Soya in the Dietary Treatment of Non Alcoholic Fatty Liver Disease

In the majority of patients, NAFLD is associated with metabolic risk factors such as obesity, diabetes mellitus, and dyslipidemia. 

The management of patients with NAFLD consists of treating liver disease as well as the associated metabolic co-morbidities.


A condition (hepatic steatosis) characterised by the accumulation of excess fat in the liver commonly caused by alcohol abuse. This condition progresses in 3 stages: 1. Hepatic steatosis; 2. Alcoholic hepatitis; and 3. Cirrhosis.


Hepatic steatosis (evidence obtained from imaging or by histology) without causes for secondary hepatic fat accumulation such as significant alcohol consumption, use of steatogenic medication or hereditary disorders.

In the majority of patients, NAFLD is associated with metabolic risk factors such as obesity, diabetes mellitus, and dyslipidemia.

NAFLD is histologically further categorized into non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH). NAFL is defined as the presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes.

NASH is defined as the presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. 


The liver has the most varied and extensive function of any organ.

It performs many functions that have an important bearing on one’s nutritional state.

  • Protein metabolism – synthesis of plasma proteins; deamination of amino acids, formation of urea.
  • Carbohydrate metabolism – synthesis, storage and release of glycogen; synthesis of heparin.
  • Lipid metabolism – synthesis of lipoproteins, phospholipids, cholesterol, formation of bile; conjugation of bile salts; oxidation of fatty acids.
  • Mineral metabolism – storage of iron, copper and other minerals.
  • Vitamin metabolism – storage of Vitamins A and D, some conversion of carotene to Vitamin A, and of Vitamin K to prothrombin.
  • Detoxification of bacterial decomposition products, mineral poisons, and certain drugs and dyes.


Conditions with established association                              Conditions with emerging association*

Obesity                                                                                                      Polycystic ovary syndrome

Type 2 diabetes mellitus                                                                        Hypothyroidism

Dyslipidemia                                                                                            Obstructive Sleep apnea

Metabolic syndrome**                                                                           Hypopituitarism


Pancreato-duodenal resection

*Few studies suggested that individuals with type1 diabetes have increased prevalence of hepatic steatosis based on liver imaging, but there is limited histological evidence.

**The Adult Treatment Panel III clinical definition of the metabolic syndrome requires the presence of three or more of the following features: (1) waist circumference greater than 102 cm in men or greater than 88 cm in women; (2) triglyceride level 150 mg/dL or greater; (3) high-density lipoprotein (HDL) cholesterol level less than 40 mg/dL in men and less than 50 mg/dL in women; (4) systolic blood pressure 130 mm Hg or greater or diastolic pressure 85 mm Hg or greater; and (5) fasting plasma glucose level 110 mg/dL or greater.


There may be no symptoms in the early stages of NASH. Most people who have NASH feel fine and don’t know that they have it.

As NASH progresses and liver damage gets worse, symptoms can occur, such as:

  • Fatigue(feeling tired all the time).
  • Weight loss for no clear reason.
  • General weakness.
  • An ache in the upper right part of your belly.
  • Non-specific
  • Feeling generally unwell
  • Possible reduced appetite


The management of patients with NAFLD consists of treating liver disease as well as the associated metabolic co-morbidities such as obesity, hyperlipidemia, insulin resistance and Type 2 DM. As patients with NAFLD without steatohepatitis have excellent prognosis from a liver standpoint, treatments aimed at improving liver disease should be limited to those with NASH.

Lifestyle intervention

Many studies indicate that lifestyle modification may reduce aminotransferases and improve hepatic steatosis.

In recent studies it is shown that lifestyle modification brings about an improvement in aminotransferases and hepatic steatosis on histology.

The best evidence for weight loss as a means to improve liver histology in NASH comes from a trial that randomized 31 obese persons with NASH to intensive lifestyle changes (diet, behaviour modification and 200 minutes a week of moderate physical activity for 48 weeks) versus structured basic education alone. The intensive arm had 9.3% weight loss (versus 0.2% in the dietary counseling alone arm) and led to an improvement in steatosis, necrosis and inflammation, but not fibrosis. Importantly, participants with 7% weight loss had significant improvement in steatosis, lobular inflammation, ballooning, and NAFLD Activity Score (NAS).

There was a similar pattern in another study where participants who lost > 5% body weight improved steatosis, whereas individuals with 9% weight loss had significant improvement in steatosis, lobular inflammation, ballooning, and NAS.

A number of recent studies used MR spectroscopy to assess changes in hepatic fat in response to lifestyle modification. The results from these studies using a variety of interventions, either by diet alone or in combination with different exercise prescriptions, have consistently reported a significant reduction in liver fat by an average of 40% (ranging from 20% to 81%). The degree of hepatic fat reduction was proportional to the intensity of the lifestyle intervention and generally required a body weight loss between 5 to 10%.

The effect of exercise without dietary modification on hepatic steatosis was investigated in four studies using MR spectroscopy. Exercise programs consisted of 2-3 sessions a week of 30-60 minutes over a period of 6 to 12 weeks. In all but one study liver fat content diminished without a significant change in body weight.


Weight loss generally reduces hepatic steatosis, achieved either by hypocaloric diet alone or in conjunction with increased physical activity. Loss of at least 3-5% of body weight appears necessary to improve steatosis, but a greater weight loss (up to 10%) may be needed to improve necroin- flammation.

Exercise alone in adults with NAFLD may reduce hepatic steatosis but its ability to improve other aspects of liver histology remains unknown.


No specific medications are approved for treating NAFLD. The current standard of care for treating patients with NAFLD focuses on lifestyle interventions, particularly diet and exercise. Sustained weight loss is the most effective treatment and should be the foundation of any treatment plan. 

Unhealthy diets, such as the so-called western diet, are enriched in fructose, trans-fatty acids and saturated fat and seem to be associated with the development of NAFLD. In human studies, certain dietary sugars, particularly fructose, are used as a substrate for lipogenesis leading to hepatic fatty infiltration, inflammation, and possibly fibrosis. Other investigations have shown that fat consumption especially cholesterol and trans/saturated fatty acids are also steatogenic and seem to increase visceral adiposity. The identification of specific dietary components that favor the development of NASH could be important for the management of this disorder.

Nutritional Guidelines for NAFLD/NASH


Weight loss10% of initial body weight over six months
Maintenance of weight loss
Bariatric surgery when individuals qualify
Calorie intake1,200 to 1,500 daily
*Energy deficit of 500 kcal/day based on Mifflin-St Jeor formula
Total fat≤ 35% of total calories
Monounsaturated fatty acids15% to 25% of total calories
Polyunsaturated fatty acids5% to 10% of total calories
Omega-3 fatty acids
Saturated fatty acids7% to 10% of total calories
Carbohydrate50% of total calories
> 50% carbohydrate sources from whole grains
Avoid high-fructose corn syrup
Added sugars < 10% of total calories
Protein15% of total calories
Lean and vegetable protein, INCLUDING SOYA
Physical activity≥ 150 minutes/week at moderate intensity or ≥ 75 minutes/week at vigorous intensity
Cardiovascular exercise five times weekly
Resistance training two or more times weekly
Decrease time spent sedentary


There is considerable evidence that soy affects serum lipids in NAFLD, NASH, metabolic syndrome, type 2 diabetes in a way that would favourably affect heart health. In addition, the research shows that there may be improvements in kidney function (also at risk in NAFLD patients).

The overall data suggest soy protein intake in the range of 20-50g daily achieves the same favourable effects on risk factors in NAFLD, and type 2 diabetes as observed in soy studies on non-diabetes study participants; and may have potential added benefit for kidney function.  

Fat in Soya

Most of the fat in soybeans is unsaturated. Polyunsaturated (primarily linoleic acid), monounsaturated (oleic acid) and saturated (primarily palmitic acid) fats make up 63 percent, 23 percent, and 14 percent respectively of the fat in soybeans. [USDA] The polyunsaturated fat content of soybeans is of interest because it includes linolenic acid (seven percent of the total fat content), an omega-3 fatty acid. Soybeans are one of the few plant sources of omega-3 fatty acids. Omega-3 fatty acids may be essential nutrients for treatment of NAFLD and they may also help to reduce risk of both heart disease.

*Carbohydrate sources must be low GI: Example Soya Life Porridge and Soya Life Drink.

In summary, soya used in daily diets for those with NAFLD and NASH, can bring about favourable benefits, and result in the risk of further complications associated with NAFLD being significantly minimised.

Soya Life Porridge and/or Soya Life Instant Meal Replacement Drinks should be used as an important daily addition in diets to treat NAFLD and NASH.

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