Introduction

Steatotic liver disease (SLD) is an umbrella term encompassing disorders characterized by hepatic steatosis and classified according to their predominant etiology. Under the current nomenclature, metabolic dysfunction-associated steatotic liver disease (MASLD) is diagnosed when hepatic steatosis occurs in the presence of at least one cardiometabolic risk factor and alcohol consumption remains below the defined thresholds [1]. Patients meeting the criteria for MASLD who consume 140-350 g of alcohol per week (20-50 g/day) for women or 210-420 g per week (30-60 g/day) for men are classified as having metabolic dysfunction- and alcohol-associated liver disease (MetALD), whereas alcohol consumption above these levels supports classification as alcohol-related liver disease (ALD) [2]. MetALD represents a continuum in which the relative contributions of metabolic dysfunction and alcohol vary among individuals [2]. This distinction is clinically important because metabolic risk factors and alcohol consumption may act synergistically to promote liver injury [1].

Within this classification, MASLD is a common chronic liver disorder encompassing a broad clinical spectrum, ranging from isolated steatosis to metabolic dysfunction-associated steatohepatitis (MASH), in which steatosis is accompanied by hepatocellular injury and inflammation [3, 4]. In susceptible individuals, MASH may lead to progressive fibrosis, cirrhosis, hepatic decompensation, and hepatocellular carcinoma [5, 6]. However, MASLD should not be considered exclusively a hepatic condition [7]. It is closely associated with obesity, insulin resistance, type 2 diabetes mellitus, dyslipidemia, hypertension, cardiovascular disease, chronic kidney disease, and other manifestations of systemic metabolic dysfunction. It is responsible for a growing clinical and economic burden [8, 9], with a global prevalence of 16-38% [3, 4], and is increasingly recognized in pediatric populations [10, 11].

The pathogenesis of MASLD is multifactorial and heterogeneous. Insulin resistance promotes adipose-tissue lipolysis and increases the delivery of non-esterified fatty acids to the liver [12]. At the same time, hyperinsulinemia and excess availability of dietary substrates stimulate hepatic de novo lipogenesis. When the capacity of hepatocytes to oxidize fatty acids or export triglycerides is exceeded, lipids accumulate within the liver [13]. The resulting lipotoxicity, mitochondrial dysfunction, oxidative stress, endoplasmic reticulum stress, inflammatory signaling, and activation of hepatic stellate cells may contribute to the transition from uncomplicated steatosis to MASH and fibrosis. Alterations in the intestinal microbiota, intestinal permeability, bile acid metabolism, and gut-derived inflammatory signals may further modulate disease development via the gut–liver axis [14-17].

Diet can influence virtually all of these pathways. Chronic energy intake exceeding expenditure promotes weight gain, visceral adiposity, insulin resistance, and increased hepatic lipid delivery [18, 19]. Nevertheless, energy balance alone does not fully explain the relationship between diet and MASLD [20]. Dietary quality, macronutrient composition, food processing, meal timing, and the overall combination of consumed foods may independently modify metabolic responses. Western-style dietary patterns characterized by high consumption of ultra-processed foods, refined grains, sugar-sweetened beverages, added fructose, saturated and trans fats, and red or processed meat have been associated with metabolic deterioration, hepatic lipotoxicity, inflammation, and disease progression [21-23].
Conversely, dietary patterns based on vegetables, fruits, legumes, whole grains, nuts, unsaturated fats, and minimally processed foods are associated with more favorable hepatic and cardiometabolic profiles [24, 25]. The management of MASLD requires an integrated approach that addresses both liver disease and its cardiometabolic determinants. Physical activity, obesity treatment, optimization of glycemic and lipid control, and management of other comorbidities remain important components of care [26, 27]. Although pharmacological options are expanding [28], lifestyle modification remains the foundation of treatment [5, 29, 30], and dietary intervention is not merely supportive advice but a potentially disease-modifying strategy. Importantly, its benefits may extend beyond the liver, because cardiovascular disease represents a major competing risk among individuals with MASLD [31].

Despite broad agreement that dietary modification is beneficial, uncertainty remains regarding the optimal dietary prescription [32, 33]. Comparisons between dietary approaches are complicated by substantial heterogeneity in intervention composition, energy intake, treatment duration, adherence, baseline metabolic status, and methods for assessing hepatic outcomes. This narrative review therefore evaluates the current evidence supporting energy restriction, weight loss, Mediterranean-style eating, and alternative dietary strategies, including low-carbohydrate, ketogenic, dietary approaches to stop hypertension (DASH), and intermittent fasting. It also discusses the food-quality principles shared across these interventions, identifies the principal limitations and knowledge gaps in the available literature, and outlines priorities for future research. Particular attention is given to whether the reported benefits reflect dietary composition, energy restriction, or weight loss; how different approaches compare in terms of efficacy and sustainability; and how dietary interventions can be individualized and implemented in routine clinical practice.

Potential dietary interventions in MASLD

Energy restriction and weight-loss-oriented dietary treatment

Current guidance does not identify a single standardized “MASLD diet”. Instead, recommendations converge on two closely related objectives: improving overall dietary quality and achieving sustained weight loss when excess body weight is present. Dietary treatment should therefore be individualized according to the patient’s nutritional status, metabolic comorbidities, food preferences, and ability to maintain the intervention over time [1, 5, 29, 34-37]. In adults with MASLD and overweight or obesity, the expected hepatic response is related to the magnitude of weight loss. A reduction of at least 5% of baseline body weight is generally recommended to decrease hepatic fat. Weight loss of approximately 7-10% may be required to improve hepatic inflammation, whereas reductions approaching 10% are associated with a greater likelihood of fibrosis improvement [1, 5, 34, 36, 38-41]. These weight-loss targets apply primarily to adults with overweight or obesity. They should not be extrapolated uncritically to normal-weight patients, those with cirrhosis, or those at risk of malnutrition or sarcopenia.

Energy restriction remains the best-supported dietary method for achieving these targets. Reviews and clinical guidance generally favor an individualized hypocaloric diet or sustained energy deficit rather than a single fixed distribution of carbohydrate, fat, and protein [36, 42-47]. Consequently, energy restriction should not be viewed as a separate competing dietary pattern. It is instead a therapeutic framework that can be applied to Mediterranean-style, low-carbohydrate, DASH, or other dietary approaches [37, 48].

Importantly, intentional weight loss should not be considered a universal therapeutic goal. In patients with lean MASLD or at increased risk of malnutrition or sarcopenia, the primary objective is to improve dietary quality, optimize cardiometabolic health, and preserve skeletal muscle mass, rather than to induce substantial weight reduction. In these individuals, nutritional management should be individualized and focus on overall metabolic health rather than energy restriction alone [1, 36, 37].

The principal clinical challenge is not merely inducing initial weight loss but maintaining it. A theoretically effective diet is unlikely to produce durable hepatic benefits when it is excessively restrictive, poorly adapted to the patient’s usual diet, or difficult to sustain. Individualization is therefore necessary even when the general therapeutic target is well established [29, 37, 40, 49-51]. Behavioral support, regular follow-up, self-monitoring, and individualized nutritional counseling substantially improve the likelihood of maintaining weight loss and long-term adherence to dietary interventions [50, 51].

Mediterranean-style diet

The Mediterranean diet is the most consistently recommended dietary pattern for MASLD. It is centered on vegetables, fruits, legumes, whole grains, nuts, olive oil, and fish, while limiting red meat, processed meat, refined products, and highly processed foods [33, 38, 40, 52-55]. This pattern incorporates several features that recur throughout MASLD guidance. It is predominantly plant-based, provides substantial amounts of fiber, prioritizes unsaturated over saturated and trans fats, and limits foods high in added sugars and refined carbohydrates. Therefore, its value lies not in any single food but in the combined improvement of overall diet quality [1, 5, 33, 35, 56].

Systematic reviews and meta-analyses of dietary interventions support the use of Mediterranean-style and hypocaloric diets to reduce liver fat. More recent syntheses of randomized controlled trials also indicate modest improvements in alanine aminotransferase and liver stiffness associated with Mediterranean dietary patterns [43, 53, 57-59]. These findings explain why the Mediterranean diet currently occupies a central position in clinical recommendations [1, 39, 60]. Nevertheless, the evidence should not be interpreted as demonstrating that every version of the Mediterranean diet is equally effective or superior to all alternative interventions. Mediterranean interventions may differ in prescribed energy intake, intensity of nutritional counseling, adherence, and the relative contribution of individual food groups. Furthermore, benefits observed in calorie-restricted Mediterranean interventions cannot always be clearly separated from the effects of weight loss itself [33, 48, 52, 53].

The Mediterranean diet should therefore be considered the best-supported default dietary pattern rather than the only acceptable option. Its principles can also be adapted to different culinary traditions. The central objective is to preserve its essential features: high consumption of minimally processed plant foods, fiber-rich products, and unsaturated fats, together with reduced consumption of sugar-sweetened beverages, ultra-processed foods, and red or processed meat [35, 37, 42, 44, 50, 51, 53].

Low-carbohydrate diets

Low-carbohydrate diets have received increasing attention as potential interventions for MASLD, particularly because metabolic dysfunction and excess body weight commonly coexist with the disease. Existing reviews describe potential benefits, but the evidence remains less well established than that supporting Mediterranean-style and general hypocaloric diets [33, 48, 49, 54, 57, 59, 61, 62].

Potential hepatic benefits of low-carbohydrate diets may result from reduced postprandial glycemia and insulinemia, decreased hepatic de novo lipogenesis, lower triglyceride synthesis, and facilitation of negative energy balance. These metabolic effects may contribute to rapid reductions in liver fat, particularly during the initial weeks of dietary intervention. However, the extent to which they are independent of weight loss remains uncertain [55, 61].

An important distinction must be made between reducing refined carbohydrates and restricting all carbohydrate-containing foods. Current dietary guidance consistently recommends minimizing simple sugars, refined carbohydrate products, sugar-sweetened beverages, and commercially produced fructose. However, it does not recommend eliminating whole grains, vegetables, legumes, or intact fruit, which are important components of Mediterranean-style and high-fiber dietary patterns [5, 20, 40, 42, 44, 55, 56]. Accordingly, the quality of a low-carbohydrate diet is likely to be clinically important. A pattern that reduces sugary drinks, sweets, and refined grains while retaining fiber-rich foods is consistent with the broader principles of MASLD dietary management. By contrast, carbohydrate restriction that substantially reduces vegetables, legumes, and other nutrient-dense foods may conflict with existing recommendations [48, 55, 61].

The current evidence does not establish low-carbohydrate diets as superior to calorie-controlled Mediterranean-style eating. Additional comparative trials are needed to determine whether their effects are primarily attributable to reduced energy intake and weight loss, or whether carbohydrate restriction provides additional hepatic benefit. Longer follow-up is also necessary to evaluate whether initial improvements can be maintained and whether they translate into meaningful effects on hepatic inflammation and fibrosis [33, 48, 57, 59, 61, 62].

Intermittent fasting

Intermittent fasting differs from other approaches because it primarily modifies the timing and frequency of food intake rather than prescribing a specific food pattern. Reviews and meta-analyses suggest that fasting-based strategies may improve selected liver-related outcomes, but their evidence base remains less settled than that for Mediterranean-style and conventional hypocaloric diets [32, 48, 49, 57, 59]. A central unresolved question is whether intermittent fasting provides benefits beyond those achieved through reduced total energy intake and subsequent weight loss [32, 48]. Fasting interventions may facilitate energy restriction for some individuals, but the dietary quality of foods consumed during eating periods remains important. An intermittent fasting schedule based on ultra-processed foods and excessive saturated fat would not align with the broader dietary recommendations for MASLD [32, 35, 37]. Therefore, intermittent fasting should be regarded as a possible method of organizing calorie intake rather than a substitute for dietary quality. Longer randomized trials should compare fasting-based strategies with continuous calorie restriction while controlling for total energy intake, weight loss, and background diet. Such studies are needed to determine whether meal timing has an independent effect on liver outcomes and whether the intervention can be maintained in routine clinical practice [32, 33, 48, 57]. Intermittent fasting may also be unsuitable for some patients, including those at risk of malnutrition or sarcopenia, individuals with advanced liver disease, older adults, and patients receiving glucose-lowering medications that increase the risk of hypoglycemia. Consequently, fasting strategies should be individualized and, when necessary, implemented under appropriate clinical supervision [49].

DASH diet

The DASH diet has also been discussed as a possible nutritional strategy for MASLD. Existing reviews classify it as a promising dietary approach, but the evidence remains less well established than that for Mediterranean-style eating [33, 48, 49, 57, 63]. The potential of the DASH diet lies in its alignment with several general recommendations for MASLD, including greater emphasis on plant-based foods, fiber-rich products, and improved overall diet quality [54, 56, 63]. It also encompasses low-fat dairy products and lean protein sources, with limited intake of sodium, saturated fat, and added sugars. However, the currently available evidence does not establish it as the optimal dietary pattern or demonstrate clear superiority over other calorie-controlled, high-quality diets [48, 63]. Further randomized trials are needed to evaluate its effects on liver fat, liver enzymes, liver stiffness, hepatic inflammation, and fibrosis. Direct comparisons with Mediterranean-style interventions would be particularly useful because both patterns share several favorable dietary characteristics [48, 63].

Vegetarian and plant-based diets

Vegetarian and plant-based diets comprise a heterogeneous group of dietary patterns. Lacto-ovo-vegetarian diets exclude meat and fish but retain eggs and dairy products, whereas vegan diets exclude all animal-derived foods; broader plant-forward or flexitarian approaches place greater emphasis on plant foods without requiring complete exclusion of animal products. Their potential relevance to MASLD depends less on the vegetarian label itself than on the quality of the foods used to replace animal products. Patterns centered on vegetables, legumes, whole grains, nuts, seeds, and minimally processed foods align with general MASLD recommendations, whereas plant-based diets dominated by refined grains, added sugars, and ultra-processed products may not confer comparable benefits [35, 38, 52]. MASLD-specific observational evidence is suggestive but not entirely consistent. Some cross-sectional studies found no protective association between vegetarianism and hepatic steatosis, whereas others found that vegetarian diets or greater adherence to healthful plant-based patterns were associated with a lower prevalence of steatosis and more favorable liver-related markers. In a prospective Korean cohort, higher adherence to a healthful plant-based diet was associated with a lower risk of MASLD in both women and men, whereas an unhealthful plant-based pattern was associated with an increased risk. These findings reinforce the importance of the quality of plant foods rather than simply excluding meat [38, 64].

Interventional evidence is also emerging. A low-fat vegan diet reduced hepatocellular lipid content, body weight, and insulin resistance in overweight adults, although the study population was not restricted to patients with MASLD. Smaller MASLD-specific trials of lacto-ovo-vegetarian diets reported improvements in hepatic steatosis, anthropometric measures, liver enzymes, and cardiometabolic markers. More recently, a six-month randomized trial involving 220 Chinese adults with MASLD found that a culturally adapted lacto-ovo-vegetarian diet produced greater reductions in body weight, fat mass, and visceral adiposity than an omnivorous diet and increased the proportion of participants achieving both clinically relevant weight loss and improvement in steatosis [65]. The findings indicate that at least part of the hepatic benefit was mediated by reductions in weight and visceral fat rather than necessarily by a weight-independent effect of vegetarianism [38, 65].

Nevertheless, the evidence remains less extensive than that available for Mediterranean-style eating. Existing studies differ in their definitions of vegetarian and plant-based diets, energy prescriptions, food quality, counseling intensity, and comparator diets. Most are relatively short and assess liver fat, enzymes, or metabolic markers rather than histological MASH resolution, fibrosis regression, or long-term clinical outcomes. It is also frequently difficult to distinguish the effects of dietary composition from those of energy restriction and weight loss. When more restrictive vegetarian or vegan diets are adopted, attention should also be paid to adequate intake of protein, vitamin B12, iron, calcium, vitamin D, and long-chain omega-3 fatty acids, particularly during long-term follow-up. Consequently, vegetarian diets cannot yet be considered superior to calorie-controlled Mediterranean-style interventions, although they represent a reasonable alternative for appropriately selected patients [38, 48].

Ketogenic diets

Ketogenic diets, which became increasingly popular in recent years, represent a more intensive form of carbohydrate restriction. It can be broadly described as a very low-carbohydrate, high-fat diet intended to induce nutritional ketosis. Reviews of dietary interventions in MASLD identify them as potentially beneficial, but the evidence remains preliminary and less consistent than that supporting Mediterranean-style or broadly hypocaloric diets [33, 48, 49, 57, 66, 67]. At present, the available evidence is insufficient to recommend ketogenic diets as the preferred first-line dietary intervention for MASLD. Published studies and reviews suggest potential benefit, but uncertainty remains regarding their comparative effectiveness, long-term sustainability, and clinical relevance beyond short-term changes in metabolic or liver-related markers [33, 59, 66, 67]. Potential safety concerns include gastrointestinal adverse effects, inadequate fiber and micronutrient intake, nephrolithiasis, and a clinically relevant increase in LDL cholesterol or apolipoprotein B in susceptible individuals, particularly with high saturated fat intake [67]. However, evidence demonstrating an increased incidence of long-term cardiovascular, renal, or liver-related clinical events remains insufficient. Future studies should clearly define the composition of ketogenic interventions, including the quality of dietary fat, protein sources, fiber intake, and total energy intake [66-68]. Without this information, studies using the same dietary label may evaluate substantially different interventions. Longer randomized trials comparing ketogenic diets with calorie-matched Mediterranean or conventional hypocaloric diets are required before their position in MASLD management can be established [48, 66, 67].

Cross-cutting food recommendations

Although dietary approaches differ in macronutrient composition and meal structure, guidelines and reviews show substantial agreement on the foods that should be emphasized or limited in MASLD management, as shown in Figure 1 and discussed in detail in this section.

Plant-rich and fiber-rich foods

Vegetables, whole grains, legumes, and other fiber-rich foods are repeatedly recommended as core components of dietary management. Their inclusion is consistent with Mediterranean-style eating and with the broader objective of improving dietary quality rather than focusing exclusively on calorie intake [41, 49, 52, 54-56, 69]. Whole fruit is generally included within the recommended dietary pattern. Restrictions should focus primarily on sugar-sweetened beverages and commercially produced fructose-containing products rather than on intact fruit [5, 40, 55, 56].

Fat quality

Dietary guidance recommends replacing saturated and trans fats with unsaturated fats. This recommendation supports the use of olive oil, nuts, fish, and other sources of unsaturated fatty acids within an otherwise balanced dietary pattern [20, 40-42, 54, 55]. This emphasis also illustrates why total fat content alone is an insufficient basis for evaluating a dietary intervention. A diet containing unsaturated fats from olive oil, nuts, and fish differs substantially from one containing large amounts of saturated fat from highly processed foods [55, 56, 70].

Protein sources

Recommended protein sources include plant proteins, fish, eggs, white meat, and low-fat dairy products. At the same time, red and processed meats should be reduced [40, 42, 44, 55, 56, 71]. The available guidance does not support defining MASLD treatment solely according to total protein intake. The source and broader dietary context of protein should also be considered [68, 71, 72].

Sugar-sweetened beverages and refined carbohydrates

Avoidance of sugar-sweetened beverages and commercially produced fructose is one of the most consistent recommendations across guidelines and reviews [5, 20, 40, 41, 54-56]. Similarly, recommendations focus on reducing refined carbohydrates and simple sugars rather than eliminating all carbohydrate-containing foods. This distinction is important because whole grains, vegetables, legumes, and fruit remain central components of the most strongly recommended dietary pattern [40, 42, 44, 55, 69, 70].

Ultra-processed foods

Ultra-processed foods (defined as mass-produced industrial formulations that contain multiple ingredients and heavily processed substances, e.g., hydrogenated oils, high-fructose corn syrup, and emulsifiers, rather than whole foods) should be limited, particularly those rich in added sugars and saturated fat. This recommendation reflects the broader shift from isolated nutrient targets towards overall dietary quality [5, 35, 52, 54, 56, 69, 70]. Reducing ultra-processed foods may simultaneously decrease intake of excess energy, refined carbohydrates, simple sugars, saturated fat, and processed meat. It therefore represents a practical component of several otherwise different dietary strategies [20, 55, 70].

Alcohol

Patients with MASLD exhibit heightened vulnerability to alcohol due to metabolic, mitochondrial, and immunologic factors that amplify oxidative stress and hepatic inflammation [73]. Therefore, all individuals with steatotic liver disease should be discouraged from consuming alcohol, as even moderate intake accelerates fibrosis and liver-related mortality, with complete and permanent abstinence advised for those with advanced fibrosis or cirrhosis [5, 34].

Coffee

Coffee consumption has been associated in observational studies with less liver damage and fewer liver-related clinical outcomes, but this evidence does not establish causality or support coffee as a treatment; however, some mechanistic pathways of hepatoprotection have been proposed [74, 75]. For patients who already drink coffee and tolerate it, unsweetened coffee without energy-dense creamers or syrups can be retained within an otherwise high-quality diet. A specific dose should not be prescribed solely for MASLD, and potential adverse effects or individual contraindications should be considered.

Special considerations

Normal weight (“lean”) MASLD

MASLD can occur at a body mass index below 25 kg/m² in non-Asian adults or below 23 kg/m² in Asian adults, and normal body weight does not exclude visceral adiposity, insulin resistance, dyslipidemia, hypertension, or low skeletal muscle mass [76]. In a recent Polish population-based cohort, approximately 12% of individuals with MASLD and 22% with MetALD had normal body weight, underscoring the clinical relevance of this phenotype in Central and Eastern Europe [77]. The goal in normal-weight MASLD is not routine large weight loss. Dietary management should prioritize reducing liver fat, improving lipid and glycemic control and blood pressure, reducing visceral adiposity where present, and maintaining or improving muscle mass. Diet and exercise are recommended even at normal body mass index; a modest 3-5% weight reduction may induce remission in selected patients with excess visceral fat, but aggressive energy restriction should be avoided, and weight trajectory, muscle strength, and nutritional adequacy should be monitored. Emphasis should remain on minimally processed foods, fiber-rich carbohydrates, unsaturated fats, and avoidance of sugar-sweetened beverages and excess fructose [37]. Evidence for effects on histological MASH, fibrosis, and clinical liver outcomes in normal-weight adults remains limited.

MASLD with cirrhosis

In MASLD-related cirrhosis, malnutrition and sarcopenia may coexist with obesity and are major determinants of frailty and clinical outcomes [78-80]. Routine hypocaloric treatment can exacerbate muscle loss, particularly in decompensated disease; nutritional assessment should therefore include recent intake and weight change, muscle mass and strength, and the presence of ascites or edema, which can mask tissue loss [78, 79]. Typical nutritional targets in cirrhosis are approximately 30-35 kcal/kg/day and 1.2-1.5 g protein/kg/day, calculated using dry or adjusted body weight as clinically appropriate, with the higher protein range often used in malnutrition or sarcopenia [78, 79, 81]. Protein should not be routinely restricted for hepatic encephalopathy. Long fasting periods should be avoided by distributing intake over three to five meals and including a late-evening snack. Sodium restriction may be required for ascites, but it should be balanced against the potential for reduced palatability and food intake. Any attempt at weight reduction in compensated cirrhosis and obesity should be modest, specialist-supervised, protein-sufficient, and combined with resistance or functional exercise, whereas decompensated cirrhosis warrants individualized hepatology and dietetic care [78, 79, 82].

Patients receiving incretin-based therapies

Glucagon-like peptide-1 receptor agonists and dual glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 receptor agonists are increasingly used for obesity and type 2 diabetes in patients with MASLD [83, 84]. These agents can facilitate substantial weight loss and reduce liver fat, or improve other liver-related outcomes [83, 85, 86]. However, nausea, vomiting, early satiety, altered food preferences, and a marked reduction in energy intake may compromise protein and micronutrient adequacy [83, 87]. A proportion of the weight lost consists of lean mass; for example, in a dual-energy X-ray absorptiometry (DXA) substudy of SURMOUNT-1, approximately 25% of the weight lost with tirzepatide was lean mass, although DXA-derived lean mass should not be equated directly with skeletal-muscle loss or functional impairment [83, 84]. Patients with low baseline muscle mass or function, older adults, those experiencing rapid or marked weight loss, and individuals with medical conditions predisposing to malnutrition or sarcopenia may warrant particularly close monitoring. Dietary counseling should therefore emphasize nutrient-dense, minimally processed foods, adequate individualized protein intake, regular hydration, and preservation or introduction of structured resistance or strength exercise. Small, frequent meals may improve nutrient intake and gastrointestinal tolerance when appetite is low or when nausea and early satiety are present. Body-weight trajectory should be interpreted alongside muscle strength, physical function, and, when feasible, body composition, rather than as an isolated treatment outcome [83, 87]. Persistent vomiting, inability to meet nutritional needs, or rapid functional decline should prompt reassessment of treatment and referral to an appropriately qualified clinician or dietitian [83, 87]. Highly restrictive diets and prolonged fasting should generally be avoided during rapid pharmacologically induced weight loss because long periods without adequate protein, energy, or dietary variety may increase the risk of nutritional inadequacy and loss of fat-free mass [83].

Overall interpretation of the evidence

The strongest evidence supports improved dietary quality and, when excess body weight is present, a sustainable energy deficit leading to clinically meaningful weight loss (Table 1). Mediterranean-style eating remains the best-supported named dietary pattern. Its evidence is moderate to high for liver fat and cardiometabolic outcomes [57, 88], low to moderate for histological MASH or fibrosis outcomes [60, 89], and low for clinical liver outcomes since, to date, only one prospective cohort study (with 47,429 MASLD patients) has linked higher Mediterranean diet adherence to reduced liver-related events (HR = 0.55) and mortality (HR = 0.85); evidence from randomized clinical trials is lacking [90].

Evidence for low-carbohydrate, ketogenic, DASH, and intermittent-fasting strategies is promising but less conclusive, and longer randomized controlled trials are required [32, 33, 48, 49, 57, 59, 61, 63, 66, 67]. Therefore, the available evidence supports a hierarchy rather than an absolute distinction between effective and ineffective diets. Alternative approaches may be suitable for selected patients, provided that they preserve adequate nutritional quality and can be maintained over time [37, 46, 48]. Special populations require different priorities: weight maintenance and metabolic-risk control in some normal-weight patients, and preservation of nutritional status and muscle mass in cirrhosis or during rapid incretin-associated weight loss. These principles are integrated into a proposed patient-centered dietary management algorithm that distinguishes between patients who are candidates for weight loss and those who require weight maintenance, muscle preservation, or specialist-modified nutritional care (Fig. 2).

Knowledge gaps

The most important gap is the absence of sufficient evidence to identify a universally optimal dietary pattern for MASLD. Although Mediterranean-style eating has the strongest and most consistent support, it remains uncertain whether its advantages are attributable to its specific composition, to associated energy reduction and weight loss, or to a combination of these factors [33, 37, 38, 48, 52]. A second limitation is the shortage of long-term comparative randomized trials. Existing evidence supports improvements in liver fat and selected biomarkers, but longer studies are required to determine whether dietary interventions produce durable changes in hepatic inflammation, liver stiffness, and fibrosis [32, 43, 48, 57-59]. Outcome-specific certainty should therefore be reported rather than assigning a single strength of evidence to Mediterranean-style eating across all hepatic and cardiometabolic endpoints.

Third, alternative diets are not always defined consistently. Low-carbohydrate and ketogenic diets may differ substantially in carbohydrate restriction, fat quality, protein sources, fiber intake, and total energy intake. Intermittent-fasting studies may use different fasting schedules and background diets. This limits direct comparison between studies and complicates translation into clinical recommendations [32, 48, 61, 66, 67].

Fourth, adherence and sustainability require greater attention. A dietary pattern may be effective in a controlled intervention but difficult to maintain in routine practice. Research should therefore evaluate not only biological efficacy but also long-term adherence, cultural adaptability, affordability, and patient acceptability [37, 49-51, 53]. Finally, more evidence is needed to guide dietary treatment in patients with advanced fibrosis, cirrhosis, diabetes, or concurrent obesity treatment. In these populations, nutritional decisions should be individualized and made in collaboration with a hepatologist, dietitian, or another appropriately qualified clinician [36, 37, 50].

Future research prospects

Future studies should prioritize long-term, adequately powered randomized trials that directly compare Mediterranean-style, low-carbohydrate, ketogenic, DASH, and intermittent fasting interventions [32, 48, 61, 63, 66, 67]. Comparators should be clearly defined, and total energy intake and achieved weight loss should be reported to help distinguish the effects of dietary composition from those of energy restriction. Dietary interventions should also be described in sufficient detail to permit replication. This includes the proportions and sources of carbohydrate, fat, and protein; fiber intake; consumption of ultra-processed foods; counseling intensity; and methods for assessing adherence [37, 48, 52]. Future research should extend beyond short-term changes in body weight and liver enzymes. Relevant outcomes include quantitative changes in liver fat, liver stiffness, and hepatic inflammation and fibrosis, as well as maintenance of weight loss and the need for pharmacological treatment [57, 58, 60]. Trials should prespecify evidence hierarchies by outcome and include histological, fibrosis-related, and clinical liver endpoints rather than combining them with short-term metabolic markers.

Greater attention should also be given to individual variability. Studies should determine which dietary strategies are most suitable for patients with different degrees of excess weight, lean MASLD, diabetes, dyslipidemia, advanced liver disease, and differing food preferences [36, 37, 91]. The objective should not necessarily be to identify a single diet for all patients, but rather to establish which evidence-based pattern is most effective and sustainable for specific clinical contexts. Implementation research will also be important. Mediterranean-style eating and other high-quality dietary patterns must be adapted to local culinary traditions, food availability, and socioeconomic conditions. The effectiveness, acceptability, and long-term sustainability of such adaptations should be assessed rather than assumed [50, 51, 53].

Challenges in achieving sustained dietary change

Translating dietary recommendations into sustained behavioral change is often more difficult than selecting a theoretically appropriate dietary pattern (Table 2). MASLD is frequently asymptomatic, and patients may underestimate its long-term hepatic and cardiometabolic consequences or may not clearly understand the relationship between diet, body weight, metabolic dysfunction, and liver injury. Generic recommendations such as “eat healthily” or “lose weight” may provide insufficient practical guidance. Adherence can be further limited by long-standing eating habits, food cravings, stress-related eating, limited time and cooking skills, financial constraints, cultural preferences, family and social influences, and easy access to inexpensive ultra-processed foods [92]. Repeated unsuccessful attempts at weight loss, unrealistic expectations, and early weight regain may additionally reduce motivation and self-efficacy [93].

Therefore, dietary implementation should focus on behavioral support rather than information alone. The selected dietary pattern and, when appropriate, the energy deficit should be agreed with the patient and adapted to nutritional status, metabolic comorbidities, culinary traditions, food availability, financial resources, and readiness to change. Broad dietary principles can be translated into a small number of specific and achievable actions, such as eliminating sugar-sweetened beverages, replacing refined grains with whole-grain products, increasing the number of plant-based meals, or preparing food in advance. Gradual changes may be more sustainable than an immediate and highly restrictive dietary transformation [94] (Fig. 2).

Because food purchasing, meal preparation, and eating often occur within a household, the involvement of partners, relatives, and other family members may substantially influence adherence. Family members can support dietary change, including in older adults, by participating in meal planning, modifying shared meals, reducing the availability of less appropriate foods at home, and reinforcing the patient’s motivation [95, 96]. Conversely, conflicting dietary preferences, unsupportive attitudes, or social pressure during family gatherings may undermine adherence. When appropriate and acceptable to the patient, dietary counseling should therefore involve key household members and encourage family-level rather than exclusively individual changes.

Self-monitoring, regular follow-up, feedback on progress, problem-solving, relapse planning, and motivational interviewing may support adherence and self-efficacy. Involvement of family members and access to dietitians, behavioral specialists, and other members of a multidisciplinary team may be particularly useful when social, psychological, or medical barriers are present. Digital tools may provide additional support through food recording, reminders, education, and remote feedback, although they should complement rather than replace individualized clinical care [97].

The risk of malnutrition, micronutrient deficiencies, and abnormalities in body mass composition should be considered in patients with MASLD [98, 99]. Chronic inflammation, insulin resistance, restricted food intake, and gut dysbiosis contribute to both liver disease progression and impaired muscle health [100, 101]. For nutritional assessment, it is important to combine nutritional screening tools with evaluation of muscle mass and body composition, accounting for changes in body weight over time, food intake, muscle strength, and muscle quality [102]. Nutritional management requires adequate energy and macronutrient intake tailored to the disease’s etiology and severity, metabolic comorbidities, and the risk of sarcopenia [72, 100, 101, 103]. In addition, evaluation of micronutrient status, particularly vitamins A, D, and E, and trace elements such as zinc, iron, copper, and selenium, might be important in patients with MASLD [37, 104-106].

Increasing dietary fiber intake is a key component of dietary management in MASLD but may initially lead to bloating, abdominal discomfort, or flatulence, particularly in individuals with previously low fiber intake. To address this, gradual increases in fiber intake over at least two weeks, together with adequate water consumption, improve gastrointestinal tolerance and support the physiological effects of fiber [107, 108]. Soluble fiber is generally better tolerated than insoluble fiber; however, most foods contain a mix of both types [107, 109]. Practical strategies to improve tolerance include introducing fiber in small portions, soaking and thoroughly cooking legumes, peeling fruits and vegetables when necessary to reduce insoluble fiber intake, and distributing fiber-rich foods evenly across meals rather than consuming large amounts at once [110, 111].

Conclusions

Dietary management is a central component of MASLD care. The strongest evidence supports a Mediterranean-style dietary pattern and, when excess body weight is present, a sustainable energy deficit that produces clinically meaningful weight loss. The evidence supporting Mediterranean-style eating is greatest for liver fat and cardiometabolic outcomes and substantially lower for histological MASH, fibrosis, and clinical liver outcomes. Normal-weight MASLD, cirrhosis, and incretin-based treatment require modified goals that prioritize metabolic control, adequate nutrient and protein intake, and preservation of muscle mass rather than indiscriminate energy restriction. Alcohol exposure should be assessed routinely and limited, with complete abstinence in advanced fibrosis or cirrhosis; coffee may be retained as an unsweetened beverage but should be presented as an observational association rather than a therapeutic intervention. Low-carbohydrate, DASH, ketogenic, intermittent-fasting, and vegetarian or plant-based approaches may improve selected hepatic and metabolic outcomes, but their comparative effectiveness, long-term sustainability, and effects on inflammation and fibrosis remain less certain. Current evidence therefore favors an individualized strategy that prioritizes overall food quality, limits sugar-sweetened beverages, refined carbohydrates, ultra-processed foods, and red or processed meat, and is maintainable over time. Future research should focus on longer comparative trials, standardized, outcome-specific hepatic endpoints, clearer intervention definitions, and the identification of dietary approaches best suited to specific patient profiles.

Disclosures

This research received no external funding.

Institutional review board statement: Not applicable.

The authors declare no conflict of interest.

References