Nutritional Management of
Liver Disease
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Review the functions of the liver
Review diseases of the liver
Major complications of liver disease
Nutritional features of end stage liver
disease
Nutritional management of end stage liver
disease
Nutritional response to hepatic
transplantation
Nutritional management of non alcoholic
fatty liver disease (NAFLD)
Hepatitis C
Functions of the Liver
 Major role of the liver is the regulation of
solutes in the blood that affect the functions
of other organs for example: the brain,
heart, muscle and kidneys
 Strategically placed such that all blood
passing from the small intestine must travel
through the liver
Functions of the Liver
 Storage and metabolism of macronutrients
such as protein, carbohydrates and lipids
 Metabolism of micronutrients – vitamins
and minerals
 Metabolism and excretion of drugs and
toxins – endogenous and exogenous
Role of the Liver in Nutrient
Metabolism
Storage and metabolism of macronutrients
such as protein, carbohydrates and lipids
Carbohydrate
 Storage of carbohydrate as
glycogen
 Gluconeogenesis
 Glycogenolysis
Role of the Liver in Nutrient
Metabolism
Protein
 Synthesis of serum proteins e.g. albumin
 Synthesis of blood clotting factors
 Formation of urea from ammonia
 Oxidation of amino acids
 Deamination or transamination of amino
acids
Role of the Liver in Nutrient
Metabolism
Fat
 Hydrolysis of triglycerides, cholesterol and
phospholipids to fatty acids and glycerol
 Formation of lipoproteins
 Ketogenesis
Role of the Liver in Nutrient
Metabolism
Fat
 Fat storage
 Cholesterol synthesis
 Production of bile necessary for
digestion of dietary fat
Role of the Liver in Nutrient
Metabolism
Vitamins
 Site of the enzymatic steps in the activation of
vitamins : thiamine
pyridoxine
folic acid
vitamin D(25 hydroxycholecalciferol)
 Site of the synthesis of carrier proteins for
vitamins: A, B12, E
Role of the Liver in Nutrient
Metabolism
 Storage site for fat soluble vitamins A, D,
E, K, B12
Minerals
 Storage site for copper iron and zinc
Diseases of the Liver
Hepatitis
 Inflammation of hepatocytes
 Reversible
 Precipitants include:
Viral infections such as hepatitis A, B,
C
Drugs such as paracetamol
Some herbal preparations
Alcohol
Fatty Liver:
Infiltration of the liver by fat
Possible causes include:
alcohol
obesity
type 2 diabetes mellitus
hyperlipidaemia
sudden rapid weight gain
hepatitis C
TPN
NAFLD (Non Alcoholic Fatty
Liver Disease)
 Resembles alcohol induced fatty liver
 Occurs in people who do not abuse
alcohol
 Has the potential to progress to cirrhosis
and liver failure
Non Alcoholic Fatty Liver Disease
(NAFLD)
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Simple steatosis
Steatohepatitis (NASH)
Fibrosing steatohepatitis
Cirrhosis
Non Alcoholic Fatty Liver Disease
(NAFLD)
Risk Factors include:
 Overweight
 Obesity
 Central Obesity
Non Alcoholic Fatty Liver Disease
(NAFLD)
Factors involved in the development of
NAFLD:
 Lifestyle :
 Weight gain
 Weight loss
 Reduced activity
 Childhood and adult obesity
 Type 2 diabetes
Non Alcoholic Fatty Liver
Disease (NAFLD)
The major underlying risk factor for the
development of NAFLD is insulin
resistance
NAFLD (Non Alcoholic Fatty
Liver Disease)
 Prevalence of obesity in patients with NAFLD
reported between 30% and 100%
 Prevalence of type 2 diabetes in patients with
NAFLD reported between 10% and 75%
 Prevalence of hyperlipidaemia in patients with
NAFLD reported between 20% and 92%
NAFLD - Symptoms
 Often asymptomatic of liver disease at
time of diagnosis
 Fatigue or malaise and/or a feeling of
fullness or discomfort on the right side of
the abdomen
NAFLD - Symptoms
 Mild to moderate elevation of the
enzymes:
aspartate amino transferase
alanine amino transferase
 Diagnosis confirmed on biopsy
Cirrhosis
 Refers to chronic scarring of the liver
 Clearly delineated nodules form within the
liver which contain connective tissue
 This leads to a significant reduction in liver
function
Fulminant Hepatic Failure
 Sudden massive necrosis of hepatocytes
 The patient rapidly becomes
encephalopathic and comatosed
 Causes may be viral or a reaction to a
drug such as paracetamol,
sulphathiazone or some herbal remedies
Autoimmune liver diseases
 Diseases of the biliary tract and include
primary sclerosing cholangitis (PSC) and
primary biliary cirrhosis (PBC)
 PSC often occurs in association with
ulcerative colitis
 Serum cholesterol levels may be elevated
and unresponsive to medication or dietary
manipulation
Alcoholic liver disease
 Alcohol is toxic to the liver
 Caused by chronic alcohol abuse
 All stages of the disease process –
hepatitis, fatty liver fibrosis and cirrhosis
Alcoholic liver disease
 Cessation of alcohol may result in
recovery in the early stages of liver
disease
 Cessation of alcohol in patient with
cirrhosis may result in an improvement in
liver function and may also result in a
slowing down of the disease progression
Wilson’s Disease
 Copper storage disease
 May result in cirrhosis if untreated
 First presentation often in adults who
present with cirrhosis
Wilson’s Disease
 If detected in childhood management
involves penecillamine which acts to bind
Cu in the GIT
 Value of dietary Cu restriction debatable in
children; of no value in adults in the
presence of cirrhosis
Hepatic tumours
 Often occur in association with Hepatitis B
or Hepatitis C
 Occur independently
 Include hepatocellular carcinomas,
cholangiosarcoma (bile duct tumours)
Portal Hypertension
 Occurs as a result of fibrous infiltration of
the liver which in turn causes increased
pressure in the portal vein
 This pressure continues back through the
system to the abdominal capillaries which
then leak serous fluid into the abdominal
cavity due to this increased pressure and
low serum albumin levels
Portal Hypertension
 Surgical interventions may be undertaken
to alleviate this pressure (TIPSS). There
are risks associated with these procedures
– infection, failed shunts, encephalopathy
Cirrhosis
 Compensated i.e. well controlled
or
 Decompensated i.e. symptomatic
Decompensated cirrhosis
Symptoms of portal hypertension include:
 Ascites and/or peripheral oedema
 Jaundice
 Oesophageal and/or gastric varices
 Encephalopathy
 Hepatorenal failure
 Malnutrition
Ascites
 Refers to the accumulation of fluid in the
abdominal cavity
 It contains protein, sodium and potassium
 It is considered to be an active metabolic
unit
Jaundice
 Refers to the yellow colour seen in
patients with liver disease
 It is caused by high circulating levels of
bilirubin
 Severe itching may be present. May be
alleviated by Questran/cholestyramine or
by phenergan
Varices
 Distended/engorged veins that can occur at
any point in the venous system of the GIT
 May bleed readily as patients with end stage
liver disease (ESLD) have poor coagulation
secondary to impaired synthesis of clotting
factors
Encephalopathy
 Impaired mental state that results in impaired
mentation and coordination
 May result in coma
 Believed to be caused by increases in plasma
ammonia and other nitrogenous waste products
 These toxins cross the blood brain barrier and
interfere with neuromuscular function and
behaviour
Precipitants of encephalopathy
include:
 Peritoneal infection (subacute bacterial
peritonitis – SBP)
 GIT bleeding
 Poor compliance with lactulose (marketed
as Duphalac) therapy
 Nitrogen overload
 Fluid and electrolyte imbalance
 Medications
 Acid-base imbalance
There are four classifications of
encephalopathy:
Grade1. foetor, impaired
coordination, tremor, altered
handwriting, reduced attention
span, mild confusion, mood
swings and altered sleep
pattern
Grade 2. asterixis (impaired ability to draw a
star), slurred speech, ataxia
inappropriate behaviour, lethargy,
impaired memory and mild
disorientation
Classifications of encephalopathy
cont…
Grade3.
bizarre behaviour, confusion,
moderate to severe
disorientation, uncharacteristic
anger, paranoia, somnolence,
stupor and muscle rigidity
Grade 4.
comatosed, dilated pupils
Nutritional Management of Liver
Disease
Early Stages of Liver Disease:
 No specific dietary management
 Healthy diet according to healthy eating
guidelines
 Beware of miracle cures
Acute Hepatitis:
 High protein/high energy intake required to
promote hepatocyte regeneration
• Fat restriction contraindicated
• Nausea/anorexia
• Consider oral supplementation such as
glucose polymers, fruit based high protein
drinks, or high protein/ high energy drinks
in the presence of nausea/anorexia
 Caution against herbal remedies as some
may be harmful and most have no
scientific basis
Nutritional Features of End Stage
Liver Disease
 Look malnourished
 Low se protein levels
albumin,
prealbumin,
transferrin, retinol
binding protein,
insulin like growth
factor-1
 Vitamin deficiencies
thiamine, vit A,
D, E
 Mineral deficiencies
Zn, Mg, Cu, Ca
Nutritional Features of Liver
Disease
 Weight and BMI do not
reflect true nutritional
status (ascites and/or
oedema)
 Oral intakes are not
necessarily poor
 Exhibit features of protein
energy malnutrition
Nutritional Assessment of patients
with ESLD
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Weight?
Weight history?
Protein markers of nutritional status?
Descriptive history of wasting?
Skinfolds?
Intake?
Appetite?
Nutritional Assessment of patients
with ESLD
SGA for patients with liver disease (Hasse)
 Anthropometry
 Food history
 Nausea
 Anorexia
 Taste changes
 Diarrhoea
 Early satiety
 Functional capacity
 Grip strength
Malnutrition in End Stage Liver
Disease
Changes in Macronutrient Metabolism:
Energy
Fat
Protein
Nutritional Management of End
Stage Liver Disease
Energy Requirements:
 Patients with compensated cirrhosis do not
appear to need modification of their energy
intakes
 Patients with decompensated liver disease
require 35 – 40 non protein kcals/kg/day*
 Ascites is a viable metabolic unit
*Plauth M, Merlim, Kondrup J, Weimann A, Ferenci P, Muller MJ.ESPEN Guidelines for Nutrition
in Liver Disease and Transplantation. Clinical Nutrition 1997; 16: 43-55
Nutritional Management of End
Stage Liver Disease
Energy
 Energy expenditure: currently there are no
metabolic equations which are able to
estimate accurately the energy
requirements of the patient with ESLD.
 Harris-Benedict, Schofields and Muller all
underestimate the energy requirements of
this group
 Indirect calorimetry
Nutritional Management of End
Stage Liver Disease
Glycogen storage
 Reduced glycogen storage capacity
 Unable to tolerate periods of prolonged
fasting – increased protein breakdown in
periods of prolonged fasting
Nutritional Management of End
Stage Liver Disease
Fat
 Altered fat synthesis
 Lipids are oxidised as a preferential
substrate
 Increased lipolysis
 Active mobilisation of lipid stores
Decompensated Liver Disease
 Fat restriction contraindicated in most
patients
 Symptoms of fat intolerance such as
steatorrhoea, abdominal pain or nausea
following a high fat intake are rare. If present
fat modification may be necessary
Nutritional Management of End
Stage Liver Disease
Protein
 Protein turnover in cirrhotic patients is normal or
increased
 Stable cirrhotics have increased protein
requirements¹‫׳‬²
 Stable cirrhotic patients are capable of achieving
positive nitrogen balance during aggressive
nutritional support regime¹‫׳‬²
¹Kondrup J, Neilsen K et al. Effect of long term refeeding on protein metabolism in
patients with cirrhosis of the liver. Br J Nutr 1997; 77: 197-212
²Swart, GR et all. Minimal protein requirements in liver cirrhosis determined by nitrogen
balance measurements at three levels of protein intake. Clin Nutr 1989; 8: 329-336
Nutritional Management of End
Stage Liver Disease
Protein
 Protein turnover in cirrhotic patients is normal or
increased
 Stable cirrhotics have increased protein
requirements¹‫׳‬²
 Stable cirrhotic patients are capable of achieving
positive nitrogen balance during aggressive
nutritional support regime¹‫׳‬²
¹Kondrup J, Neilsen K et al. Effect of long term refeeding on protein metabolism in
patients with cirrhosis of the liver. Br J Nutr 1997; 77: 197-212
²Swart, GR et all. Minimal protein requirements in liver cirrhosis determined by nitrogen
balance measurements at three levels of protein intake. Clin Nutr 1989; 8: 329-336
Nutritional Management of End
Stage Liver Disease
Protein
 Protein refeeding showed a 30% increase
in protein synthesis*
 Protein refeeding did not show a
significant increase in protein degradation*
*Kondrup J, Neilsen, K,and Anders J. Effect of long term refeeding on protein metabolism
in patients with cirrhosis of the liver. Br J Nutrition (1997), 77, 197-212
Nutritional Management of End
Stage Liver Disease
Protein
 Patients with cirrhosis have been shown to
have high protein requirements to maintain
positive nitrogen balance*
*Konrup J, Nielsen K, Juul A. Effect of long-term refeeding on protein metabolism in
patients with cirrhosis of the liver. Br. J. Nutr. 1997; 77: 197-212
Nutritional Management of End
Stage Liver Disease
Protein
 The protein restricted diets used
traditionally have probably arisen
historically from the response to a dietary
protein load seen in cirrhotic patients who
have some form of portocaval shunt
surgery
Nutritional Management of End
Stage Liver Disease
Protein requirements in episodic hepatic
encephalopathy
 62 patients with acute encephalopathy
assessed – 32 excluded
 30 patients randomised into two groups
 All patients received lactulose enema and
then identical oral neomycin dosage
Cordoba J, Lopez-Hellin J et al. Normal protein diet for episodic hepatic encephalopathy:
results of a randomised study. J of Hepatology 41 2004) 38-43
Nutritional Management of End
Stage Liver Disease
 20 patients completed study
 5 patients in each arm dropped out – 4
deaths in each. Group A: additional
variceal bleed; group B: additional
voluntary abandon
Nutritional Management of End
Stage Liver Disease
 2 groups – 15 in each group
 14 days
 Group A: 0g protein/day for 3 days. Protein increased
incrementally to 1.2g protein/kg/day
 Group B: 1.2g protein/kg/day
 Protein synthesis and breakdown studied at day 2 and
day 14
Nutritional Management of End
Stage Liver Disease
Day 2:
 Increased protein breakdown in protein
restricted group
 No statistically significant difference in
protein synthesis
Nutritional Management of End
Stage Liver Disease
Nutritional Management of End
Stage Liver Disease
Restricting protein
intake did not have
any positive effect
on the evolution of
episodic hepatic
encephalopathy
Nutritional Management of End
Stage Liver Disease
Protein
 Protein restriction is contra - indicated for
patients with decompensated cirrhosis
 Recommended protein intake for cirrhotics
is 1.0 – 1.5g protein/kg/day¹
 Dietary protein restriction does not appear
to be of any benefit in episodic hepatic
encephalopathy²
¹Plauth M, Merlim, Kondrup J, Weimann A, Ferenci P, Muller MJ.ESPEN Guidelines for
nutrition in Liver Disease and Transplantation. Clinical Nutrition 1997; 16: 43-55²
²Cordoba J, Lopez-Hellin J et al. Normal protein diet for episodic hepatic encephalopathy:
results of a randomised study. J of Hepatology 41 2004) 38-43
Nutritional Management of End
Stage Liver Disease
Does the type of protein matter?
Nutritional Management of End
Stage Liver Disease
Amino Acids in Encephalopathy
 Patients with advanced liver disease have an
altered ratio of branched chain amino (leucine
valine, isoleucine) acids to aromatic amino acids
(phenylalanine, tyrosine)
 Aromatic amino acids are catabolised in the liver
and their metabolism is impaired in cirrhosis
resulting in an increase in circulating levels of
AAAs
Nutritional Management of End
Stage Liver Disease
Amino Acids in Encephalopathy
 Branched chain amino acids (BCAA) are
metabolised predominantly in the skeletal
muscle and fat
 Plasma BCAA levels fall due to their
utilisation as an energy substrate and a
substrate in gluconeogenesis
Nutritional Management of End
Stage Liver Disease
Amino Acids in Encephalopathy
 The alteration in the ratio of BCAA:AAA
has been proposed as an aetiological
factor in the development of
encephalopathy*
*Fischer JE, Rosen HM, Ebeid AM et al. The effect of normalisation of plasma amino
acids on hepatic encephalopathy in man. Surgery. 1976 Jul. 80 (1): 77-91.
Nutritional Management of End
Stage Liver Disease
Amino Acids in Encephalopathy
 Marchesini et al carried out a multicentre
double blind randomised trial in which
BCAA supplementation was compared
with an isocaloric casein supplementation
in 64 patients with encephalopathy*
*G Marchesini, FS Dioguardi, GP Bianchi et al. Long- term oral branched chain amino
acid treatment in chronic hepatic encephalopathy. J of Hepatol, 1990; 11:92-101
Nutritional Management of End
Stage Liver Disease
 16/34 patients in the BCAA group regained
normal mental state compared with 9/30 in
the casein treated group (p<0.05)
 After 6 months on BCAA treatment
nitrogen balance improved and was
suggestive of decreased nitrogen
catabolism in the BCAA treated group
G Marchesini, FS Dioguardi, GP Bianchi et al. Long- term oral branched chain amino acid
treatment in chronic hepatic encephalopathy. J of Hepatol, 1990; 11:92-101
Nutritional Management of End
Stage Liver Disease
 Long-term oral BCAA supplementation(6
months) resulted in an increase in body
weight
G Marchesini, FS Dioguardi, GP Bianchi et al. Long- term oral branched chain amino acid treatment in
chronic hepatic encephalopathy. J of Hepatol, 1990; 11:92-101
Nutritional Management of End
Stage Liver Disease
 15 centres over up to 15.5 months*
 174 patients with Childs B or C cirrhosis
*Marchesini G, Bianchi G, Merli M et al. Nutritional supplementation with branched
chain amino acids in advanced cirrhosis: a double blind randomised trial.
Gastroenterology 2003;124:1792-1801
Nutritional Management of End
Stage Liver Disease
Methods:
 Three types of nutritional supplements.
Each 10g package supplied:
 14.4g BCAA/day (leucine, isoleucine, valine
and saccharose providing 37.5 kcal)
 2.1g lacto-albumin/day (lacto-albumin,
saccharose and mannitol providing 33.6 kcal)
 2.4g maltodextrose/day (maltodextrose,
saccharose providing 34.9 kcal)
Nutritional Management of End
Stage Liver Disease
Methods:
 All subjects were instructed to take 2
packets three times daily dissolved in
200ml water half an hour before meals
 Patients were maintained on self selected
diet. No new dietary restrictions were
recommended or prescribed
 Standard therapies (albumin, diuretics,
lactulose) were allowed but registered
Nutritional Management of End
Stage Liver Disease
Results:
 115 patients remained in the study
 59 patients were withdrawn for a variety
reasons:
• Death
• Deterioration in liver function
• Non-compliance (palatability, nausea,
gastrointestinal discomfort and diarrhoea)
• Psychiatric disease
Nutritional Management of End
Stage Liver Disease
Results:
 Patients treated with BCAAs were admitted to
hospital less frequently:
195 days in BCAA group;
327days in L-ALB group and
520days in M-DXT group
 Length of stay varied within the treated groups:
0-24 days in BCAA group
0-31 days in the L-ALB group
0-77 days in the M-DXT group
Nutritional Management of End
Stage Liver Disease
Results:
 Improved triceps skinfold thickness in the BCAA
group
 Improved midarm fat area in the BCAA group
 Reduction in the prevalence and severity of
ascites in the BCAA group
 Shift towards better scoring of health only in the
BCAA group
 M-DXT supplementation therapy did not require
increase in insulin therapy
Nutritional Management of End
Stage Liver Disease
Results:
 Total bilirubin levels decreased in the BCAA
group and increased in the M-DXT group
 Improvement in the CTP score in the BCAA
group
 CTP was stable in the L-Alb group and M-DXT
group
 Reduced prevalence of anorexia in the BCAA
group
Nutritional Management of End
Stage Liver Disease
To summarise:
 There are benefits to routinely supplement
patients with advanced cirrhosis with
branched chain amino acids
 Patient compliance
Nutritional Management of End
Stage Liver Disease
Current Criteria for use of Oral BCAA
Supplementation at RPAH:
 chronic encephalopathy
 frequent hospital admissions due to
encephalopathy
 severe depletion of fat and muscle
stores
 elevated blood sugar levels
Nutritional Management of End
Stage Liver Disease
Does the timing or frequency of
meals of meals matter?
Nutritional Management of End
Stage Liver Disease
• Reduced glycogen storage capacity
Nutritional Management of End
Stage Liver Disease
Eating Pattern
 Swart and Zillikens demonstrated that
spreading food intake and inclusion of a late
evening meal significantly improved
nitrogen balance in cirrhotics*
*Swart G, Zillikens M. Effect of a late evening meal on nitrogen balance in patients with
cirrhosis of the liver Med J 1989;299: 1202-3
Nutritional Management of End
Stage Liver Disease
Eating Pattern
 A modified eating pattern should be
recommended to all patients with ESLD.
 This would include eating at regular intervals –
perhaps 5-7 small HP/HE meals/snacks per day
 Include a pre-bedtime HP/HE snack to provide
substrate for the liver to work with during sleep
(supplements)
Ascites
 Patients with ascites usually have a high total
body sodium but often have a low se sodium
 Generally have a poor intake secondary to
abdominal distension
 Early Satiety
 Delayed gastric emptying
 Frequent snacking important to achieve high
energy intake
Ascites
 Sodium restricted diet. Most common restriction
is a no added salt diet which can range
between 50Mm Na and 100Mm Na
 Diuretics. Most commonly used are Lasix and
Aldactone.
 Salt substitutes contraindicated due to
potassium sparing effect of aldactone
Ascites
 Fluid restriction
 Moderate (1500ml )to severe (≤ 800ml)
 ≤800ml used to treat intractable ascites
unresponsive to diuretic therapy or when
diuretic therapy no longer possible due to
compromised renal function
• Don’t measure: custards, ice cream
Oesophageal Varices
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Varices can occur at any point along the
GIT

Oesophageal varices may bleed easily and
bleeding further compromises the patient's
nutritional status
Oesophageal Varices

Varices can occur at any point along the
GIT

Oesophageal varices may bleed easily and
bleeding further compromises the patient's
nutritional status
Oesophageal Varices
 Following an oesophageal bleed the
patient will be nil by mouth
 Varices will be banded
 Oral intake recommenced when patient’s
condition stabilises
Oesophageal Varices
When allowed to eat patients should be advise to:
 Eat carefully and avoid large bolus of food which
might dislodge a clot
 Avoid over distension of the stomach which
might lead to regurgitation or vomiting
 Avoid foods with sharp bones that might be
accidentally swallowed
Diabetes in Liver Disease
Patients with ESLD may present with impaired
glucose tolerance. This may be due to a
number of factors:
 Depleted hepatic glycogen stores
 Impaired glucose tolerance
 Hyperinsulinaemia
 Insulin resistance
Diabetes in Liver Disease
 Management involves diabetic education
without restriction of energy intake
 Insulin therapy
 BCAA supplementation has been shown to
facilitate control of blood sugar levels in
patients with ESLD
Nutritional Management of End
Stage Liver Disease
 Achieve and maintain high energy
intake(35-40 non protein kcal/kg/day)
 Achieve and maintain a high protein
intake(1.0-1.5g/kg/day)
 Avoid unnecessary fat restriction
 Encourage frequent snacking
Nutritional Management of End
Stage Liver Disease
 Restrict dietary sodium intake in the
presence of ascites and/or oedema
 Restrict fluid intake to assist in the
management of ascites/oedema
associated with hyponatraemia
Nutritional Management of End
Stage Liver Disease
 Consider branched chain amino acid
supplementation
 Significant pre-bedtime snack
Nutritional Response to Hepatic
Transplantation
Hepatotoxicity of Herbal
Remedies
 Herbs are potent medicines
 The community is increasingly seeking out
alternative or “natural” therapies
 Patients with hepatitis C frequently seek
out alternative therapies
Hepatotoxicity of Herbal
Remedies
 Important to be aware of the possible
harmful effects of herbs
 Some herbs are hepatotoxic and patients
with known liver disease should avoid
using them
Nutritional Management of
NAFLD
Treatment centres around reducing insulin
resistance
 Dietary intervention
 Increased physical activity
 Metformin
Nutritional Management of
NAFLD
 Weight loss strategies in presence of
overweight/obesity. Weight loss results in
improved lipid and carbohydrate metabolism.
 Weight loss must be slow. Rapid weight loss
results in worsening liver function tests and
hepatomegaly
 Rapid weight loss may promote or worsen
NAFLD, NASH and may result in liver failure
Nutritional Management of
NAFLD
• Normal weight subjects: dietary and
pharmacological treatment of altered lipid
and /or carbohydrate metabolism
• In overweight individuals with elevated
aminotransferase levels weight loss of
10% or more corrects aminotransferase
levels and decreases hepatomegaly
Nutritional Management of
NAFLD
Modification in lifestyle which
involves weight reduction and
regular exercise are the mainstay
of treatment and prevention of
NAFLD
Nutritional Management of
NAFLD
Summary
There is no quick fix and there are no
gimmicks for the consumer
– Weight control
– Increased exercise/physical activity
– Good Diabetic control
– Manage lipid abnormalities