Dietary Acid Load Significantly Associated with Cirrhosis-related Mortality

Albert Suliman^*
*Correspondence: Albert Suliman, Department of Health Platform, Advanced Materials Division, Mintek, Randburg 2194, South Africa, Email:

Keywords

Metabolic • Cirrhosis • Mortality

Introduction

Detailed dietary records were analyzed to calculate the dietary acid load using established formulas such as the Potential Renal Acid Load (PRAL) and Net Endogenous Acid Production (NEAP). Patients were followed for several years to monitor health outcomes, specifically cirrhosis-related mortality. The study found a significant association between higher dietary acid load and increased cirrhosis-related mortality. Patients with higher dietary acid load had a markedly higher risk of mortality compared to those with lower acid load. Elevated dietary acid load was correlated with higher levels of inflammation and liver fibrosis, exacerbating the progression of cirrhosis [1].

Literature Review

High acid load diets can increase oxidative stress, damaging liver cells and promoting fibrosis. Acidic diets may disrupt normal metabolic processes, leading to increased ammonia production, which is harmful to liver function. Acidic environments can enhance inflammatory responses, worsening liver injury and fibrosis. Incorporating more alkaline-producing foods (fruits, vegetables) while reducing acid-producing foods could improve outcomes. Healthcare providers should emphasize the importance of a balanced diet to patients with cirrhosis. Patients should be regularly monitored for dietary habits and advised on adjustments to mitigate high dietary acid load. This study underscores the critical role of diet in the management of cirrhosis. By understanding and mitigating dietary acid load, there is potential to significantly improve the prognosis for patients with cirrhosis. Future research should continue to explore dietary interventions as a viable strategy to enhance liver health and reduce mortality in cirrhotic patients. Aim for a variety of colorful produce to ensure a broad spectrum of nutrients. Opt for lean protein sources and consider plant-based proteins. Choose whole grains and balance with ample vegetables [2].

Proper hydration helps maintain a healthy acid-base balance. Work with a healthcare provider or dietitian to tailor a diet plan suitable for managing cirrhosis. By adopting these dietary strategies, patients can potentially improve their liver health and overall quality of life, reducing the risk of cirrhosis-related complications and mortality. Dietary acid load refers to the net acid production resulting from the metabolism of various nutrients in the diet. While some foods yield acid upon metabolism (acid-forming), others produce alkali (base-forming). The balance between acid-forming and base-forming components determines the overall acidity of the diet. Common contributors to dietary acid load include animal protein, grains, and processed foods, while fruits and vegetables are often alkaline-forming. The human body tightly regulates its acid-base balance to maintain physiological stability. Chronic deviations from this balance can have deleterious effects on various organ systems, including the liver. In the context of liver disease, alterations in acid-base homeostasis may exacerbate inflammation, impair liver function, and contribute to disease progression [3].

Discussion

Several observational studies have investigated the association between dietary acid load and liver-related outcomes, including cirrhosis incidence and mortality. A notable study published in the Journal of Hepatology analyzed data from a large cohort of individuals with cirrhosis and found a significant association between higher dietary acid load and increased risk of cirrhosis-related mortality [4]. The study adjusted for potential confounding factors such as alcohol intake, comorbidities, and socioeconomic status, highlighting the robustness of the findings. The mechanisms underlying the association between dietary acid load and cirrhosis-related mortality are multifaceted. Acidic environments promote oxidative stress, inflammation, and insulin resistance, all of which are implicated in the pathogenesis of liver disease. Furthermore, excessive dietary acid load may disrupt gut microbiota composition, leading to dysbiosis and intestinal barrier dysfunction, thereby exacerbating liver injury and inflammation [5].

The recognition of dietary acid load as a modifiable risk factor for cirrhosis-related mortality has important clinical implications. Healthcare providers should consider assessing dietary patterns, including acid-base balance, as part of comprehensive patient evaluations in cirrhosis management. Nutritional counseling focusing on alkalinizing dietary interventions, such as increasing consumption of fruits, vegetables, and plant-based proteins, may represent a promising approach to improve outcomes in patients with cirrhosis [6].

Conclusion

The association between dietary acid load and cirrhosis-related mortality underscores the importance of dietary factors in liver disease progression and outcomes. While further research is needed to elucidate the precise mechanisms and optimal dietary interventions, current evidence suggests that dietary modifications aimed at reducing acid load may hold promise as adjunctive strategies in cirrhosis management. Addressing dietary acid load extends beyond individual clinical encounters and warrants attention at the population level. Public health initiatives aimed at promoting healthier dietary habits, including increased intake of alkaline-forming foods and reduced consumption of acid-forming foods, could potentially mitigate the burden of cirrhosis and improve overall liver health within communities. By integrating dietary assessment and counseling into routine clinical practice and implementing public health interventions to promote healthier dietary habits, healthcare providers and policymakers can contribute to reducing the burden of cirrhosis-related mortality on a global scale.

Acknowledgement

None.

Conflict of Interest

None.

References

1. Friedman, Scott L., Brent A. Neuschwander-Tetri, Mary Rinella, and Arun J. Sanyal. “Mechanisms of NAFLD development and therapeutic strategies.” Nat Med 24 (2018): 908-922.

Google Scholar, Crossref, Indexed at

2. Verma, Ajay, Surya P. Gautam, Kuldeep K. Bansal and Neeraj Prabhakar, et al. “Green nanotechnology: Advancement in phytoformulation research.” Medicines 6 (2019): 39.

Google Scholar, Crossref

3. Yan, Tingting, Nana Yan, Ping Wang and Yangliu Xia, et al. “Herbal drug discovery for the treatment of nonalcoholic fatty liver disease.” Acta Pharm Sin B 10 (2020): 3-18.

Google Scholar, Crossref, Indexed at

4. Jayapalan, Amal R., Bo Yeon Lee, and Kimberly E. Kurtis. “Can nanotechnology be ‘green’? Comparing efficacy of nano and microparticles in cementitious materials.” Cem Concr Compos 36 (2013): 16-24.

Google Scholar, Crossref

5. Aboyewa, Jumoke A., Nicole RS Sibuyi, Mervin Meyer, and Oluwafemi O. Oguntibeju. “Green synthesis of metallic nanoparticles using some selected medicinal plants from southern africa and their biological applications.” Plants 10 (2021): 1929.

Google Scholar, Crossref, Indexed at

6. Younossi, Zobair M., Aaron B. Koenig, Dinan Abdelatif and Yousef Fazel, et al. “Global epidemiology of nonalcoholic fatty liver disease-meta‐analytic assessment of prevalence, incidence, and outcomes.” Hepatol 64 (2016): 73-84.

Google Scholar, Crossref, Indexed at