Dietary intervention as a therapeutic tool in Non-Alcoholic Fatty Liver Disease: A case-based approach

Dietary intervention as a therapeutic tool in Non-Alcoholic Fatty Liver Disease: A case-based approach | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Dietary intervention as a therapeutic tool in Non-Alcoholic Fatty Liver Disease: A case-based approach W.M.S. Pushpakumara, R.A.M.D. Ranathunga, J.F. Zimra, M.S.H.Banu This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6981390/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Introduction: Non Alcoholic Fatty Liver disease (NAFLD) is a spectrum of liver disorders which is characterized by excessive fat accumulation in the liver that ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), and NASH may develop up to hepatocellular carcinoma. NAFLD is the most common liver disease in the world. Since NAFLD is associated with many risk factors including obesity, metabolic syndrome, insulin resistance and diabetes, weight loss and dietary management are proven supportive therapies in NAFLD management. Therefore this study aimed Case: A 35-year-old obese male garment industry worker presented with left abdominal pain, frothy urine, and fatigue. Clinical and dietary assessments revealed central adiposity, sedentary lifestyle, and high intake of refined carbohydrates and saturated fats with minimal fruits, vegetables, and fiber. Biochemical findings indicated dyslipidemia (TG: 154 mg/dL, HDL: 34 mg/dL, LDL: 134 mg/dL), elevated ALT (58 U/L), and grade II fatty liver on imaging. A calorie-restricted, macronutrient-balanced diet (1500 kcal/day: 50% carbs, 30% fat, 20% protein) with nutrition counseling was initiated to promote weight loss and improve liver and lipid profiles. After 2 months, the patient showed significant improvements: weight reduced from 95.1 kg to 91.8 kg, BMI from 30.2 to 29.1 kg/m², and waist circumference from 103 cm to 99 cm. Biochemical parameters improved with ALT decreasing to 39 U/L, HDL increasing to 41 mg/dL, and LDL, VLDL, and triglycerides all moving closer to recommended levels. These outcomes demonstrate that personalized dietary interventions can effectively reduce hepatic steatosis and correct lipid abnormalities, highlighting the importance of early nutrition management in non-alcoholic fatty liver disease (NAFLD). Conclusion: The study concludes that individualized dietary interventions, including weight reduction and evidence-based dietary modifications—such as adequate hydration, replacement of low-quality nutrient sources with nutrient-dense alternatives, and adherence to a balanced diet—are effective in the management of non-alcoholic fatty liver disease (NAFLD), as evidenced by improvements in liver enzyme levels and overall lipid profile. Nutrition & Dietetics NAFLD Obesity Nutrition assessment Dietary management Introduction Obesity-driven metabolic dysfunction has re-branded non-alcoholic fatty liver disease (NAFLD) as metabolic dysfunction-associated steatotic liver disease (MASLD), reflecting its tight coupling to global surges in adiposity and type 2 diabetes (Allen et al., 2024 ). Excess adipose tissue delivers a continuous flux of free fatty acids to the liver, amplifies de novo lipogenesis via insulin-resistant hyperinsulinaemia, and suppresses very-low-density-lipoprotein export. Together these processes saturate hepatocellular triglyceride-handling capacity, initiating lipotoxic stress that can progress from simple steatosis to steatohepatitis and fibrosis. Contemporary European guidelines emphasise that each kilogram of sustained weight gain further accelerates this trajectory, whereas 7–10% weight loss can reverse it (Esler and Cohen, 2024 ). Serum alanine- and aspartate-aminotransferase (ALT, AST) remain the most accessible biochemical sentinels of hepatocellular injury; elevations usually track with histological activity, although normal values do not exclude disease. Gamma-glutamyl-transferase, fasting insulin, HOMA-IR, and atherogenic lipid profiles often rise in parallel, mirroring the systemic insulin resistance that both triggers and perpetuates hepatic fat accumulation (Bril et al., 2020). Obesity’s chronic, low-grade inflammatory milieu—characterised by increased C-reactive protein, interleukin-6, tumour-necrosis-factor-α, and pro-inflammatory adipokines—further aggravates steatotic hepatocytes, drives Kupffer-cell activation, and fuels fibrogenesis. These circulating markers therefore provide additional prognostic insight and underscore why MASLD is now viewed as a liver-centred component of a whole-body inflammatory syndrome (Vlad TARU et al., 2024 ). Management still begins with intensive lifestyle therapy: hypocaloric Mediterranean-style diets, progressive aerobic-plus-resistance training, and behavioural support that together target ≥ 7% weight loss. When cardiometabolic comorbidities demand pharmacological help, agents chosen primarily for glycaemic or lipid control—e.g., GLP-1 receptor agonists, SGLT2 inhibitors, pioglitazone—offer collateral hepatic benefit; obeticholic acid, an FXR agonist, is the first drug authorised for NASH with fibrosis but requires careful monitoring. Bariatric surgery delivers the most durable histological improvement in eligible patients, and liver transplantation remains the rescue option for decompensated cirrhosis. Importantly, no medication obviates the need to correct the underlying obesogenic environment, so long-term success depends on sustained lifestyle and risk-factor modification (Basil et al., 2024 ). Case A 35-year-old male quality supervisor from the garment industry presented with left-sided abdominal pain, frothy urine, and generalized fatigue. He had no prior history of chronic illness or family history of metabolic disorders. Anthropometric examination indicated obesity (BMI-30.2 kg/m²) and central adiposity (waist circumference-103 cm). He reported a sedentary lifestyle and dietary patterns that included frequent consumption of refined carbohydrates, fried foods, coconut milk, and minimal fruit and vegetable intake. Clinical and Biochemical Assessment Biochemical analysis confirmed the presence of dyslipidemia (Triglycerides: 154 mg/dl, HDL: 34 mg/dl, LDL: 134 mg/dl, VLDL: 31 mg/dl) and elevated liver enzyme levels (ALT: 58 U/L). Imaging studies revealed grade II fatty liver changes. A comprehensive nutrition assessment identified high carbohydrate and saturated fat intake, minimal dietary fiber, and no structured physical activity. Dietary assessment Dietary evaluation via dietary recall revealed several nutrition-relevant behaviours that may adversely affect metabolic health. The participant habitually eats dinner away from home at least three times per week, primarily selecting quick-service or fast-food outlets, thereby increasing exposure to energy-dense, nutrient-poor meals. At home, dietary variety is limited: the respondent routinely classifies potato or dhal as the sole “vegetable” serving at both breakfast and lunch, which are themselves obtained from the company buffet and therefore largely outside personal control. Household use of coconut products is substantial—approximately one whole coconut is blended each day for milk—contributing considerable saturated fat to the diet. Fruit intake is markedly inadequate, with no daily consumption reported, and there are no snacks between main meals that might otherwise supply additional micronutrients or fibre. Alcohol is abstained from entirely, yet there is also an absence of planned physical activity, underscoring a sedentary lifestyle that, combined with the aforementioned dietary patterns, may potentiate dyslipidaemia, weight gain, and non-alcoholic fatty liver disease. Nutritional diagnosis The nutritional assessment indicates multiple interrelated metabolic concerns primarily driven by dietary and lifestyle behaviors. Hepatic fat accumulation appears to be associated with excessive energy intake and reduced energy expenditure, as evidenced by the individual's dietary pattern and sedentary lifestyle history. Additionally, elevated plasma triglyceride levels are likely attributable to excessive carbohydrate consumption, particularly from refined sources, as revealed through detailed dietary assessment. The presence of high plasma LDL and VLDL concentrations may be linked to a diet high in saturated fats and low in dietary fiber, further supporting the role of poor dietary quality in lipid abnormalities. Moreover, excess adiposity, reflected in anthropometric measurements, is consistent with chronic energy imbalance—specifically, high caloric intake coupled with insufficient physical activity. Collectively, these findings underscore the critical role of dietary composition and physical inactivity in the development of metabolic disturbances such as dyslipidemia and hepatic steatosis. Nutritional Management Hepatocyte regeneration and the healing of liver disease begin with appropriate nutritional management from the initial stage of diagnosis. Early nutritional intervention significantly reduces the adverse effects caused by impaired nutrient metabolism associated with liver dysfunction. Additionally, through proper dietary management of dyslipidemia, ectopic fat accumulation and cardiovascular diseases can be prevented by decreasing low-density lipoprotein (LDL) levels and improving high-density lipoprotein (HDL) levels. The primary goals of medical nutrition therapy for patients with liver disease include weight reduction, maintaining normal blood glucose levels, achieving normal ranges of liver enzymes, and stabilizing the lipid profile within recommended limits. These objectives may vary depending on the stage and severity of the disease, and often require integration with medical management to support effective lifestyle modifications. Among these goals, weight reduction should be prioritized. A weight loss of 7% to 10% has been associated with reduced liver fat content and significant improvements in liver fibrosis (Miller and Henry, 2019). Furthermore, non-alcoholic steatohepatitis (NASH) has been found to occur at higher rates in obese individuals compared to those with lean body mass (Quek et al., 2023). Implementing a low-fat, hypocaloric diet that provides approximately 750 kcal/day less than the patient's daily requirement has shown promising results, including a reduction in fibrosis score by at least one point in patients who presented with baseline fibrosis (Vilar-Gomea et al., 2015). Improving insulin sensitivity is another key nutritional objective. In patients with non-alcoholic fatty liver disease (NAFLD), insulin resistance promotes gluconeogenesis through two main mechanisms: by increasing adipocyte lipolysis and circulating fatty acid levels, and by reducing hepatic glycogen storage capacity (Chen et al., 2017). Addressing these metabolic disruptions through tailored dietary strategies is essential for mitigating disease progression and improving overall liver health. Dietary Intervention Plan The patient underwent a calorie-restricted, macronutrient-balanced dietary plan designed to induce weight loss of approximately 0.5–1 kg per week. Daily caloric intake was limited to 1500 kcal/day with a macronutrient split of approximately 50% carbohydrates, 30% fats (with <10% saturated fats), and 20% protein. High-fiber foods, low-glycemic index carbohydrates, unsaturated fats, and lean protein sources were emphasized. Nutritional counseling sessions were conducted twice weekly, and meals were supervised during hospitalization. Considering the macro nutrient compositions to achieve the medical nutrition therapy goals, of non-alcoholic fatty liver patients, Kargulewicz et al., 2014 have given the dietary recommendations as follows: Personalized Diet Plan Calorie – 1500 kcal Carbohydrate – 50%; (1500 kcal * 0.5) / (4 kcal/g) = 187.5 g Fat – 30%; (1500 * 0.3) / (9 kcal/g) = 50 g Protein – 20% (1500 * 0.2) / (4 kcal/g) = 75 g Food Exchange List Table1: food exchange list for personalized diet plan Food Group Exchanges Carbohydrate (g) Fat (g) Protein (g) Energy (kcal) Milk, skimmed 2 24 0.4 14 155.6 Pulses 2 30 1 14 185 Non-starchy vegetables 6 18 - 4 88 Fruit 1 15 - - 60 Sugar 2 10 - - 40 Starch 7 105 3.5 21 535.5 Protein 3 - 9 21 165 Coconut 1 - 20 - 180 Oil 2 - 10 - 90 Total 202 43.9 74 1499.1 Percentages 54% 26% 20% Pre- and Post-Intervention Clinical Parameters Over the course of the hospital stay anthropometric and biochemical parameters were monitored after 2 months. No pharmacological agents targeting liver enzymes or lipids were introduced during the study period to isolate the dietary effect. Table 2 - Baseline and follow-up assessment of the patient Parameter Baseline (Day 0) Follow-up (Afetr 2 months) Reference Range Weight (kg) 95.1 91.8 - BMI (kg/m²) 30.2 29.1 18.5 – 24.9 Waist Circumference (cm) 103 99 <90 (Asian males) ALT (U/L) 58 39 <45 AST (U/L) 27 25 <40 Triglycerides (mg/dL) 154 129 40 LDL (mg/dL) 134 110 <130 VLDL (mg/dL) 31 23 <30 Total Cholesterol / HDL Ratio 5.9 4.3 <5 Discussion Grade 2 fatty liver—now classified as moderate metabolic-dysfunction-associated steatotic liver disease (MASLD)—is considered a reversible stage as long as intensive lifestyle therapy is initiated early. Contemporary society guidelines from both Europe (EASL–EASD–EASO, 2024) and the United States (AASLD update, 2023) position personalised nutrition, intentional weight loss and exercise as first-line treatment, ahead of, and complementary to, any pharmacotherapy. These documents emphasise that dietary counselling should aim not only to normalise aminotransferases but also to mitigate future cardiovascular and oncologic risk, which together account for most MASLD-related mortality (Tack et al., 2024 ). Energy restriction sufficient to produce a sustained 7–10% reduction in body weight remains the single most powerful intervention for improving hepatic steatosis and even regressing early fibrosis. A 2025 narrative review pooling recent clinical trials found that every additional percentage point of weight lost translated into incremental improvements in liver fat, with resolution of steatohepatitis often achieved once the 10% threshold was crossed. Conversely, crash diets producing rapid, unstructured losses are discouraged because they are rarely maintained, can exacerbate ketone production and have been linked to transient rises in bilirubin and worsening fibrosis in susceptible individuals (Takawy and Abdelmalek, 2025 ). In qualitative terms, a Mediterranean-style eating pattern—rich in vegetables, whole fruit, pulses, extra-virgin olive oil, nuts and oily fish—has repeatedly shown superiority over Western or convenience-food patterns for reducing intra-hepatic triglyceride content and improving insulin sensitivity, even without large calorie deficits. A longitudinal analysis of PREDIMED participants published in 2025 demonstrated significant reductions in the Hepatic Steatosis Index as adherence scores rose, and systematic reviews of randomised trials in both adults and children report parallel falls in ALT and γ-GT (Cueto-Galán et al., 2025 ). Within this pattern, fat quality matters. Substituting saturated and trans-fat-rich foods (processed meats, commercial bakery items, deep-fried snacks) with monounsaturated (olive, canola, avocado) and polyunsaturated (marine and certain plant oils) sources down-regulates de-novo lipogenesis and may favourably shift the LDL-to-HDL ratio. Both the European and American position statements explicitly endorse liberal use of unsaturated fats within total calorie targets (Rinella et al., 2023 ). Carbohydrate quality is equally critical. Fructose and sucrose delivered in sugar-sweetened beverages, confectionery and refined cereals drive hepatic de-novo lipogenesis and worsen insulin resistance; limiting these products is therefore strongly advised. Where a low-carbohydrate approach is preferred, short-term trials show quicker reductions in liver fat than iso-caloric low-fat diets, but after 12–24 month weight loss and biochemical outcomes converge, underscoring that sustainability and food quality trump macronutrient ratios. Whole-grain breads, legumes and low-glycaemic fruit remain the staple carbohydrate choices in most successful long-term regimens (Zelber-Sagi and Moore, 2024 ). Alcohol intake requires individualised counselling. For patients whose steatosis is purely metabolic, even light drinking (< 10 g day⁻¹) has been associated with faster fibrosis progression in cohort studies, and the 2024 EASL guidance therefore “discourages” alcohol altogether; for those with alcoholic fatty liver disease, total abstinence is mandatory (Tack et al., 2024 ). A 2023 Cedars-Sinai study suggested that minimal consumption may be tolerated in very mild disease, yet its findings have not altered consensus recommendations, which continue to prioritise abstinence until clear longitudinal safety data emerge (Zhu et al., 2024 ) Practical behaviour strategies—mindful portion control, three balanced meals spaced across the day to avoid large post-prandial glucose and lipid excursions, and replacing caloric beverages with plain water—help patients adhere to calorie goals and may confer independent metabolic benefits. A 2024 NHANES analysis showed that NAFLD participants in the highest quartile of plain-water intake had significantly lower all-cause mortality than low-intake peers, lending empirical support to the long-standing clinical advice to “drink mostly water.” (Zhao et al., 2024 ). Dietary management of Grade 2 fatty liver combines a modest, sustainable calorie deficit with a Mediterranean-leaning, low-sugar, unsaturated-fat-rich eating pattern, strict limits on alcohol, ample hydration and attention to behavioural factors that promote long-term adherence. When implemented alongside regular physical activity and optimisation of comorbidities, this strategy not only reverses hepatic fat accumulation but also addresses the cardio-metabolic milieu that drives disease progression. Continuous monitoring by a multidisciplinary team allows timely adjustment of nutrition targets and consideration of emerging pharmacotherapies when lifestyle measures alone do not halt fibrosis. Conclusion The study concludes that personalized dietary management including weight reduction and other evidence based diet related behaviour changes as proper hydration, substitution of low quality nutrient sources with high quality sources and management of a balanced diet in general supports the management of NAFLD by means of improving liver enzymes and total lipid profile. Declarations The patient involved in this clinical case study was fully informed about the purpose, content, and potential implications of the publication. Written informed consent was obtained from the patient, confirming their voluntary agreement to the inclusion and publication of relevant clinical details and data in the preprint. The patient was assured that their identity would be protected and that all information would be handled with strict confidentiality. Competing interests: The authors declare that they have no competing interests. Funding: Self-funded Acknowledgments: We thank the participant of this study. Author contributions: All authors have contributed to the manuscript through data collection, data analysis, and writing. References Allen, A.M., Pose, E., K. Rajender Reddy, Russo, M.W. and Kamath, P.S. (2024). Nonalcoholic Fatty Liver Disease Gets Renamed as Metabolic Dysfunction–Associated Steatotic Liver Disease: Progress But With Challenges. Gastroenterology , 166(2), pp.229–234. https://doi.org/10.1053/j.gastro.2023.11.007. Basil, B., Myke-Mbata, B.K., Eze, O.E. and Akubue, A.U. (2024). From adiposity to steatosis: metabolic dysfunction-associated steatotic liver disease, a hepatic expression of metabolic syndrome – current insights and future directions. Clinical Diabetes and Endocrinology , [online] 10(1). https://doi.org/10.1186/s40842-024-00187-4. ‌Bril, F., McPhaul, M.J., Caulfield, M.P., Clark, V.C., Soldevilla-Pico, C., Firpi-Morell, R.J., Lai, J., Shiffman, D., Rowland, C.M. and Cusi, K. (2020). Performance of Plasma Biomarkers and Diagnostic Panels for Nonalcoholic Steatohepatitis and Advanced Fibrosis in Patients With Type 2 Diabetes. Diabetes Care , [online] 43(2), pp.290–297. https://doi.org/10.2337/dc19-1071. Cueto-Galán, R., Fontalba-Navas, A., Gutiérrez-Bedmar, M., Ruiz-Canela, M., Martínez-González, M.A., Alves, L., Babio, N., Montserrat Fitó, Ros, E., Fiol, M., Ramón Estruch, Arós, F., Serra-Majem, L., Pintó, X., Muñoz-Bravo, C., García-Rodríguez, A. and Gómez-Gracia, E. (2025). Adherence to the Mediterranean diet to prevent or delay hepatic steatosis: a longitudinal analysis within the PREDIMED study. Frontiers in Nutrition , 12. https://doi.org/10.3389/fnut.2025.1518082. Esler, W.P. and Cohen, D.E. (2024). Pharmacologic inhibition of lipogenesis for the treatment of NAFLD. Journal of hepatology , 80(2), pp.362–37. https://doi.org/10.1016/j.jhep.2023.10.042. Kargulewicz, A., Stankowiak-Kulpa, H. and Grzymisławski, M. (2014) ‘Dietary recommendations for patients with non-alcoholic fatty liver disease’, Gastroenterology Review , 9(1), pp. 18–23. https://doi.org/10.5114/pg.2014.40850. Miller, J., Hepatology, Z. and Henry (n.d.). NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #191 Diet in Non-Alcoholic Fatty Liver Disease Pathophysiology of NAFLD . [online] Available at: https://practicalgastro.com/wp-content/uploads/2019/11/Parrish-October-2019.pdf. Quek, J., Chan, K.E., Wong, Z.Y., Tan, C., Tan, B., Lim, W.H., Tan, D.J.H., Tang, A.S.P., Tay, P., Xiao, J., Yong, J.N., Zeng, R.W., Chew, N.W.S., Nah, B., Kulkarni, A., Siddiqui, M.S., Dan, Y.Y., Wong, V.W.-S., Sanyal, A.J. and Noureddin, M. (2023). Global prevalence of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in the overweight and obese population: a systematic review and meta-analysis. The Lancet Gastroenterology & Hepatology , 8(1), pp.20–30. https://doi.org/10.1016/s2468-1253(22)00317-x. Rinella, M.E., Neuschwander-Tetri, B.A., Siddiqui, M.S., Abdelmalek, M.F., Caldwell, S., Barb, D., Kleiner, D.E. and Loomba, R. (2023). AASLD Practice Guidance on the Clinical Assessment and Management of Nonalcoholic Fatty Liver Disease. Hepatology , [online] 77(5), p.10. https://doi.org/10.1097/HEP.0000000000000323 Tack, F., Horn, P., Vincent Wai-Sun Wong, Vlad Ratziu, Elisabetta Bugianesi, Sven Francque, Zelber-Sagi, S., Valenti, L., Roden, M., Schick, F., Hannele Yki-Järvinen, Gastaldelli, A., Vettor, R., Frühbeck, G. and Dicker, D. (2024). EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD): Executive Summary. Diabetologia . https://doi.org/10.1007/s00125-024-06196-3. Takawy, M.W. and Abdelmalek, M.F. (2025). Impact of Weight Loss on Metabolic Dysfunction Associated Steatohepatitis and Hepatic Fibrosis. Current diabetes reports , [online] 25(1), p.23. https://doi.org/10.1016/s2468-1253(22)00317-x Vilar-Gomez, E., Martinez-Perez, Y., Calzadilla-Bertot, L., Torres-Gonzalez, A., Gra-Oramas, B., Gonzalez-Fabian, L., Friedman, S.L., Diago, M. and Romero-Gomez, M. (2015). Weight Loss Through Lifestyle Modification Significantly Reduces Features of Nonalcoholic Steatohepatitis. Gastroenterology , [online] 149(2), pp.367-378.e5. https://doi.org/10.1053/j.gastro.2015.04.005. Vlad TARU, SZABO, G., MEHAL, W. and REIBERGER, T. (2024). Inflammasomes in chronic liver disease: hepatic injury, fibrosis progression and systemic inflammation. Journal of Hepatology . https://doi.org/10.1016/j.jhep.2024.06.016. Zelber-Sagi, S. and Moore, J.B. (2024). Practical Lifestyle Management of Nonalcoholic Fatty Liver Disease for Busy Clinicians. Diabetes Spectrum: A Publication of the American Diabetes Association , [online] 37(1), pp.39–47. https://doi.org/10.2337/dsi23-0009. Zhao, N., He, Y., Li, Y., Zhang, N. and Wang, Y. (2024). Association of plain water intake with risk of all-cause and cause-specific mortality in individuals with non-alcoholic fatty liver disease or metabolic dysfunction-associated steatotic liver disease. Frontiers in Nutrition , 11. https://doi.org/10.3389/fnut.2024.1478194. Zhu, Y., Xu, X., Fan, Z., Ma, X., Rui, F., Ni, W., Hu, X., Gu, Q., Shi, J., Wu, C., Yeo, Y.H. and Li, J. (2024) ‘Different minimal alcohol consumption in male and female individuals with metabolic dysfunction‑associated fatty liver disease’, Liver International , 44(3), pp. 865–875. https://doi.org/10.1111/liv.15849. Additional Declarations The authors declare no competing interests. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6981390","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":476751114,"identity":"5897b15a-40c9-474a-aa0f-d91a46981e74","order_by":0,"name":"W.M.S. Pushpakumara","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABBElEQVRIiWNgGAWjYHACNiBOgPPkQMSBB6RoMQZrScCuFLuWxAYGFD4mMJdIf/a4oCYtcW372YefeXPq0ueHHX4ItMVOTrcBuxbLGTnmxjOO5SRuO5NuLM277XDuxttpBkAtycZmB7BrMbiRwybNw1aRuO1AGoN07rYDuRtnJ4C0HACK4NKS/kya5x9Qy/lnzL9zt9WlG85O/0BAS4KZNG8b0GE30tiAtjAnyEvn4LfFsueNmfTMvjTjbTeesVn/3XbYcIN0TsGBBAPcfjFnBzqs4Fuy7Lbzacw3Z26rk5efnb75w4cKOzmc3gdiZlSRAzBxHABTi3wDbtWjYBSMglEwMgEAc99lMuHztSYAAAAASUVORK5CYII=","orcid":"https://orcid.org/0009-0006-0303-2501","institution":"Wayamba University of Sri Lanka","correspondingAuthor":true,"prefix":"","firstName":"W.M.S.","middleName":"","lastName":"Pushpakumara","suffix":""},{"id":476751115,"identity":"416e5153-9982-4cf0-9f27-e7129adce105","order_by":1,"name":"R.A.M.D. Ranathunga","email":"","orcid":"https://orcid.org/0009-0003-0484-8578","institution":"University of Colombo","correspondingAuthor":false,"prefix":"","firstName":"R.A.M.D.","middleName":"","lastName":"Ranat","suffix":"M.D."},{"id":476751116,"identity":"4d5d329a-ca75-4bab-a4be-aa81aac67c80","order_by":2,"name":"J.F. Zimra","email":"","orcid":"https://orcid.org/0009-0001-4905-5139","institution":"Wayamba University of Sri Lanka","correspondingAuthor":false,"prefix":"","firstName":"J.F.","middleName":"","lastName":"Zimra","suffix":""},{"id":476751117,"identity":"0897e86a-1bc2-4afb-992f-f8f0406db34f","order_by":3,"name":"M.S.H.Banu","email":"","orcid":"https://orcid.org/0009-0000-0219-4273","institution":"Wayamba University of Sri Lanka","correspondingAuthor":false,"prefix":"","firstName":"","middleName":"","lastName":"M.S.H.Banu","suffix":""}],"badges":[],"createdAt":"2025-06-26 08:50:42","currentVersionCode":1,"declarations":{"humanSubjects":true,"vertebrateSubjects":false,"conflictsOfInterestStatement":false,"humanSubjectEthicalGuidelines":true,"humanSubjectConsent":true,"humanSubjectClinicalTrial":false,"humanSubjectCaseReport":true,"vertebrateSubjectEthicalGuidelines":false},"doi":"10.21203/rs.3.rs-6981390/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6981390/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":85651015,"identity":"0049c6ba-4049-4bbd-ae3e-e673becdf378","added_by":"auto","created_at":"2025-06-30 09:13:05","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":566836,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6981390/v1/6a80ba98-8262-4fc7-aa46-9a8a007f93d1.pdf"}],"financialInterests":"The authors declare no competing interests.","formattedTitle":"\u003cp\u003e\u003cstrong\u003eDietary intervention as a therapeutic tool in Non-Alcoholic Fatty Liver Disease: A case-based approach\u003c/strong\u003e\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eObesity-driven metabolic dysfunction has re-branded non-alcoholic fatty liver disease (NAFLD) as metabolic dysfunction-associated steatotic liver disease (MASLD), reflecting its tight coupling to global surges in adiposity and type 2 diabetes (Allen et al., \u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e2024\u003c/span\u003e). Excess adipose tissue delivers a continuous flux of free fatty acids to the liver, amplifies de novo lipogenesis via insulin-resistant hyperinsulinaemia, and suppresses very-low-density-lipoprotein export. Together these processes saturate hepatocellular triglyceride-handling capacity, initiating lipotoxic stress that can progress from simple steatosis to steatohepatitis and fibrosis. Contemporary European guidelines emphasise that each kilogram of sustained weight gain further accelerates this trajectory, whereas 7\u0026ndash;10% weight loss can reverse it (Esler and Cohen, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e2024\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eSerum alanine- and aspartate-aminotransferase (ALT, AST) remain the most accessible biochemical sentinels of hepatocellular injury; elevations usually track with histological activity, although normal values do not exclude disease. Gamma-glutamyl-transferase, fasting insulin, HOMA-IR, and atherogenic lipid profiles often rise in parallel, mirroring the systemic insulin resistance that both triggers and perpetuates hepatic fat accumulation (Bril et al., 2020). Obesity\u0026rsquo;s chronic, low-grade inflammatory milieu\u0026mdash;characterised by increased C-reactive protein, interleukin-6, tumour-necrosis-factor-α, and pro-inflammatory adipokines\u0026mdash;further aggravates steatotic hepatocytes, drives Kupffer-cell activation, and fuels fibrogenesis. These circulating markers therefore provide additional prognostic insight and underscore why MASLD is now viewed as a liver-centred component of a whole-body inflammatory syndrome (Vlad TARU et al., \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e2024\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eManagement still begins with intensive lifestyle therapy: hypocaloric Mediterranean-style diets, progressive aerobic-plus-resistance training, and behavioural support that together target\u0026thinsp;\u0026ge;\u0026thinsp;7% weight loss. When cardiometabolic comorbidities demand pharmacological help, agents chosen primarily for glycaemic or lipid control\u0026mdash;e.g., GLP-1 receptor agonists, SGLT2 inhibitors, pioglitazone\u0026mdash;offer collateral hepatic benefit; obeticholic acid, an FXR agonist, is the first drug authorised for NASH with fibrosis but requires careful monitoring. Bariatric surgery delivers the most durable histological improvement in eligible patients, and liver transplantation remains the rescue option for decompensated cirrhosis. Importantly, no medication obviates the need to correct the underlying obesogenic environment, so long-term success depends on sustained lifestyle and risk-factor modification (Basil et al., \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2024\u003c/span\u003e).\u003c/p\u003e"},{"header":"Case","content":"\u003cp\u003eA 35-year-old male quality supervisor from the garment industry presented with left-sided abdominal pain, frothy urine, and generalized fatigue. He had no prior history of chronic illness or family history of metabolic disorders. Anthropometric examination indicated obesity (BMI-30.2 kg/m\u0026sup2;) and central adiposity (waist circumference-103 cm). He reported a sedentary lifestyle and dietary patterns that included frequent consumption of refined carbohydrates, fried foods, coconut milk, and minimal fruit and vegetable intake.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical and Biochemical Assessment\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eBiochemical analysis confirmed the presence of dyslipidemia (Triglycerides: 154 mg/dl, HDL: 34 mg/dl, LDL: 134 mg/dl, VLDL: 31 mg/dl) and elevated liver enzyme levels (ALT: 58 U/L). Imaging studies revealed grade II fatty liver changes. A comprehensive nutrition assessment identified high carbohydrate and saturated fat intake, minimal dietary fiber, and no structured physical activity.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDietary assessment\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDietary evaluation via dietary recall revealed several nutrition-relevant behaviours that may adversely affect metabolic health. The participant habitually eats dinner away from home at least three times per week, primarily selecting quick-service or fast-food outlets, thereby increasing exposure to energy-dense, nutrient-poor meals. At home, dietary variety is limited: the respondent routinely classifies potato or dhal as the sole \u0026ldquo;vegetable\u0026rdquo; serving at both breakfast and lunch, which are themselves obtained from the company buffet and therefore largely outside personal control. Household use of coconut products is substantial\u0026mdash;approximately one whole coconut is blended each day for milk\u0026mdash;contributing considerable saturated fat to the diet. Fruit intake is markedly inadequate, with no daily consumption reported, and there are no snacks between main meals that might otherwise supply additional micronutrients or fibre. Alcohol is abstained from entirely, yet there is also an absence of planned physical activity, underscoring a sedentary lifestyle that, combined with the aforementioned dietary patterns, may potentiate dyslipidaemia, weight gain, and non-alcoholic fatty liver disease.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eNutritional diagnosis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe nutritional assessment indicates multiple interrelated metabolic concerns primarily driven by dietary and lifestyle behaviors. Hepatic fat accumulation appears to be associated with excessive energy intake and reduced energy expenditure, as evidenced by the individual\u0026apos;s dietary pattern and sedentary lifestyle history. Additionally, elevated plasma triglyceride levels are likely attributable to excessive carbohydrate consumption, particularly from refined sources, as revealed through detailed dietary assessment. The presence of high plasma LDL and VLDL concentrations may be linked to a diet high in saturated fats and low in dietary fiber, further supporting the role of poor dietary quality in lipid abnormalities. Moreover, excess adiposity, reflected in anthropometric measurements, is consistent with chronic energy imbalance\u0026mdash;specifically, high caloric intake coupled with insufficient physical activity. Collectively, these findings underscore the critical role of dietary composition and physical inactivity in the development of metabolic disturbances such as dyslipidemia and hepatic steatosis.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eNutritional Management\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eHepatocyte regeneration and the healing of liver disease begin with appropriate nutritional management from the initial stage of diagnosis. Early nutritional intervention significantly reduces the adverse effects caused by impaired nutrient metabolism associated with liver dysfunction. Additionally, through proper dietary management of dyslipidemia, ectopic fat accumulation and cardiovascular diseases can be prevented by decreasing low-density lipoprotein (LDL) levels and improving high-density lipoprotein (HDL) levels. The primary goals of medical nutrition therapy for patients with liver disease include weight reduction, maintaining normal blood glucose levels, achieving normal ranges of liver enzymes, and stabilizing the lipid profile within recommended limits. These objectives may vary depending on the stage and severity of the disease, and often require integration with medical management to support effective lifestyle modifications. Among these goals, weight reduction should be prioritized. A weight loss of 7% to 10% has been associated with reduced liver fat content and significant improvements in liver fibrosis (Miller and Henry, 2019). Furthermore, non-alcoholic steatohepatitis (NASH) has been found to occur at higher rates in obese individuals compared to those with lean body mass (Quek et al., 2023). Implementing a low-fat, hypocaloric diet that provides approximately 750 kcal/day less than the patient\u0026apos;s daily requirement has shown promising results, including a reduction in fibrosis score by at least one point in patients who presented with baseline fibrosis (Vilar-Gomea et al., 2015).\u003c/p\u003e\n\u003cp\u003eImproving insulin sensitivity is another key nutritional objective. In patients with non-alcoholic fatty liver disease (NAFLD), insulin resistance promotes gluconeogenesis through two main mechanisms: by increasing adipocyte lipolysis and circulating fatty acid levels, and by reducing hepatic glycogen storage capacity (Chen et al., 2017). Addressing these metabolic disruptions through tailored dietary strategies is essential for mitigating disease progression and improving overall liver health.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDietary Intervention Plan\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe patient underwent a calorie-restricted, macronutrient-balanced dietary plan designed to induce weight loss of approximately 0.5\u0026ndash;1 kg per week. Daily caloric intake was limited to 1500 kcal/day with a macronutrient split of approximately 50% carbohydrates, 30% fats (with \u0026lt;10% saturated fats), and 20% protein. High-fiber foods, low-glycemic index carbohydrates, unsaturated fats, and lean protein sources were emphasized. Nutritional counseling sessions were conducted twice weekly, and meals were supervised during hospitalization.\u003c/p\u003e\n\u003cp\u003eConsidering the macro nutrient compositions to achieve the medical nutrition therapy goals,\u0026nbsp;of\u0026nbsp;non-alcoholic\u0026nbsp;fatty\u0026nbsp;liver\u0026nbsp;patients,\u0026nbsp;Kargulewicz\u0026nbsp;et\u0026nbsp;al.,\u0026nbsp;2014\u0026nbsp;have\u0026nbsp;given\u0026nbsp;the\u0026nbsp;dietary recommendations as follows:\u003c/p\u003e\n\u003cp\u003e\u003cimg src=\"https://myfiles.space/user_files/58895_8739fc6c57c1c19a/58895_custom_files/img1751274031.png\" width=\"504\" height=\"204\"\u003e\u003c/p\u003e\n\u003ch3\u003e\u0026nbsp;\u003c/h3\u003e\n\u003ch3\u003ePersonalized Diet Plan\u003c/h3\u003e\n\u003cp\u003eCalorie\u0026nbsp;\u0026ndash;\u0026nbsp;1500 kcal\u003c/p\u003e\n\u003cp\u003eCarbohydrate\u0026nbsp;\u0026ndash;\u0026nbsp;50%;\u0026nbsp;(1500 kcal *\u0026nbsp;0.5)\u0026nbsp;/\u0026nbsp;(4\u0026nbsp;kcal/g)\u0026nbsp;= 187.5 g\u003c/p\u003e\n\u003cp\u003eFat\u0026nbsp;\u0026ndash;\u0026nbsp;30%; (1500\u0026nbsp;*\u0026nbsp;0.3)\u0026nbsp;/\u0026nbsp;(9 kcal/g)\u0026nbsp;= 50 g\u003c/p\u003e\n\u003cp\u003eProtein \u0026ndash; 20% (1500 * 0.2) / (4 kcal/g) = 75 g\u003c/p\u003e\n\u003ch3\u003eFood Exchange List\u003c/h3\u003e\n\u003cp\u003eTable1:\u0026nbsp;food\u0026nbsp;exchange\u0026nbsp;list\u0026nbsp;for\u0026nbsp;personalized\u0026nbsp;diet plan\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eFood Group\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eExchanges\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCarbohydrate\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003e(g)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eFat\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003e(g)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eProtein\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003e(g)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eEnergy (kcal)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eMilk,\u003c/p\u003e\n \u003cp\u003eskimmed\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e24\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e0.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e14\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e155.6\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003ePulses\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e14\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e185\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eNon-starchy vegetables\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e18\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e88\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eFruit\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e60\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eSugar\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e40\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eStarch\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e105\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e3.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e21\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e535.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eProtein\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e21\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e165\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eCoconut\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e20\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e180\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003eOil\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e90\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003eTotal\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e202\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e43.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e1499.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 18.7156%;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003ePercentages\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 21.2844%;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e54%\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 11.5596%;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e26%\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 15.5963%;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e20%\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 17.2477%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePre- and Post-Intervention Clinical Parameters\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOver the course of the hospital stay anthropometric and biochemical parameters were monitored after 2 months. No pharmacological agents targeting liver enzymes or lipids were introduced during the study period to isolate the dietary effect.\u003c/p\u003e\n\u003cp\u003eTable 2 -\u0026nbsp;Baseline and follow-up assessment of the patient\u003c/p\u003e\n\u003ctable border=\"0\" cellpadding=\"0\" align=\"\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eParameter\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eBaseline\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e(Day 0)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eFollow-up\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e(Afetr 2 months)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eReference Range\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eWeight (kg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e95.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e91.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eBMI (kg/m\u0026sup2;)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e30.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e29.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e18.5 \u0026ndash; 24.9\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eWaist Circumference (cm)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e103\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026lt;90 (Asian males)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eALT (U/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e58\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e39\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026lt;45\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eAST (U/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e27\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e25\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026lt;40\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eTriglycerides (mg/dL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e154\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e129\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026lt;150\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eHDL (mg/dL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e34\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026gt;40\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eLDL (mg/dL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e134\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e110\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026lt;130\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eVLDL (mg/dL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e31\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e23\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026lt;30\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 217px;\"\u003e\n \u003cp\u003eTotal Cholesterol / HDL Ratio\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 84px;\"\u003e\n \u003cp\u003e5.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 130px;\"\u003e\n \u003cp\u003e4.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 129px;\"\u003e\n \u003cp\u003e\u0026lt;5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e"},{"header":"Discussion","content":"\u003cp\u003eGrade 2 fatty liver\u0026mdash;now classified as moderate metabolic-dysfunction-associated steatotic liver disease (MASLD)\u0026mdash;is considered a reversible stage as long as intensive lifestyle therapy is initiated early. Contemporary society guidelines from both Europe (EASL\u0026ndash;EASD\u0026ndash;EASO, 2024) and the United States (AASLD update, 2023) position personalised nutrition, intentional weight loss and exercise as first-line treatment, ahead of, and complementary to, any pharmacotherapy. These documents emphasise that dietary counselling should aim not only to normalise aminotransferases but also to mitigate future cardiovascular and oncologic risk, which together account for most MASLD-related mortality (Tack et al., \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e2024\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eEnergy restriction sufficient to produce a sustained 7\u0026ndash;10% reduction in body weight remains the single most powerful intervention for improving hepatic steatosis and even regressing early fibrosis. A 2025 narrative review pooling recent clinical trials found that every additional percentage point of weight lost translated into incremental improvements in liver fat, with resolution of steatohepatitis often achieved once the 10% threshold was crossed. Conversely, crash diets producing rapid, unstructured losses are discouraged because they are rarely maintained, can exacerbate ketone production and have been linked to transient rises in bilirubin and worsening fibrosis in susceptible individuals (Takawy and Abdelmalek, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e2025\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn qualitative terms, a Mediterranean-style eating pattern\u0026mdash;rich in vegetables, whole fruit, pulses, extra-virgin olive oil, nuts and oily fish\u0026mdash;has repeatedly shown superiority over Western or convenience-food patterns for reducing intra-hepatic triglyceride content and improving insulin sensitivity, even without large calorie deficits. A longitudinal analysis of PREDIMED participants published in 2025 demonstrated significant reductions in the Hepatic Steatosis Index as adherence scores rose, and systematic reviews of randomised trials in both adults and children report parallel falls in ALT and γ-GT (Cueto-Gal\u0026aacute;n et al., \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e2025\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eWithin this pattern, fat quality matters. Substituting saturated and trans-fat-rich foods (processed meats, commercial bakery items, deep-fried snacks) with monounsaturated (olive, canola, avocado) and polyunsaturated (marine and certain plant oils) sources down-regulates de-novo lipogenesis and may favourably shift the LDL-to-HDL ratio. Both the European and American position statements explicitly endorse liberal use of unsaturated fats within total calorie targets (Rinella et al., \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e2023\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eCarbohydrate quality is equally critical. Fructose and sucrose delivered in sugar-sweetened beverages, confectionery and refined cereals drive hepatic de-novo lipogenesis and worsen insulin resistance; limiting these products is therefore strongly advised. Where a low-carbohydrate approach is preferred, short-term trials show quicker reductions in liver fat than iso-caloric low-fat diets, but after 12\u0026ndash;24 month weight loss and biochemical outcomes converge, underscoring that sustainability and food quality trump macronutrient ratios. Whole-grain breads, legumes and low-glycaemic fruit remain the staple carbohydrate choices in most successful long-term regimens (Zelber-Sagi and Moore, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e2024\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eAlcohol intake requires individualised counselling. For patients whose steatosis is purely metabolic, even light drinking (\u0026lt;\u0026thinsp;10 g day⁻\u0026sup1;) has been associated with faster fibrosis progression in cohort studies, and the 2024 EASL guidance therefore \u0026ldquo;discourages\u0026rdquo; alcohol altogether; for those with alcoholic fatty liver disease, total abstinence is mandatory (Tack et al., \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e2024\u003c/span\u003e). A 2023 Cedars-Sinai study suggested that minimal consumption may be tolerated in very mild disease, yet its findings have not altered consensus recommendations, which continue to prioritise abstinence until clear longitudinal safety data emerge (Zhu et al., \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e2024\u003c/span\u003e)\u003c/p\u003e \u003cp\u003ePractical behaviour strategies\u0026mdash;mindful portion control, three balanced meals spaced across the day to avoid large post-prandial glucose and lipid excursions, and replacing caloric beverages with plain water\u0026mdash;help patients adhere to calorie goals and may confer independent metabolic benefits. A 2024 NHANES analysis showed that NAFLD participants in the highest quartile of plain-water intake had significantly lower all-cause mortality than low-intake peers, lending empirical support to the long-standing clinical advice to \u0026ldquo;drink mostly water.\u0026rdquo; (Zhao et al., \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e2024\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eDietary management of Grade 2 fatty liver combines a modest, sustainable calorie deficit with a Mediterranean-leaning, low-sugar, unsaturated-fat-rich eating pattern, strict limits on alcohol, ample hydration and attention to behavioural factors that promote long-term adherence. When implemented alongside regular physical activity and optimisation of comorbidities, this strategy not only reverses hepatic fat accumulation but also addresses the cardio-metabolic milieu that drives disease progression. Continuous monitoring by a multidisciplinary team allows timely adjustment of nutrition targets and consideration of emerging pharmacotherapies when lifestyle measures alone do not halt fibrosis.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThe study concludes that personalized dietary management including weight reduction and other evidence based diet related behaviour changes as proper hydration, substitution of low quality nutrient sources with high quality sources and management of a balanced diet in general supports the management of NAFLD by means of improving liver enzymes and total lipid profile.\u003c/p\u003e "},{"header":"Declarations","content":"\u003cp\u003e\u003cspan\u003eThe patient involved in this clinical case study was fully informed about the purpose, content, and potential implications of the publication. Written informed consent was obtained from the patient, confirming their voluntary agreement to the inclusion and publication of relevant clinical details and data in the preprint. The patient was assured that their identity would be protected and that all information would be handled with strict confidentiality.\u003c/span\u003e\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eCompeting interests:\u0026nbsp;\u003c/strong\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding:\u003c/strong\u003e Self-funded\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgments:\u003c/strong\u003e We thank the participant of this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor contributions:\u003c/strong\u003e All authors have contributed to the manuscript through data collection, data analysis, and writing.\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eAllen, A.M., Pose, E., K. Rajender Reddy, Russo, M.W. and Kamath, P.S. (2024). Nonalcoholic Fatty Liver Disease Gets Renamed as Metabolic Dysfunction\u0026ndash;Associated Steatotic Liver Disease: Progress But With Challenges. \u003cem\u003eGastroenterology\u003c/em\u003e, 166(2), pp.229\u0026ndash;234. https://doi.org/10.1053/j.gastro.2023.11.007. \u003c/li\u003e\n\u003cli\u003eBasil, B., Myke-Mbata, B.K., Eze, O.E. and Akubue, A.U. (2024). From adiposity to steatosis: metabolic dysfunction-associated steatotic liver disease, a hepatic expression of metabolic syndrome \u0026ndash; current insights and future directions. \u003cem\u003eClinical Diabetes and Endocrinology\u003c/em\u003e, [online] 10(1). https://doi.org/10.1186/s40842-024-00187-4. \u003c/li\u003e\n\u003cli\u003e\u0026zwnj;Bril, F., McPhaul, M.J., Caulfield, M.P., Clark, V.C., Soldevilla-Pico, C., Firpi-Morell, R.J., Lai, J., Shiffman, D., Rowland, C.M. and Cusi, K. (2020). Performance of Plasma Biomarkers and Diagnostic Panels for Nonalcoholic Steatohepatitis and Advanced Fibrosis in Patients With Type 2 Diabetes. \u003cem\u003eDiabetes Care\u003c/em\u003e, [online] 43(2), pp.290\u0026ndash;297. https://doi.org/10.2337/dc19-1071. \u003c/li\u003e\n\u003cli\u003eCueto-Gal\u0026aacute;n, R., Fontalba-Navas, A., Guti\u0026eacute;rrez-Bedmar, M., Ruiz-Canela, M., Mart\u0026iacute;nez-Gonz\u0026aacute;lez, M.A., Alves, L., Babio, N., Montserrat Fit\u0026oacute;, Ros, E., Fiol, M., Ram\u0026oacute;n Estruch, Ar\u0026oacute;s, F., Serra-Majem, L., Pint\u0026oacute;, X., Mu\u0026ntilde;oz-Bravo, C., Garc\u0026iacute;a-Rodr\u0026iacute;guez, A. and G\u0026oacute;mez-Gracia, E. (2025). Adherence to the Mediterranean diet to prevent or delay hepatic steatosis: a longitudinal analysis within the PREDIMED study. \u003cem\u003eFrontiers in Nutrition\u003c/em\u003e, 12. https://doi.org/10.3389/fnut.2025.1518082. \u003c/li\u003e\n\u003cli\u003eEsler, W.P. and Cohen, D.E. (2024). Pharmacologic inhibition of lipogenesis for the treatment of NAFLD. \u003cem\u003eJournal of hepatology\u003c/em\u003e, 80(2), pp.362\u0026ndash;37. https://doi.org/10.1016/j.jhep.2023.10.042. \u003c/li\u003e\n\u003cli\u003eKargulewicz, A., Stankowiak-Kulpa, H. and Grzymisławski, M. (2014) \u0026lsquo;Dietary recommendations for patients with non-alcoholic fatty liver disease\u0026rsquo;, \u003cem\u003eGastroenterology Review\u003c/em\u003e, 9(1), pp. 18\u0026ndash;23. https://doi.org/10.5114/pg.2014.40850.\u003c/li\u003e\n\u003cli\u003eMiller, J., Hepatology, Z. and Henry (n.d.). \u003cem\u003eNUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #191 Diet in Non-Alcoholic Fatty Liver Disease Pathophysiology of NAFLD\u003c/em\u003e. [online] Available at: https://practicalgastro.com/wp-content/uploads/2019/11/Parrish-October-2019.pdf. \u003c/li\u003e\n\u003cli\u003eQuek, J., Chan, K.E., Wong, Z.Y., Tan, C., Tan, B., Lim, W.H., Tan, D.J.H., Tang, A.S.P., Tay, P., Xiao, J., Yong, J.N., Zeng, R.W., Chew, N.W.S., Nah, B., Kulkarni, A., Siddiqui, M.S., Dan, Y.Y., Wong, V.W.-S., Sanyal, A.J. and Noureddin, M. (2023). Global prevalence of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in the overweight and obese population: a systematic review and meta-analysis. \u003cem\u003eThe Lancet Gastroenterology \u0026amp; Hepatology\u003c/em\u003e, 8(1), pp.20\u0026ndash;30. https://doi.org/10.1016/s2468-1253(22)00317-x. \u003c/li\u003e\n\u003cli\u003eRinella, M.E., Neuschwander-Tetri, B.A., Siddiqui, M.S., Abdelmalek, M.F., Caldwell, S., Barb, D., Kleiner, D.E. and Loomba, R. (2023). AASLD Practice Guidance on the Clinical Assessment and Management of Nonalcoholic Fatty Liver Disease. \u003cem\u003eHepatology\u003c/em\u003e, [online] 77(5), p.10. https://doi.org/10.1097/HEP.0000000000000323 \u003c/li\u003e\n\u003cli\u003eTack, F., Horn, P., Vincent Wai-Sun Wong, Vlad Ratziu, Elisabetta Bugianesi, Sven Francque, Zelber-Sagi, S., Valenti, L., Roden, M., Schick, F., Hannele Yki-J\u0026auml;rvinen, Gastaldelli, A., Vettor, R., Fr\u0026uuml;hbeck, G. and Dicker, D. (2024). EASL\u0026ndash;EASD\u0026ndash;EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD): Executive Summary. \u003cem\u003eDiabetologia\u003c/em\u003e. https://doi.org/10.1007/s00125-024-06196-3. \u003c/li\u003e\n\u003cli\u003eTakawy, M.W. and Abdelmalek, M.F. (2025). Impact of Weight Loss on Metabolic Dysfunction Associated Steatohepatitis and Hepatic Fibrosis. \u003cem\u003eCurrent diabetes reports\u003c/em\u003e, [online] 25(1), p.23. https://doi.org/10.1016/s2468-1253(22)00317-x \u003c/li\u003e\n\u003cli\u003eVilar-Gomez, E., Martinez-Perez, Y., Calzadilla-Bertot, L., Torres-Gonzalez, A., Gra-Oramas, B., Gonzalez-Fabian, L., Friedman, S.L., Diago, M. and Romero-Gomez, M. (2015). Weight Loss Through Lifestyle Modification Significantly Reduces Features of Nonalcoholic Steatohepatitis. \u003cem\u003eGastroenterology\u003c/em\u003e, [online] 149(2), pp.367-378.e5. https://doi.org/10.1053/j.gastro.2015.04.005. \u003c/li\u003e\n\u003cli\u003eVlad TARU, SZABO, G., MEHAL, W. and REIBERGER, T. (2024). Inflammasomes in chronic liver disease: hepatic injury, fibrosis progression and systemic inflammation. \u003cem\u003eJournal of Hepatology\u003c/em\u003e. https://doi.org/10.1016/j.jhep.2024.06.016. \u003c/li\u003e\n\u003cli\u003eZelber-Sagi, S. and Moore, J.B. (2024). Practical Lifestyle Management of Nonalcoholic Fatty Liver Disease for Busy Clinicians. \u003cem\u003eDiabetes Spectrum: A Publication of the American Diabetes Association\u003c/em\u003e, [online] 37(1), pp.39\u0026ndash;47. https://doi.org/10.2337/dsi23-0009. \u003c/li\u003e\n\u003cli\u003eZhao, N., He, Y., Li, Y., Zhang, N. and Wang, Y. (2024). Association of plain water intake with risk of all-cause and cause-specific mortality in individuals with non-alcoholic fatty liver disease or metabolic dysfunction-associated steatotic liver disease. \u003cem\u003eFrontiers in Nutrition\u003c/em\u003e, 11. https://doi.org/10.3389/fnut.2024.1478194.\u003c/li\u003e\n\u003cli\u003eZhu, Y., Xu, X., Fan, Z., Ma, X., Rui, F., Ni, W., Hu, X., Gu, Q., Shi, J., Wu, C., Yeo, Y.H. and Li, J. (2024) \u0026lsquo;Different minimal alcohol consumption in male and female individuals with metabolic dysfunction‑associated fatty liver disease\u0026rsquo;, \u003cem\u003eLiver International\u003c/em\u003e, 44(3), pp. 865\u0026ndash;875. https://doi.org/10.1111/liv.15849. \u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"NAFLD, Obesity, Nutrition assessment, Dietary management","lastPublishedDoi":"10.21203/rs.3.rs-6981390/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6981390/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eIntroduction:\u003c/strong\u003e Non Alcoholic Fatty Liver disease (NAFLD) is a spectrum of liver disorders which is characterized by excessive fat accumulation in the liver that ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), and NASH may develop up to hepatocellular carcinoma. NAFLD is the most common liver disease in the world. Since NAFLD is associated with many risk factors including obesity, metabolic syndrome, insulin resistance and diabetes, weight loss and dietary management are proven supportive therapies in NAFLD management. Therefore this study aimed\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase:\u003c/strong\u003e A 35-year-old obese male garment industry worker presented with left abdominal pain, frothy urine, and fatigue. Clinical and dietary assessments revealed central adiposity, sedentary lifestyle, and high intake of refined carbohydrates and saturated fats with minimal fruits, vegetables, and fiber. Biochemical findings indicated dyslipidemia (TG: 154 mg/dL, HDL: 34 mg/dL, LDL: 134 mg/dL), elevated ALT (58 U/L), and grade II fatty liver on imaging. A calorie-restricted, macronutrient-balanced diet (1500 kcal/day: 50% carbs, 30% fat, 20% protein) with nutrition counseling was initiated to promote weight loss and improve liver and lipid profiles. After 2 months, the patient showed significant improvements: weight reduced from 95.1 kg to 91.8 kg, BMI from 30.2 to 29.1 kg/m², and waist circumference from 103 cm to 99 cm. Biochemical parameters improved with ALT decreasing to 39 U/L, HDL increasing to 41 mg/dL, and LDL, VLDL, and triglycerides all moving closer to recommended levels. These outcomes demonstrate that personalized dietary interventions can effectively reduce hepatic steatosis and correct lipid abnormalities, highlighting the importance of early nutrition management in non-alcoholic fatty liver disease (NAFLD).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion:\u003c/strong\u003e The study concludes that individualized dietary interventions, including weight reduction and evidence-based dietary modifications—such as adequate hydration, replacement of low-quality nutrient sources with nutrient-dense alternatives, and adherence to a balanced diet—are effective in the management of non-alcoholic fatty liver disease (NAFLD), as evidenced by improvements in liver enzyme levels and overall lipid profile.\u003c/p\u003e","manuscriptTitle":"Dietary intervention as a therapeutic tool in Non-Alcoholic Fatty Liver Disease: A case-based approach","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-06-30 09:04:56","doi":"10.21203/rs.3.rs-6981390/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"9e07db68-7827-40cd-8baa-d9cc75395251","owner":[],"postedDate":"June 30th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":50626616,"name":"Nutrition \u0026 Dietetics"}],"tags":[],"updatedAt":"2025-06-30T09:04:56+00:00","versionOfRecord":[],"versionCreatedAt":"2025-06-30 09:04:56","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6981390","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6981390","identity":"rs-6981390","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}