–30% of the global population. In people with HIV (PWH), NAFLD prevalence ranges from 13–65%, with two meta-analyses reporting approximately 35% prevalence in HIV mono-infected patients. NAFLD is not only more common but also more severe in PWH, with pooled prevalences of biopsy-proven NASH and significant liver fibrosis of up to 49% and 23%, respectively. Pathogenesis in PWH involves classic metabolic risk factors plus unique determinants including HIV chronic inflammation and lifelong exposure to antiretroviral therapy, particularly older nucleoside reverse transcriptase inhibitors and ritonavir-boosted protease inhibitors. Currently, no NASH-targeted therapies have been FDA-approved, making lifestyle intervention the cornerstone of treatment.
**Methods:** This narrative review conducted a comprehensive literature search using PubMed for peer-reviewed articles from 1996 to February 2023. Search terms matched 'Non-alcoholic fatty liver disease' or 'Non-alcoholic steatohepatitis' with 'HIV' or 'HIV infection' and related terms including nutrition, diet, carbohydrates, lipids, fatty acids, proteins, vitamins, alcohol, coffee, cannabinoids, food insecurity, lifestyle, exercise, physical activity, lean NAFLD, and gut microbiota. Only English-language papers were included.
**Key Results:** Regarding macronutrients, a Brazilian cross-sectional study of 451 PWH found that high fat intake was associated with 91% higher odds of NAFLD, while moderate monounsaturated fatty acid intake was associated with lower odds of NAFLD and liver fibrosis. Moderate fiber intake was also associated with lower odds of NAFLD. A Canadian study comparing 20 PWH with NAFLD to 21 HIV-negative NAFLD subjects found that PWH had higher hepatic n-6/n-3 ratios and lower dietary intake of n-3 polyunsaturated fatty acids. For alcohol, a Danish cross-sectional study of 453 PWH found that moderate alcohol consumption (<14 units/week for men, <7 for women) was associated with lower odds of moderate-to-severe hepatic steatosis. Coffee studies from the ANRS CO13 HEPAVIH cohort showed that high coffee intake (≥3 cups/day) was associated with a 50% reduction in all-cause mortality risk and lower prevalence of advanced liver fibrosis in HIV/HCV coinfected patients. For micronutrients, a Canadian open-label trial of 27 PWH with NASH found that vitamin E 800 IU/day for 24 weeks improved liver inflammation, steatosis (CAP −22 dB/m), and hepatocyte apoptosis (cytokeratin 18 −123 U/L) with a good safety profile. Vitamin D deficiency was associated with NAFLD with liver fibrosis in a cross-sectional study of 707 PWH (OR 1.94, 95% CI 1.18–3.24). Regarding lifestyle interventions, a Portuguese randomized trial of 55 PWH with NAFLD allocated to Mediterranean diet-based intervention showed significant weight loss (−1.5 kg vs. +0.65 kg, p < 0.001) compared to standard of care after 5 months. Pharmacotherapy trials showed that tesamorelin reduced hepatic fat content by 37% and prevented liver fibrosis progression (10.5% vs. 37.5%, p = 0.04) in 61 PWH, while pioglitazone reduced CAP by −23.5 dB/m (p < 0.001) in 98 PWH. Aramchol and maraviroc showed no significant benefit. Food insecurity was identified as an independent predictor of higher mortality in NAFLD and was linked to increased odds of NAFLD and liver fibrosis in PWH.
**Clinical Implications:** Lifestyle intervention remains the cornerstone of NAFLD treatment in PWH, with weight loss targets of 7–10% for overweight/obese patients and 3–5% for lean individuals. PWH with NAFLD should avoid diets rich in saturated fatty acids, refined carbohydrates, fructose-added beverages, and red processed meat. Vitamin E is a viable short-term option for NASH in PWH. Coffee consumption appears beneficial for liver fibrosis, though data are primarily from HIV/HCV coinfected cohorts. Food insecurity must be addressed as a social determinant of liver health. The exclusion of PWH from most NASH drug trials represents an ethical concern that needs to be addressed through more inclusive trial designs.