Dietary Fats and Fatty Liver Disease

1. Introduction

When most people think about dietary fats and liver health, they imagine butter, lard, and bacon as the primary culprits. The reality is far more nuanced. While all fats impact liver metabolism, the type, processing, and ratio of fats we consume matter profoundly.

This chapter examines the complex relationship between dietary fats and metabolic dysfunction-associated steatotic liver disease (MASLD), with particular attention to the often-overlooked story of omega-6 fatty acids and their dramatic increase in the modern Western diet.

Before diving into the specifics, it’s essential to understand that the terminology for fatty liver disease has evolved. In June 2023, the international consensus renamed nonalcoholic fatty liver disease (NAFLD) to metabolic dysfunction-associated steatotic liver disease (MASLD) to better reflect the metabolic nature of the condition and reduce stigma.

This change is more than semantic, it emphasizes that this liver disease is fundamentally linked to metabolic dysfunction, including obesity, insulin resistance, and dyslipidemia. Importantly, 99% of individuals previously diagnosed with NAFLD meet the criteria for MASLD, and clinical outcomes are essentially identical between the two definitions.^1,2^ Throughout this chapter, we use MASLD as the primary term while acknowledging that much of the existing research was conducted under the NAFLD nomenclature.

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2. Understanding Dietary Fats

Before examining how specific fats influence liver health, we need a framework for understanding fat classification. Dietary fats can be categorized by their source (plant or animal) and their chemical structure and both matter for metabolic health.

DIETARY FATS
│
├── SATURATED FATS (0 double bonds)
│ ├── Short-Chain (2-5 carbons): Butyric, Caproic
│ ├── Medium-Chain (6-12 carbons): Caprylic, Capric, Lauric
│ └── Long-Chain (13+ carbons): Myristic, Palmitic, Stearic, etc.
│
└── UNSATURATED FATS (1+ double bonds)
├── MONOUNSATURATED (1 double bond)
│ └── Omega-9: Oleic acid
│
├── POLYUNSATURATED (2+ double bonds)
│ ├── Omega-3: ALA, EPA, DHA
│ └── Omega-6: Linoleic acid, etc.
│
└── TRANS FATS (double bonds in trans configuration)
├── Industrial trans fats (avoid)
└── Natural trans fats (CLA, Vaccenic acid)

Classification by Chemical Structure

Saturated Fats: These fats have no double bonds in their carbon chains, making them solid at room temperature. Common sources include animal fats (butter, lard, tallow), coconut oil, and palm oil. For decades, saturated fats were demonized as the primary dietary villain in metabolic disease. However, recent evidence suggests a more nuanced picture, not all saturated fats behave identically, and their effects may depend heavily on the overall dietary context and individual metabolic health.
Monounsaturated Fats (MUFAs): Containing one double bond in their carbon chain, these fats are generally liquid at room temperature but may solidify when refrigerated. Olive oil, avocados, and nuts are rich in MUFAs, particularly oleic acid. Fatty acids are categorized into families based on the position of the first double bond, so oleic acid and erucic acid are called omega-9 fats. The Mediterranean diet’s emphasis on olive oil has been associated with lower MASLD prevalence and improved metabolic health (Del Bo, 2023).
Polyunsaturated Fats (PUFAs): These fats contain two or more double bonds and remain liquid even when refrigerated. PUFAs are further divided into omega-3 and omega-6 families, based on the position of the first double bond from the methyl end of the fatty acid chain. This distinction is not merely chemical pedantry, it has profound metabolic implications.
Trans Fats: Created through industrial hydrogenation or formed naturally in small amounts in ruminant animals, trans fats have been largely eliminated from the food supply in many countries due to their clear association with cardiovascular disease and metabolic dysfunction. They have no place in any healthy dietary pattern.

The Omega Fatty Acid Families

Omega-3 Fatty Acids: These include alpha-linolenic acid (ALA) from plant sources like flaxseed and walnuts, and the longer-chain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found primarily in fatty fish. ALA is an essential fatty acid, our bodies cannot synthesize it, so we must obtain it from diet. While EPA and DHA can technically be synthesized from ALA, conversion rates are very low (<5% for EPA, <0.5% for DHA), making dietary sources important. They serve as precursors for anti-inflammatory mediators and play crucial roles in cell membrane structure and function.
Omega-6 Fatty Acids: The primary omega-6 fatty acid is linoleic acid (LA), found abundantly in industrial seed oils like soybean, corn, sunflower, and safflower oils. Like omega-3s, omega-6 fatty acids are essential and cannot be synthesized by the human body. Linoleic acid can be converted through a series of enzymatic steps to arachidonic acid (AA), which serves as a precursor for both pro-inflammatory and anti-inflammatory signaling molecules.
Omega-9 Fatty Acids: Primarily oleic acid, these are non-essential fatty acids that our bodies can synthesize. They are abundant in olive oil, avocados, and many nuts. Unlike omega-3 and omega-6 fatty acids, omega-9s do not compete for the same enzymatic pathways and are generally considered metabolically neutral to beneficial.

2.1 SATURATED FATS (No double bonds)

Fatty Acid Name	Chemical Notation	Common Sources	Notes
Lauric Acid	12:0	Coconut oil (47%), Palm kernel oil	Medium-chain fatty acid
Myristic Acid	14:0	Coconut oil, Palm kernel oil, Dairy fat	Raises LDL cholesterol
Palmitic Acid	16:0	Palm oil (44%), Meat, Dairy, Cocoa butter	Most common saturated fat
Stearic Acid	18:0	Cocoa butter, Animal fat, Shea butter	Neutral effect on cholesterol
Arachidic Acid	20:0	Peanut oil	Less common
Behenic Acid	22:0	Peanut oil, Rapeseed oil	Less common
SHORT-CHAIN (2-5 carbons)
Butyric Acid	4:0	Butter (3-4%), Milk fat, Ghee	Gut health benefits; distinctive butter flavor
Caproic Acid	6:0	Butter, Milk fat, Coconut oil	Also called Hexanoic acid
MEDIUM-CHAIN (6-12 carbons)
Caprylic Acid	8:0	MCT oil, Coconut oil (8%), Palm kernel oil, Dairy fat	Rapidly absorbed; ketogenic
Capric Acid	10:0	MCT oil, Coconut oil (7%), Palm kernel oil, Dairy fat	Rapidly absorbed; ketogenic
Lauric Acid	12:0	Coconut oil (47%), Palm kernel oil, Dairy fat (2-3%)	Borderline medium/long chain

Key Sources High in Saturated Fats:

Coconut oil (92% saturated)
Palm oil (50% saturated)
Butter (63% saturated)
Animal fats (lard, tallow: 40-50% saturated)
Dairy products (butter, milk, cream, whey protein, milk powder): Rich in butyric, caproic, caprylic, capric acids
MCT Oil supplements: Concentrated caprylic (C8) and capric (C10) acids
Coconut oil: High in caprylic, capric, and especially lauric acid
Butter/Ghee: 11-17% short and medium-chain fatty acids

Why dairy fats are unique:

Milk fat contains ALL chain lengths from 4 to 18 carbons
Whey protein powders and milk powders retain these milk fats unless specifically removed
Short-chain fatty acids like butyric acid support gut health and are anti-inflammatory

2.2 UNSATURATED FATS (Contains double bonds)

A. MONOUNSATURATED FATS (MUFA) - One double bond

Fatty Acid Name	Chemical Notation	Common Sources	Notes
Oleic Acid (Omega-9)	18:1 n-9	Olive oil (73%), Avocado oil (71%), Canola oil (63%), Almonds, Macadamia nuts	Most abundant MUFA; heart-healthy
Palmitoleic Acid (Omega-7)	16:1 n-7	Macadamia nuts, Sea buckthorn oil	Less common
Erucic Acid (Omega-9)	22:1 n-9	Old-style rapeseed oil	Modern canola is bred to be low in this

Key Sources High in MUFAs:

Olive oil (73% MUFA)
Avocado oil (71% MUFA)
Canola oil (63% MUFA)
Peanut oil (46% MUFA)
Almonds, cashews, pecans

B. POLYUNSATURATED FATS (PUFA) - Multiple double bonds

B1. OMEGA-3 FATTY ACIDS (n-3 or ω-3)

Fatty Acid Name	Chemical Notation	Type	Common Sources	Notes
Alpha-Linolenic Acid (ALA)	18:3 n-3	Plant-based	Flaxseed oil (53g/100g), Chia seeds, Walnuts, Hemp seeds, Canola oil (9g/100g), Soybean oil	Essential fatty acid; body converts ~10% to EPA/DHA
Eicosapentaenoic Acid (EPA)	20:5 n-3	Marine	Fatty fish (salmon, mackerel, sardines, herring), Fish oil supplements, Algae oil	Anti-inflammatory; directly usable
Docosahexaenoic Acid (DHA)	22:6 n-3	Marine	Fatty fish (salmon, mackerel, sardines), Fish oil, Algae oil, Krill oil	Brain & eye health; directly usable
Docosapentaenoic Acid (DPA)	22:5 n-3	Marine	Fatty fish, Seal oil	Less studied; intermediate form

Key Omega-3 Sources:

PLANT-BASED (ALA):

Flaxseed oil: 7,260 mg per tablespoon
Chia seeds: 5,060 mg per tablespoon
Walnuts: 2,570 mg per ounce
Hemp seeds, hemp oil
Canola oil: 1,280 mg per tablespoon

MARINE-BASED (EPA + DHA):

Mackerel: 4,580 mg per 100g
Salmon: 2,260 mg per 100g
Sardines: 2,000 mg per 100g
Herring: 1,700 mg per 85g
Anchovies, tuna

B2. OMEGA-6 FATTY ACIDS (n-6 or ω-6)

Fatty Acid Name	Chemical Notation	Common Sources	Notes
Linoleic Acid (LA)	18:2 n-6	Safflower oil (75%), Sunflower oil (66%), Corn oil (54%), Soybean oil (51%), Walnuts, Sunflower seeds	Essential fatty acid; most abundant omega-6
Gamma-Linolenic Acid (GLA)	18:3 n-6	Borage oil, Evening primrose oil, Black currant seed oil	Anti-inflammatory properties
Arachidonic Acid (AA)	20:4 n-6	Egg yolks, Meat, Poultry, Fish	Precursor to inflammatory compounds
Conjugated Linoleic Acid (CLA)	18:2 (various isomers)	Grass-fed beef, Dairy products	May have metabolic benefits

Key Omega-6 Sources:

Safflower oil: 74,600 mg per tablespoon
Sunflower oil: 65,700 mg per tablespoon
Corn oil: 53,520 mg per tablespoon
Grapeseed oil: 69% omega-6
Soybean oil: 51,000 mg per tablespoon
Walnuts: 10,800 mg per ounce
Sunflower seeds, pumpkin seeds
Poultry, eggs, nuts

B3. OMEGA-9 FATTY ACIDS (n-9 or ω-9)

Fatty Acid Name	Chemical Notation	Common Sources	Notes
Oleic Acid	18:1 n-9	Olive oil (73%), Avocado oil (71%), Canola oil (60%), Almonds, Cashews	Non-essential (body can produce it); heart-healthy
Erucic Acid	22:1 n-9	Mustard seed oil, Old rapeseed varieties	Modern canola bred to reduce this
Mead Acid	20:3 n-9	Produced in body during omega-³⁄₆ deficiency	Biomarker of essential fatty acid deficiency

Key Omega-9 Sources:

Olive oil (especially extra virgin): 73% MUFA (mostly oleic)
Avocado oil: 71% MUFA
Canola oil: 60% MUFA
High-oleic sunflower/safflower oils
Almonds, cashews, pecans, macadamia nuts
Avocados

D. TRANS FATS (Industrial & Natural) Unsaturated fats with trans configuration of double bonds

Trans Fat Type	Chemical Notation	Common Sources	Notes
INDUSTRIAL TRANS FATS
Elaidic Acid	18:1 trans-9	Partially hydrogenated oils, Margarine (old formulas), Fried foods, Baked goods	Trans version of oleic acid; raises LDL, lowers HDL
Linoelaidic Acid	18:2 trans	Partially hydrogenated oils	Trans version of linoleic acid
NATURAL TRANS FATS
Vaccenic Acid	18:1 trans-11	Dairy fat, Beef, Lamb	Natural ruminant trans fat; may be neutral or beneficial
Conjugated Linoleic Acid (CLA)	18:2 (cis-9, trans-11)	Grass-fed dairy, Grass-fed beef	Natural trans fat; potential health benefits

Key Sources:

AVOID: Industrial trans fats
- Partially hydrogenated vegetable oils
- Many processed foods, baked goods (cookies, crackers, pastries)
- Fried fast foods
- Stick margarine (old formulas)
Natural trans fats (small amounts, generally considered safe):
- Dairy products: 2-5% of fat
- Beef and lamb: 3-9% of fat
- These include vaccenic acid and CLA

Health note: Industrial trans fats are strongly linked to heart disease and should be avoided. Natural trans fats from dairy/meat are present in small amounts and are not associated with the same health risks.

2.3 QUICK REFERENCE: Common Cooking Oils Breakdown

Oil	Saturated	MUFA (mainly Omega-9)	PUFA	Omega-3	Omega-6	Omega-6:3 Ratio
Canola	7%	63% (oleic acid)	28%	9.1g	18.6g	2:1 (ideal)
Olive	14%	73% (oleic acid)	11%	0.8g	9.8g	12:1
Avocado	12%	71% (oleic acid)	13%	1.0g	12.5g	13:1
Peanut	17%	46% (oleic acid)	32%	0g	32g	∞:1
Coconut	92% (lauric, myristic, palmitic)	6%	2%	0g	1.8g	N/A
Palm	50% (palmitic)	40% (oleic acid)	10%	0.2g	9.1g	46:1
Soybean	15%	23%	58%	7.0g	51g	7:1
Corn	13%	28%	55%	1.2g	53.5g	46:1
Sunflower (standard)	10%	20%	66%	0.2g	65.7g	329:1 (poor)
Safflower	7%	15%	75%	0g	74.6g	∞:1 (poor)
Flaxseed	9%	18%	68%	53.4g	14.3g	0.3:1 (excellent)
Walnut	9%	23%	63%	10.4g	52.9g	5:1
Sesame	14%	40% (oleic acid)	42%	0.3g	41.7g	138:1
Cottonseed	26% (palmitic)	18%	52%	0.2g	51.5g	258:1
Grapeseed	10%	16%	70%	0.1g	69.6g	696:1 (very poor)

(Values per 100g oil)

COMPLETE DAIRY FAT PROFILE What’s in milk, butter, whey protein powder, milk powder

Fat Component	% in Milk Fat	% in Butter	Notes
Short-chain (4:0 to 6:0)	8-11%	8-11%	Butyric, caproic acids
Medium-chain (8:0 to 12:0)	5-8%	5-8%	Caprylic, capric, lauric
Palmitic acid (16:0)	25-30%	25-30%	Major saturated fat
Stearic acid (18:0)	10-13%	10-13%	Saturated fat
Oleic acid (18:1 n-9)	20-30%	20-30%	Major MUFA (omega-9)
Linoleic acid (18:2 n-6)	1-3%	1-3%	Omega-6 PUFA
Alpha-linolenic acid (18:3 n-3)	0.5-1.5%	0.5-1.5%	Omega-3 (higher in grass-fed)
CLA (conjugated linoleic acid)	0.5-2%	0.5-2%	Higher in grass-fed
Trans fats (natural)	2-5%	2-5%	Vaccenic acid, CLA

In whey protein powders:

Whey protein concentrate (WPC): Contains 1-9% fat (includes all above dairy fats)
Whey protein isolate (WPI): Contains <1% fat (most dairy fats removed)
Milk protein powder/whole milk powder: Contains 26-27% fat (full dairy fat profile)
Skim milk powder: <1% fat

Understanding the Notation

Number before colon (18): Number of carbon atoms
Number after colon (1, 2, 3): Number of double bonds
n-3, n-6, n-9: Position of first double bond from the methyl end
Example: Oleic acid = 18:1 n-9 means 18 carbons, 1 double bond, first double bond at position 9

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3. Historical Context: How We Got Here

For millennia, humans consumed traditional fats, butter, lard, tallow, and olive oil, with relatively balanced omega-6 to omega-3 ratios estimated at 1:1 to 4:1, though precise historical ratios are difficult to establish with certainty and likely varied considerably by geography and season. The 20th century brought dramatic changes to our fat consumption patterns:

1900s-1920s: Introduction of cottonseed oil and the development of hydrogenation technology for creating solid vegetable shortening
1950s-1960s: The “vegetable oil” marketing push gained momentum, positioning seed oils as healthier alternatives to animal fats
1970s-1980s: Large-scale anti-saturated fat campaigns based on the diet-heart hypothesis led to widespread replacement of animal fats with seed oils in both home cooking and food manufacturing
1990s-Present: Industrial seed oils became ubiquitous in processed foods, restaurant cooking, and home kitchens, resulting in a 20-fold increase in omega-6 consumption

The result? Modern Western diets now exhibit omega-6 to omega-3 ratios of 15:1 to 20:1 (Simopoulos AP, 1999), compared to the historical ratio of approximately 1:1 to 4:1. This dramatic shift occurred over just a few generations, far too rapidly for our metabolism to adapt. While evolutionary arguments alone don’t prove harm, they provide context for understanding why modern dietary patterns may create metabolic stress.

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4. Saturated Fat and Liver Health

For decades, saturated fat has been cast as the dietary villain responsible for metabolic disease, cardiovascular disease, and presumably, fatty liver disease. But when we examine the evidence specifically for MASLD, the picture becomes considerably more complex.

The relationship between saturated fat and liver health cannot be reduced to simple cause and effect, context, quantity, food matrix, and individual metabolic health all play crucial roles.

Does Saturated Fat Independently Increase MASLD Risk?

The short answer: it’s complicated. Research suggests that saturated fat intake does have immediate metabolic effects. A controlled study in humans found that a single bolus of saturated fat resulted in measurable increases in insulin resistance, hepatic triglycerides, and gluconeogenesis.(Chavez & Summers 2017)

In animal models, high saturated fat diets consistently promote hepatic steatosis and metabolic dysfunction. However, these controlled experiments don’t fully capture the complexity of real-world eating patterns.

The challenge lies in disentangling saturated fat from calories, dietary pattern, and food quality. Most high-saturated-fat diets in observational studies also tend to be high in processed foods, refined carbohydrates, and total calories. When researchers compare isocaloric diets with varying saturated fat content while keeping other variables constant, the picture becomes less clear.

Current evidence suggests that saturated fat’s effects on the liver are likely dose-dependent and context-dependent. Moderate intake from whole food sources (such as dairy, eggs, and unprocessed meat) in the context of a nutrient-dense, minimally processed diet appears less problematic than high intake from ultra-processed foods rich in both saturated fat and refined carbohydrates.

The 2024 EASL-EASD-EASO Clinical Practice Guidelines on MASLD emphasize the importance of minimizing processed foods while encouraging whole, nutrient-dense options, implicitly recognizing that food quality matters as much as macronutrient composition.

4.1 Is Reducing Saturated Fat Useful for MASLD Reversal?

Evidence consistently shows that MASLD reversal is based on overall dietary patterns than isolated nutrients. Weight loss of 7-10% body weight consistently improves MASLD markers including liver fat, inflammation, and even fibrosis.^5,6^ But is this benefit specific to reducing saturated fat, or is it primarily about caloric restriction and weight loss regardless of fat composition?

Research comparing different dietary approaches suggests that multiple dietary patterns can improve MASLD when they achieve weight loss and improve metabolic health. The Mediterranean diet, which is relatively high in monounsaturated fats from olive oil but also contains moderate amounts of saturated fat from dairy and meat, has shown consistent benefits for liver health even without significant weight loss (Del Bo et al, 2023) This suggests that the quality of the overall dietary pattern, emphasizing whole foods, vegetables, fruits, fish, nuts, and olive oil while minimizing processed foods and added sugars, may be more important than simply reducing saturated fat.

That said, replacing some saturated fat with healthier fat sources (particularly olive oil, nuts, avocados, and fatty fish) appears beneficial. The question is not whether you should eliminate butter and ghee entirely, but whether you should make them your primary fat sources or consume them in excess. For most people with MASLD, moderate intake of traditional saturated fats from whole food sources, in the context of a nutrient-dense diet emphasizing plants, fish, and olive oil, represents a sensible middle ground.

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5. Omega-6 Biochemistry and Liver Metabolism

To understand why omega-6 fatty acids might influence liver health, we need to examine their metabolic fate in the body. Unlike saturated and monounsaturated fats, which are primarily used for energy or incorporated into cell membranes in their original form, polyunsaturated fatty acids (PUFA) undergo enzymatic conversion to bioactive signaling molecules that influence inflammation, immunity, and cellular function.

The Linoleic Acid Pathway

Dietary linoleic acid (LA, 18:2 n-6), the predominant omega-6 fatty acid in modern diets, follows a well-characterized metabolic pathway:

Linoleic Acid (LA, 18:2 n-6)

↓ (Δ6-desaturase enzyme)

γ-Linolenic Acid (GLA, 18:3 n-6)

↓ (Elongase enzyme)

Dihomo-γ-linolenic Acid (DGLA, 20:3 n-6)

↓ (Δ5-desaturase enzyme)

Arachidonic Acid (AA, 20:4 n-6)

↓ (COX and LOX enzymes)

Pro-inflammatory Eicosanoids (PGE2, LTB4, TXA2)

Note: ALl dietary LA does NOT get fully converted to AA and eicosanoids, the majority is oxidized for energy or stored.

This pathway is tightly regulated under normal circumstances. The rate-limiting enzyme, Δ6-desaturase, is influenced by dietary factors, insulin status, and inflammatory signals. Under conditions of excess omega-6 intake and metabolic stress, both characteristic of modern Western diets and MASLD, this pathway can become dysregulated, potentially leading to excessive production of arachidonic acid and its downstream inflammatory mediators.

5.1 The Inflammation Connection

Arachidonic acid serves as the substrate for several enzyme systems that produce bioactive lipid mediators:

Cyclooxygenase (COX) enzymes convert arachidonic acid to prostaglandins, including PGE₂, which has complex context-dependent effects. While PGE₂ can be pro-inflammatory in some settings, it also has immunomodulatory functions. In the liver, excessive PGE₂ production has been associated with inflammation and fibrosis progression.
Lipoxygenase (LOX) enzymes produce leukotrienes like LTB₄, potent pro-inflammatory mediators that recruit immune cells and amplify inflammatory responses. In fatty liver disease, elevated leukotrienes contribute to hepatic inflammation and the progression from simple steatosis to steatohepatitis.
Thromboxane synthase converts arachidonic acid to thromboxanes, which promote platelet aggregation and vasoconstriction. In the context of liver disease, excessive thromboxane production may contribute to microvascular dysfunction and fibrosis.

It’s crucial to understand that these mediators aren’t inherently “bad”, they play essential roles in normal physiology, including wound healing, immune function, and vascular regulation. The problem arises when their production becomes excessive and chronic, contributing to sustained inflammation and tissue damage. This is where the balance between omega-6 and omega-3 fatty acids becomes critical.

5.2 Competition with Omega-3 Fatty Acids

Omega-3 and omega-6 fatty acids compete for the same enzymatic machinery. This metabolic competition has profound implications for inflammatory balance:

Enzyme competition: Δ6-desaturase, the rate-limiting enzyme in both pathways, has higher affinity for omega-3 fatty acids. However, when omega-6 intake vastly exceeds omega-3 intake (as in modern diets), the sheer abundance of omega-6 substrates means more omega-6 conversion occurs, effectively blocking omega-3 metabolism.
Reduced EPA and DHA production: Excess dietary omega-6 impairs the conversion of plant-based omega-3 (alpha-linolenic acid) to the more bioactive EPA and DHA. This is particularly problematic for individuals who rely primarily on plant sources of omega-3s, as the conversion efficiency is already low (typically <5% for EPA and <0.5% for DHA).
Inflammatory mediator balance: EPA and DHA serve as substrates for anti-inflammatory and pro-resolution mediators, including resolvins, protectins, and maresins. These specialized pro-resolving mediators (SPMs) actively resolve inflammation and promote tissue repair. High omega-6 to omega-3 ratios shift the balance toward inflammatory eicosanoids at the expense of SPMs.

Recent research in MASLD patients has found that hepatic polyunsaturated fatty acid composition is altered in liver disease, with lower levels of both n-3 and n-6 PUFAs in the liver (Arendt, et al 2015). However, the ratio of omega-3 to omega-6 is key, a lower n-3:n-6 ratio correlates with worse disease severity and altered gene expression patterns associated with inflammation and metabolism.

5.3 Oxidative Stress and Lipid Peroxidation

Polyunsaturated fatty acids, by virtue of their multiple double bonds, are inherently susceptible to oxidation. This vulnerability has important implications for both industrial processing and in vivo metabolism:

Industrial Processing: The extraction and refinement of seed oils involves high heat, chemical solvents, and extended exposure to oxygen. These conditions promote lipid peroxidation, creating oxidized linoleic acid metabolites (OXLAMs) and other harmful byproducts even before consumption.

In Vivo Oxidation: Once consumed, omega-6 fatty acids incorporated into cell membranes and lipoproteins remain vulnerable to oxidative damage. In conditions of metabolic stress, characteristic of obesity and insulin resistance, oxidative stress is elevated, leading to increased in vivo peroxidation of omega-6 fatty acids. These oxidized lipids can trigger inflammatory responses, endoplasmic reticulum stress, and cellular dysfunction.

OXLAMs and Metabolic Dysfunction: Oxidized linoleic acid metabolites are not merely inactive degradation products, they are bioactive molecules that can bind to receptors, modify proteins, and influence gene expression. While direct evidence linking OXLAMs to liver disease progression is still emerging, the mechanistic plausibility is strong.

The oxidative vulnerability of omega-6 fatty acids explains, in part, why source matters. Omega-6 from whole food sources like nuts and seeds comes packaged with protective antioxidants (vitamin E, polyphenols) that help prevent oxidation. Industrial seed oils, stripped of these protective compounds during processing, are more prone to oxidation both in the bottle and in the body.

5.4 Database Analysis of Omega-6 in Processed Foods

Understanding omega-6 biochemistry is one thing; recognizing where these fats appear most commonly in the modern food supply is quite another. Industrial seed oils have become so ubiquitous that avoiding them requires vigilance, label-reading skills, and often, complete avoidance of packaged and restaurant foods. This section examines where omega-6 fatty acids appear most abundantly in the food supply and why they’ve become so prevalent.

The Industrial Seed Oil Takeover

A handful of oils dominate modern food production, all characterized by high omega-6 content:

Soybean Oil: The most widely used oil in the United States, accounting for approximately 60% of edible oil consumption. Soybean oil is roughly 54% linoleic acid. It’s virtually impossible to find processed foods, restaurant meals, or even “healthy” salad dressings without soybean oil.
Corn Oil: Approximately 57% linoleic acid, corn oil appears frequently in processed snacks, baked goods, and frying applications.
Sunflower Oil (conventional): Contains up to 70% linoleic acid in conventional varieties. High-oleic sunflower oil, bred to contain more monounsaturated fat, is a notable exception with only 10-20% linoleic acid, but it remains relatively uncommon compared to conventional sunflower oil.
Safflower Oil (conventional): Can be up to 75% linoleic acid in conventional form. Like sunflower oil, high-oleic varieties exist but are less common.
Cottonseed Oil: Approximately 52% linoleic acid. Once the most common seed oil in the US, it’s now less prevalent but still appears in many processed foods.
Canola Oil (rapeseed): A partial exception with only about 20% linoleic acid and higher monounsaturated content. However, canola oil still undergoes extensive industrial processing and may contain trace levels of trans fats as processing artifacts.
Palm Oil: Lower in omega-6 (about 10% linoleic acid) but high in saturated fat. Palm oil poses different concerns related to sustainability and processing, but from an omega-6 perspective, it’s less problematic than other seed oils.

These oils appear in thousands of products, often disguised under terms like “vegetable oil”, “vegetable oil blend”, or simply listed as specific oils (soybean oil, sunflower oil). Food manufacturers favor these oils for several reasons: low cost, neutral flavor, long shelf life, and high smoke points for frying.

5.4.1 Worst Offender Categories

Certain food categories are particularly problematic for omega-6 content. Here’s where the omega-6 overload is most severe:

1. Salad Dressings and Condiments

Ironically, foods marketed as “healthy” options for adding flavor to vegetables are often loaded with omega-6 fats. A typical commercial salad dressing can contain 10-12g of omega-6 per serving (often 2 tablespoons), with some ranch or thousand island dressings exceeding this. Mayonnaise is essentially emulsified seed oil, typically providing 3-8g of omega-6 per tablespoon. Even seemingly innocuous condiments like pesto or hummus often contain added seed oils, dramatically increasing their omega-6 content beyond what the base ingredients would provide.

2. Fried Foods

Nearly all commercial frying, whether at fast food restaurants, casual dining establishments, or food manufacturers producing packaged fried snacks uses high omega-6 seed oils. A single serving of french fries can contain 5-10g of omega-6. Fried chicken, fish and chips, tempura, and donuts all represent concentrated sources of oxidized, heat-damaged omega-6 fatty acids. The situation worsens when frying oil is reused, as repeated heating accelerates oxidation and generates more toxic byproducts.

3. Baked Goods and Pastries

Cookies, cakes, muffins, croissants, and other baked goods typically use seed oils (often along with sugar and refined flour) as primary ingredients. A single muffin or slice of cake might contain 3-8g of omega-6. The high-heat baking process also promotes lipid oxidation, creating OXLAMs and other damaged fats.

4. Snack Foods

Potato chips, tortilla chips, crackers, and similar snack foods are typically fried or heavily oiled with seed oils. A standard serving (about 1 oz) of potato chips contains 3-6g of omega-6. Many people consume multiple servings in a sitting, easily accumulating 10-15g or more.

5. Frozen Convenience Foods

Frozen dinners, pizza, fish sticks, chicken nuggets, and similar convenience items almost universally contain seed oils. These foods combine the omega-6 overload with refined carbohydrates, creating a particularly problematic combination for liver health.

6. Restaurant Food

Perhaps most concerning is the near-universal use of seed oils in restaurant cooking. Even upscale, health-conscious establishments typically use seed oils for economic reasons and high smoke points. Chefs use these oils for sautéing, roasting, making sauces, and preparing vinaigrettes. A single restaurant meal can easily provide 10-40g of omega-6, depending on preparation methods.

5.4.2 The ‘Healthy’ Deception

Some of the most problematic omega-6 sources hide behind health halos. Products marketed as healthy alternatives often contain substantial amounts of seed oils:

Sunflower seed butter: Marketed as an allergen-free alternative to peanut butter, conventional sunflower seed butter can contain enormous amounts of omega-6 (unless made from high-oleic sunflower seeds). A 2-tablespoon serving might provide 10-12g of omega-6, five times more than the same amount of peanut butter.
Trail mixes and granola: When nuts and seeds are roasted in vegetable oil rather than dry-roasted, omega-6 content skyrockets. What appears to be a wholesome snack becomes an omega-6 loaded snack no worse than regular nonhealthy option.
‘Baked not fried’ chips: These products still contain seed oils, often in large amounts, to achieve crispness and flavor.
Low-fat products: To compensate for reduced fat content and maintain texture, manufacturers often add seed oils. Low-fat salad dressings, for example, typically use seed oils along with thickeners and emulsifiers.
Vegan and plant-based products: Plant-based meat alternatives, vegan cheeses, and dairy-free products rely heavily on seed oils for texture and fat content. A single serving of plant-based burger can contain 5-10g of omega-6.

The health halo surrounding these products can lead people with MASLD to consume them liberally, unknowingly increasing their omega-6 burden while believing they’re making healthy choices.

5.4.3 Hidden Sources and Cumulative Exposure

The cumulative nature of omega-6 exposure is worth emphasizing. Consider a typical day for someone eating a standard American diet:

Breakfast: Muffin or pastry (5g omega-6) + coffee with flavored creamer (2g) = 7g
Snack: Granola bar (3g) = 3g
Lunch: Salad with commercial dressing (15g) + crackers (2g) = 17g
Snack: Chips (6g) = 6g
Dinner: Restaurant meal with sautéed protein and vegetables (20g) = 20g

Total: 53g of omega-6 in one day.

This example represents a high but realistic intake for someone consuming a processed food-heavy diet.

If this individual consumes even modest amounts of omega-3 (perhaps 1-2g from fish a few times per week), their omega-6 to omega-3 ratio easily exceeds 20:1. The historical ratio of 1:1 to 4:1 seems impossibly distant under these dietary circumstances. For someone with MASLD, who needs to optimize every aspect of their diet to support liver healing, this omega-6 overload can represent a significant and modifiable risk factor.

5.5 The Evidence for Omega-6 and Liver Disease

Now we arrive at the critical question: what does the scientific evidence actually say about omega-6 fatty acids and liver disease? The answer requires nuance. Unlike the clear evidence linking fructose consumption to MASLD, the omega-6 story is more complex, context-dependent, and evolving. We must acknowledge both what we know and what remains uncertain.

Direct Evidence: Hepatic PUFA Composition and Liver Disease

The most direct evidence comes from studies examining fatty acid composition in liver tissue from MASLD patients. A landmark 2015 study by Arendt and colleagues analyzed hepatic gene expression and fatty acid composition in NAFLD patients.^7^ Key findings included:

NAFLD patients showed altered hepatic polyunsaturated fatty acid composition compared to healthy controls, with overall lower levels of both n-3 and n-6 PUFAs in the liver.
The ratio of n-3 to n-6 fatty acids was lower in NAFLD patients, and this lower ratio correlated with disease severity.
Gene expression changes in NAFLD livers showed alterations in lipid metabolism pathways that correlated with PUFA composition abnormalities.

This study is particularly important because it doesn’t just show correlation, it demonstrates that the PUFA composition of the liver itself is altered in NAFLD, and that these changes correlate with the molecular signatures of disease progression. The key finding wasn’t simply about elevated omega-6—both types were lower, but that the balance between omega-3 and omega-6 is disturbed and the ratio was skewed toward omega-6 dominance.

5.6 Indirect Evidence: The Omega-3 Mirror Image

While direct evidence linking high omega-6 intake to liver disease is limited, there’s robust evidence that increasing omega-3 intake improves NAFLD/MASLD outcomes. This provides indirect support for the importance of the omega-6 to omega-3 ratio.

Multiple systematic reviews and meta-analyses have examined omega-3 supplementation in NAFLD/MASLD:

Musa-Veloso et al. (2018): This meta-analysis of controlled intervention studies found that omega-3 supplementation significantly reduced liver fat content, as well as serum ALT and AST levels in NAFLD patients.^8^ The benefits were consistent across studies, suggesting a real therapeutic effect.

Aziz et al. (2024): A more recent systematic review and meta-analysis including studies through 2023 confirmed that omega-3 PUFA supplementation significantly decreased ALT and AST levels, with a trend toward reduction in GGT.^9^ The study also demonstrated improvements in serum lipid profiles and anthropometric measures.

Plant-based omega-3 supplementation: Even plant-based omega-3 sources (primarily alpha-linolenic acid) have shown benefits in NAFLD, with a 2024 systematic review finding significant reductions in ALT levels with plant-based n-3 supplementation.^10^ This is notable given the poor conversion of ALA to EPA and DHA, suggesting that even modest increases in omega-3 status can benefit liver health.

The consistency of omega-3 benefits across multiple meta-analyses and diverse study populations strongly suggests that improving the omega-3 to omega-6 balance is beneficial for liver health. While we can’t prove that high omega-6 is harmful from these studies alone, they support the mechanistic rationale that balance matters.

Mechanistic Evidence from Animal Models

Animal studies, while not directly translatable to humans, provide important mechanistic insights. Rodent studies consistently show that:

High omega-6, low omega-3 diets promote hepatic steatosis, inflammation, and insulin resistance in multiple animal models.
Diets enriched with omega-3 fatty acids (particularly EPA and DHA) reduce hepatic fat accumulation, inflammation, and fibrosis in animal models of fatty liver disease.
The ratio of omega-6 to omega-3 influences the inflammatory profile of the liver, with high ratios promoting pro-inflammatory eicosanoid production and low ratios favoring anti-inflammatory lipid mediators.

These animal data support the mechanistic plausibility of the omega-6 hypothesis but must be interpreted cautiously. Rodents have different fatty acid metabolism compared to humans, and controlled feeding studies in animals don’t capture the complexity of human dietary patterns.

The Complexity and Context Dependence

Here’s where we must exercise intellectual honesty: the omega-6 story is not as clear-cut as we might wish. Recent research suggests important contextual factors:

Source matters profoundly: A 2025 systematic review examining omega-6 fatty acids and MASLD found that the effects of omega-6 vary by subtype and source.^11^ Omega-6 from whole food sources (nuts, seeds, whole grains) consistently associates with better metabolic health, while omega-6 from refined oils shows more concerning patterns. This suggests that the food matrix matters; omega-6 consumed with fiber, antioxidants, and other protective compounds behaves differently than omega-6 consumed from processed oils.

Baseline omega-3 status matters: The impact of omega-6 may depend heavily on concurrent omega-3 intake. In populations with adequate omega-3 consumption, moderate omega-6 intake appears less problematic. This aligns with the mechanistic understanding of enzyme competition—adequate omega-3 may partially offset the effects of elevated omega-6.

Oxidative stress context: In individuals with high oxidative stress (obesity, diabetes, smoking), the potential for omega-6 oxidation and OXLAM formation is greater. This may explain why omega-6 effects appear more pronounced in metabolically unhealthy populations.

Genetic factors: Polymorphisms in genes encoding fatty acid desaturases (FADS1 and FADS2) influence how efficiently individuals convert linoleic acid to arachidonic acid. People with highly active desaturases may be more susceptible to the inflammatory effects of high omega-6 intake.

Interestingly, some epidemiological studies have found that higher dietary omega-6 intake associates with lower cardiovascular disease risk.^12^ This apparent paradox likely reflects the fact that in these studies, people consuming more omega-6 were often consuming nuts, seeds, and plant-based diets, not just industrial seed oils. When omega-6 comes packaged with protective nutrients in whole foods, it may behave very differently than when consumed as refined oil. This remains an active area of research and hence at this moment, instead of advocating against cutting down all omega-6 consumption, we should instead try to just cut down on seed oil based omega-6 and try to consume whole foods (seeds, nuts etc.).

Current Evidence Summary for MASLD and Omega-6 Consumption

Given the current evidence, what can we reasonably conclude about omega-6 fatty acids and MASLD?

Strong evidence: Improving the omega-6 to omega-3 ratio benefits liver health. This is supported by consistent findings from omega-3 supplementation studies and hepatic PUFA composition research.

Mechanistic plausibility: The biochemical pathways linking high omega-6 intake to inflammation, oxidative stress, and insulin resistance are well-established. The mechanisms exist for omega-6 overload to contribute to liver disease.

Source-dependent effects: Omega-6 from whole food sources (nuts, seeds, avocados) appears benign or beneficial, while omega-6 from industrial seed oils, particularly when oxidized through processing or high-heat cooking, is more concerning.

Limited direct human RCT evidence: We lack large-scale randomized controlled trials specifically testing omega-6 reduction on liver disease outcomes in humans. This is a significant gap in the evidence.

The most intellectually honest statement is this: while we cannot prove that high omega-6 intake directly causes or worsens MASLD based on human RCT evidence alone, the mechanistic rationale is strong, the circumstantial evidence is compelling, and the potential benefits of reducing industrial seed oil consumption while increasing omega-3 intake are substantial with minimal downside risk. For individuals with MASLD, optimizing the omega-6 to omega-3 ratio represents a prudent, evidence-based dietary strategy.

5.7 High-Oleic Versions: A Better Option?

Recognizing the above mentioned problems of high-polyunsaturated oils including shelf stability issues, plant breeders have developed high-oleic versions of several seed oil crops. These varieties have been selectively bred (not genetically modified, in most cases) to produce oils with 70-80% oleic acid (a monounsaturated omega-9 fatty acid) instead of high linoleic acid content.

Examples include:

High-oleic sunflower oil: ~80% oleic acid, ~10% linoleic acid (compared to ~70% linoleic in conventional sunflower oil)
High-oleic safflower oil: ~75% oleic acid, ~15% linoleic acid (compared to ~75% linoleic in conventional safflower oil)
High-oleic canola oil: ~70% oleic acid, ~3% linoleic acid (conventional canola already has relatively lower linoleic at ~20%)

From an omega-6 perspective, high-oleic versions represent a significant improvement. The much lower polyunsaturated fat content means:

Much less omega-6 per serving
Greater oxidative stability (monounsaturated fats are much more resistant to oxidation than polyunsaturated fats)
Fewer oxidation products formed during processing and cooking

However, high-oleic oils still undergo the same industrial refining process with all its attendant problems. They’re still heavily processed, heat-damaged products stripped of natural protective compounds. While they’re likely a better choice than conventional high-linoleic seed oils, they’re not equivalent to minimally processed fats like cold-pressed extra virgin olive oil or butter from grass-fed cows.

For individuals with MASLD seeking to optimize their dietary fat intake, high-oleic seed oils represent a reasonable middle ground when olive oil or avocado oil is cost-prohibitive, but they should not be considered an optimal choice. Extra virgin olive oil which is cold-pressed, minimally processed, and rich in protective polyphenols, remains the gold standard for liquid cooking oil.

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6. Omega-6:Omega-3 Ratios - What’s Optimal for MASLD?

We’ve established that the balance between omega-6 and omega-3 fatty acids matters. But what ratio should we actually aim for? And how do we translate population-level dietary recommendations into practical guidance for individuals with MASLD?

6.1 Historical and Contemporary Ratios

Context matters when discussing “optimal” ratios. Different populations throughout history and across contemporary societies have thrived on various ratios:

Paleolithic estimate: 1:1 to 2:1 (omega-6:omega-3). Our hunter-gatherer ancestors consumed diets rich in fish, wild game, nuts, seeds, and leafy plants. Wild game contains substantially more omega-3 than conventionally raised livestock. This very low ratio likely represents the evolutionary baseline.
Mediterranean diet (traditional): 4:1 to 8:1. The traditional Mediterranean diet includes moderate amounts of omega-6 from nuts, seeds, and poultry, balanced by fatty fish, greens, and olive oil. This pattern has been associated with lower rates of metabolic disease, cardiovascular disease, and all-cause mortality.
Traditional Asian diets: 6:1 to 10:1. Japanese and Okinawan diets, famous for longevity and low disease rates, included significant fish consumption balanced with modest amounts of omega-6 from soybeans and grains.
Modern Western diet: 15:1 to 20:1 (or higher). The dramatic shift toward seed oils and away from omega-3-rich foods has created historically unprecedented ratios.

Our metabolic machinery likely evolved under conditions of lower omega-6:omega-3 ratios, and the rapid shift to 15-20:1 may create metabolic stress in susceptible individuals.

6.2 Evidence for Optimal Ratios in MASLD

We must acknowledge uncertainty: there’s no single “perfect” ratio supported by high-quality randomized controlled trials specifically in MASLD patients. The evidence is indirect, coming from omega-3 supplementation studies, observational research, and mechanistic understanding.

What we can reasonably infer:

The current Western ratio of 15-20:1 is almost certainly too high. The preponderance of evidence suggests this ratio promotes inflammation and metabolic dysfunction.
Ratios below 5:1 are likely beneficial. This approximates traditional healthy dietary patterns and would represent a significant improvement for most Western populations.
Very low ratios (1-2:1) might offer additional benefits, particularly for individuals with active inflammation or metabolic dysfunction, though this remains speculative.

The critical point is this: for most people with MASLD, the goal isn’t to achieve a specific ratio with mathematical precision. Rather, the goal is a substantial shift from the current Western pattern toward something closer to traditional healthy diets, which means both reducing industrial seed oils (lowering omega-6) and increasing omega-3 intake.

6.3 Practical Targets for MASLD Management

Rather than obsessing over calculated ratios, individuals with MASLD should focus on achievable intake targets:

Total Omega-6 Intake: Aim for less than 15g per day, ideally 10-12g. The current American average is 20-30g per day. This reduction is achievable by eliminating industrial seed oils and being selective about processed foods. This doesn’t mean eliminating all omega-6, nuts, seeds, avocados, and even whole grains contain some omega-6, and these foods provide valuable nutrients. The goal is eliminating the concentrated sources from refined oils.

EPA and DHA Intake: Target 2-4g per day combined EPA+DHA for therapeutic benefits in MASLD. This is substantially higher than population-level recommendations for general health (which are typically 250-500mg per day). Meta-analyses of omega-3 supplementation in NAFLD/MASLD typically used doses of 2-4g per day, with consistent benefits observed.^8,9^ This level of intake generally requires either very high fish consumption (3-4 servings of fatty fish per week) or supplementation.

Resulting Ratio: If you achieve 12g omega-6 and 3g EPA+DHA daily, your ratio would be approximately 4:1, within the range of healthy traditional diets and likely optimal for liver health. This represents a dramatic shift from the standard Western 20:1 ratio without requiring perfect dietary adherence.

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7. Saturated Fats and Omega-6 in Cirrhosis: Special Considerations

Cirrhosis, the end stage of chronic liver disease, requires different nutritional considerations. Individuals with cirrhosis often experience malnutrition, muscle wasting (sarcopenia), and altered fat metabolism. In this population, adequate calories and protein are paramount. While the same principles of emphasizing whole foods and healthy fats apply, the priority shifts toward preventing malnutrition rather than optimizing macronutrient ratios.

The 2024 EASL-EASD-EASO guidelines recommend nutritional counseling for patients with advanced liver disease, emphasizing adequate protein and energy intake, frequent small meals to prevent overnight fasting, and late-evening snacks.^5^ For patients with cirrhosis, moderate intake of all fat types from nutrient-dense whole foods is appropriate. The focus should be on meeting nutritional needs rather than restriction.

That said, the general principles of healthy fat intake still apply:

Emphasize whole food sources of fats: olive oil, avocados, nuts (if tolerated), fatty fish, and moderate amounts of traditional fats like butter
Continue omega-3 supplementation as per your hepatologist’s advice or regular fatty fish consumption, as omega-3s may help reduce inflammation and potentially slow fibrosis progression
Minimize industrial seed oils and fried foods, which provide calories but potentially contribute to ongoing liver stress
Ensure adequate fat intake to meet energy needs, malnutrition is a greater risk than excessive fat intake in cirrhosis

The omega-6:omega-3 ratio remains important, but it should not be pursued at the expense of adequate caloric and protein intake. For cirrhotic patients, a pragmatic approach might target an EPA+DHA intake of 1-2g daily (through fish or supplementation) while minimizing but not eliminating all omega-6 sources. The focus should be on nutrient-dense whole foods that provide calories, protein, and essential micronutrients.

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8. Summary and Practical Recommendations

This chapter has explored the complex relationship between dietary fats and MASLD, with particular attention to the role of omega-6 fatty acids and the omega-6:omega-3 balance. Let’s distill the key takeaways into actionable guidance:

Key Principles

Not all fats are created equal: The type of fat matters at least as much as the amount. Focus on fat quality, not just quantity.
Source matters profoundly: Omega-6 from whole foods (nuts, seeds, avocados) is not equivalent to omega-6 from industrial seed oils. The food matrix and processing matter.
Balance is key: The omega-6 to omega-3 ratio influences inflammatory balance and metabolic health. Modern Western ratios of 15-20:1 are problematic; ratios below 5:1 are likely beneficial.
Processing degrades fat quality: The industrial refining process transforms seed oils into products laden with oxidation products and stripped of protective compounds. Minimally processed fats are superior.
Context-dependent effects: The impact of fatty acids depends on overall dietary pattern, baseline omega-3 status, metabolic health, and genetics. No single approach works for everyone.

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9. Practical Action Steps for MASLD Management

Implementing all the changes mentioned below may feel overwhelming. Our suggestion is to Start with step 1 and gradually add other changes and focus on the changes that feel most achievable for your situation.

Remember, this is a marathon and not a race, and last thing you want is to try and drastically change your lifestyle which may lead you to abondon the entire attempt itself, instead go slow and take this as a roadmap.

1. Eliminate or Drastically Reduce Industrial Seed Oils

Remove from your kitchen: soybean oil, corn oil, conventional sunflower oil, conventional safflower oil, cottonseed oil, and generic “vegetable oil” blends
Read labels carefully, these oils hide in nearly all processed foods, salad dressings, and condiments
Be aware that restaurant food almost universally contains seed oils

2. Choose Better Cooking Fats

Primary choice: Extra virgin olive oil (cold-pressed, high in polyphenols) for most cooking and dressings
High-heat cooking: Avocado oil, high-oleic sunflower oil, or refined olive oil (not extra virgin)
Traditional fats in moderation: Butter, ghee, tallow, or lard from high-quality sources can be part of a healthy pattern when not overconsumed
Specialty uses: Toasted sesame oil for Asian cooking (small amounts for flavor)

3. Increase Omega-3 Intake Substantially

Fatty fish: Aim for 3-4 servings per week of salmon, mackerel, sardines, herring, or anchovies (prioritize wild-caught or responsibly farmed)
Supplementation: For individuals with MASLD, consider omega-3 supplements providing 2-4g combined EPA+DHA daily. Choose distilled, tested-for-purity supplements.
Plant sources: Include walnuts, flaxseeds, chia seeds, and hemp seeds for ALA, though these don’t replace EPA/DHA needs

4. Embrace Whole Food Sources of Healthy Fats

Nuts and seeds: almonds, walnuts, macadamias, pecans, pumpkin seeds, chia seeds (moderate portions, 1-2 oz daily)
Avocados: excellent source of monounsaturated fat with protective compounds
Olives: whole olives provide fat along with polyphenols and other beneficial compounds
Eggs: from pasture-raised chickens when possible (better omega-3 profile)

5. Minimize Fried and Heavily Processed Foods

Avoid deep-fried foods from restaurants and fast food entirely
Limit packaged baked goods, snack foods, and frozen convenience meals
When eating out, choose grilled, baked, or steamed preparations over fried or heavily sautéed dishes

6. Consider the Overall Dietary Pattern

Focus on whole, minimally processed foods: vegetables, fruits, whole grains, legumes, fish, poultry, eggs, and moderate amounts of dairy
Emphasize a Mediterranean-style dietary pattern, which has strong evidence for liver health benefits
Prioritize vegetables, particularly leafy greens and cruciferous vegetables
Minimize added sugars, refined grains, and ultra-processed foods

Fat optimization is one piece of the MASLD management puzzle, not the entire solution. These recommendations should be implemented alongside weight loss (if needed), regular physical activity, management of metabolic comorbidities, and other lifestyle modifications outlined in comprehensive MASLD guidelines. No single dietary change will reverse MASLD, but optimizing fat intake, particularly the omega-6 to omega-3 balance, represents a significant and achievable step toward liver health.

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10. References

1. Rinella ME, Lazarus JV, Ratziu V, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology. 2023;78(6):1966-1986. link

2. Younossi ZM, Paik JM, Stepanova M, et al. Clinical profiles and mortality rates are similar for metabolic dysfunction-associated steatotic liver disease and non-alcoholic fatty liver disease. J Hepatol. 2024;80(5):694-701. link

3 Del Bo C, Perna S, Allehdan S, et al. Does the Mediterranean Diet Have Any Effect on Lipid Profile, Central Obesity and Liver Enzymes in Non-Alcoholic Fatty Liver Disease (NAFLD) Subjects? A Systematic Review and Meta-Analysis of Randomized Control Trials. Nutrients. 2023;15(10):2250. link

4. Parks E et. al. Out of the frying pan: dietary saturated fat influences nonalcoholic fatty liver disease. J Clin Invest. 2017;127(2):454-456. Link

5. European Association for the Study of the Liver (EASL), European Association for the Study of Diabetes (EASD), European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). J Hepatol. 2024;81(3):492-542. Link

6. Rinella ME, Neuschwander-Tetri BA, Siddiqui MS, et al. AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology. 2023;77(5):1797-1835. Link

7. Arendt BM, Comelli EM, Ma DW, et al. Altered hepatic gene expression in nonalcoholic fatty liver disease is associated with lower hepatic n-3 and n-6 polyunsaturated fatty acids. Hepatology. 2015;61(5):1565-1578. Link

8. Musa-Veloso K, Venditti C, Lee HY, et al. Systematic review and meta-analysis of controlled intervention studies on the effectiveness of long-chain omega-3 fatty acids in patients with nonalcoholic fatty liver disease. Nutr Rev. 2018;76(8):581-602.Link

9. Aziz T, Niraj MK, Kumar S, et al. Effectiveness of Omega-3 Polyunsaturated Fatty Acids in Non-alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis. Cureus. 2024;16(8):e68002. Link

10. Buckley E, Williams AD, Liddle L, et al. A systematic review and meta-analysis of randomized controlled trials to evaluate plant-based omega-3 polyunsaturated fatty acids in nonalcoholic fatty liver disease patient biomarkers and parameters. Nutr Rev. 2024;82(2):182-198. Link

11. Hegazy MA, Ahmed SM, Sultan SM, Afifi OF. Metabolic dysfunction-associated steatotic liver disease and omega-6 polyunsaturated fatty acids: Friends or foes. World J Hepatol. 2025;17(3):102286. Link

12. Fallahzadeh A, Hosseini-Esfahani F, Daneshzad E, et al. Dietary and circulating omega-6 fatty acids and their impact on cardiovascular disease, cancer risk, and mortality: a global meta-analysis of 150 cohorts and meta-regression. Crit Rev Food Sci Nutr. 2025. Link

Additional References

13. Yki-Järvinen H, Luukkonen PK, Hodson L, Moore JB. Dietary carbohydrates and fats in nonalcoholic fatty liver disease. Nat Rev Gastroenterol Hepatol. 2021;18(11):770-786. Link

14. Jump DB, Lytle KA, Depner CM, Tripathy S. Omega-3 fatty acids, hepatic lipid metabolism, and nonalcoholic fatty liver disease. Annu Rev Nutr. 2013;33:231-248.Link

15. Jang H, Park K. Omega-3 and omega-6 polyunsaturated fatty acids and metabolic syndrome: A systematic review and meta-analysis. Clin Nutr. 2020;39(3):765-773. Link

16. Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ. 2016;353:i1246. Link

17. Younossi ZM, Golabi P, Paik JM, Henry A, Van Dongen C, Henry L. The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): a systematic review. Hepatology. 2023;77(4):1335-1347. Link

18. Hagström H, Vessby J, Ekstedt M, Shang Y. 99% of patients with NAFLD meet MASLD criteria and natural history is therefore identical. J Hepatol. 2024;80(2):e76-e77.Link

19. Wang X, Jin X, Li H, et al. Effects of various interventions on non-alcoholic fatty liver disease (NAFLD): A systematic review and network meta-analysis. Front Pharmacol. 2023;14:1180016.Link

20. Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018;67(1):328-357. Link

21. Simopoulos AP. Essential fatty acids in health and chronic disease. Am J Clin Nutr 1999;70(suppl):560S–9S Link. This is an excellent article that articulates historical shift in omega 3: omega 6 ratios and its overall health impact.

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