NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #82
Carol Rees Parrish, R.D., M.S., Series Editor
Nutritional Recommendations for Patients with Non-Alcoholic Fatty Liver Disease: An Evidence Based Review Non-alcoholic fatty liver disease (NAFLD) includes a spectrum of liver disorders due to abnormal fat deposition in the liver. These range histopathologically from simple steato- sis to steatohepatitis (NASH) which can progress to cirrhosis and end stage liver disease. NAFLD is the most common cause of chronic liver disease in the developed world and is generally a component of the underlying “metabolic syndrome.” It is likely to emerge as the most common cause of liver disease associated mortality in the next decade. Cur- rently, there is no specific drug therapy approved for the treatment of this condition. This article reviews the role of weight loss measures and nutritional supplements such as antioxidants and n-3 polyunsaturated fatty acids in the treatment of NAFLD. INTRODUCTION
trum of liver disorders occurring due to abnormal fat
Non-alcoholic fatty liver disease (NAFLD) is the deposition in the liver, which ranges in severity from
most common cause of chronic liver disease in
simple hepatic steatosis with no inflammation, to
the developed world (1). NAFLD refers to a spec-
steatohepatitis (NASH) which can progress to liver cir-rhosis. The diagnosis of NAFLD by definition impliesthe exclusion of significant alcohol intake (i.e., >140gm/week in men; >70 gm/week in women). Histologi-
Ashutosh S.Naniwadekar, M.B.B.S, M.S., Fellow,Division of Gastroenterology, Hepatology and Nutri-
cally, it is characterized by a spectrum of findings rang-
tion, Department of Internal Medicine, Virginia Com-
ing from macrovesicular steatosis alone, mixed portal
monwealth University Medical Center, Richmond, VA.
and lobular inflammation of varying degrees, balloon-
PRACTICAL GASTROENTEROLOGY • FEBRUARY 2010 Nutritional Recommendations for Patients NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #82
ing degeneration of hepatocytes with perisinusoidal
PATHOGENESIS OF NAFLD
deposition of collagen, and finally full blown cirrhosis
Excess energy intake and obesity, in combination with
(2,5). Recent epidemiologic studies support the role of
different genetic and environmental factors, can lead
antecedent NASH in causing about two-thirds to three-
to the development of insulin resistance. A combina-
fourths of all cryptogenic cirrhosis cases (3).
tion of insulin resistance, along with excess accumula-
NAFLD is generally found as a component of the
tion of free fatty acids (FFA) and increased
“metabolic syndrome” which is characterized by cen-
intracellular formation of toxic lipid metabolites (such
tral obesity, hypertension, hyperlipedemia, and
as products of lipid peroxidation), is thought to elicit
impaired glucose tolerance. Up to 90% of patients with
an inflammatory response that triggers the progression
NAFLD have at least one of these features (4). The
to NASH. The accumulation of triglycerides them-
incidence of NAFLD and NASH in the general popu-
selves in the hepatocytes is merely a marker for the
lation varies widely depending on the test used to diag-
deranged lipid metabolism and indicates increased
nose it. Liver biopsy remains the gold standard of
lipid trafficking (12). Since lipotoxicity is thought to
diagnosis. However, different tests, including liver
be a major player in the pathogenesis, both dietary
enzymes (AST, ALT) and imaging (liver ultrasound,
modifications and exercise seem theoretically the best
MR spectroscopy), have been used. Studies looking at
options for preventing the progression to NASH and
the Third National Health and Nutrition Examination
for management of NASH once it develops. This
Survey (NHANES III) using AST and ALT as criteria
review focuses on the nutritional interventions that can
for NAFLD (after excluding alcohol and hepatitis B, C
potentially make a difference in the management of
as causes) found a prevalence of 5.4% in the U.S pop-
ulation (6,7). However, liver enzymes have beenshown to be non-specific and poorly sensitive forchronic liver disease (8). Use of liver ultrasound to
DIETARY MODIFICATIONS AND
diagnose hepatic steatosis has shown a prevalence of
LIFESTYLE CHANGES IN NAFLD
NAFLD ranging from 57–75% in obese, non-drinking
Several studies have shown beneficial effects of
patients (9). Use of MR spectroscopy in a large multi-
dietary modification, weight loss and exercise in
ethnic patient population shows a prevalence of
reducing insulin resistance and in normalization of
NAFLD of 34% in the general population with major
ALT in patients with NAFLD (13–20). However, only
a few studies have evaluated histological improvementin NAFLD based on biopsy results (14,19,20).
NATURAL HISTORY OF NAFLD
One of the best studies to date looking at the naturalhistory of NAFLD in the general population was donein the Mayo Clinic by Adams et al. A total of 420
patients in Olmstead County, Rochester, diagnosed
Diet Trials in NAFLD
with NAFLD, using imaging or with a liver biopsy,were followed for a median period of 7 years. Twenty-
• Daily 600–800 calorie intake reduction (13)
one patients (5%) developed cirrhosis during this
• Restriction of caloric intake to <25 kcals/kg/day of
period, and thirteen (3.1%) developed complications
of cirrhosis, including two patients who developed
• Restriction of total dietary fat content to <30% of the
hepatocellular cancer (11). Even though only a minor-
caloric intake with <10% of the caloric intake from
ity (<10%) of patients with NAFLD develop cirrhosis
• Restriction of caloric intake to <30 kcals/kg/day (18)
and end stage liver disease, the sheer numbers of
• Low calorie/low carbohydrate(40–45% of caloric
patients who have NAFLD in the general population
make this a significant health care concern. PRACTICAL GASTROENTEROLOGY • FEBRUARY 2010 Nutritional Recommendations for Patients NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #82
Different diets have all documented a normaliza-
weight reduction program, showed that a higher per-
tion of the ALT levels 1–3 months after initiation of
centage of patients receiving orlistat with reduced ALT
dietary changes (see Table 1). At least three studies on
levels (48% in orlistat group vs. 26% in placebo).
weight loss in NAFLD patients (14,19,20) have docu-
There was a statistically significant reduction in fatty
mented histologic improvement in steatosis and
liver by ultrasound in the orlistat group compared to
inflammation with biopsies, including one in children
placebo. This was despite a similar reduction in BMI
(20). Studies comparing the efficacy of different types
of diets (i.e., traditional low fat vs. calorie restriction
In the largest meta-analysis looking at the use of
with low carbohydrate diet) in producing weight loss
orlistat in obese patients, a total of 16 clinical trials with
have not been able to prove the superiority of one over
10,631 patients were identified (29). Orlistat improved
the other. However, none of these studies have looked
blood pressure and glycemic control, decreased LDL
and total cholesterol levels, and reduced the incidence
Of interest, all studies support the fact that even
of diabetes, and produced a mean weight reduction of
small degrees of weight loss of around 5–10% of the
2.9 kg compared to the placebo group when followed
total body weight show a clear benefit. This seems to
for one year (29). However, NAFLD was not specifi-
indicate that changes in the amount of fat delivery to
the liver related to dietary fats and the subsequent
Orlistat should therefore be considered in obese
alterations in lipid metabolism are as important as the
patients with NAFLD, particularly when they fail to
actual weight loss (19). This would be an important
lose weight, despite an adequate program of nutritional
point for clinicians to emphasize to NAFLD patients
during weight loss counseling, as the weight loss itselfis just one of the goals of the intervention.
There is concern that very rapid weight loss (gen-
ANTIOXIDANTS IN NAFLD
erally >1.6 kg/week) may cause worsening of the
A recently published Cochrane database meta-analysis
inflammation with NASH, and thereby accelerate pro-
looked at six trials which used a combination of
gression of the disease by drastically increasing vis-
different antioxidants including selenium, vitamin C
ceral adipose tissue breakdown and delivery to the
and vitamin E to evaluate their effects on the progres-
sion of NAFLD. It concluded that there was insuffi-
All of the above studies combined dietary changes
cient evidence to support or refute a role for these in
with aerobic exercise in varying intervals and varying
NAFLD patients (30). Another recently published
levels of supervision. No studies looking at exercise
study looked at the effects of lifestyle changes and
alone without the confounding effect of weight loss
weight loss with or without the use of vitamin C and
E in 53 children with NAFLD. The authors showedthat a mean weight loss of around 4.7 kg produced sig-nificant histologic improvement in the degree of
ROLE OF ORLISTAT IN AUGMENTING
steatosis, lobular inflammation and ballooning degen-
WEIGHT LOSS IN NAFLD PATIENTS:
eration in hepatocytes as determined by a liver biopsy
Orlistat is an inhibitor of gastric and pancreatic lipase,
at 24 months of treatment. The study showed no addi-
which reduces the absorption of long chain fatty acids
tional effect of using vitamin C or E over weight loss
and cholesterol by approximately 30%, with the unab-
sorbed fat excreted in the stool. Four published studies
Betaine is a methyl group donor which increases
have shown the benefit of adding orlistat in obese
the hepatic S-adenosyl-methionine levels and thereby
patients with NAFLD (25–28). A double blind,
may help combat oxidative stress in the liver. A recent
placebo controlled study with 44 patients randomized
randomized controlled trial looking at the effect of
to either receive orlistat 120 mg thrice daily or placebo
daily betaine supplementation in patients with NASH
for six months, with all patients undergoing a similar
failed to show a clear benefit (31). PRACTICAL GASTROENTEROLOGY • FEBRUARY 2010 Nutritional Recommendations for Patients NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #82 n-3 POLYUNSATURATED FATTY ACIDS (n-3 PUFA) AND NAFLD Practical Recommendations for Management of NAFLD
Animal studies have shown that n-3 PUFA enricheddiets reduce hepatic triglyceride content and the devel-
1. Nutritional counseling and appropriate follow-up
opment of steatohepatitis (45). The benefit is thought
with a dietitian is the first line of therapy with spe-
to be due to the modulation of lipid processing by n-3
cific emphasis on the role of daily exercise/activity.
PUFA’s by acting as ligands of the peroxisome prolif-
2. Walking or some form of daily aerobic exercise at
least 30–45 minutes daily is encouraged.
erator-activated receptor α (PPARα) and reducing
3. No clear evidence to recommend the traditional low
hepatic inflammation and oxidative stress (32).
fat vs. the newer high fat, low carbohydrate diets.
The first clinical trial studying the role of n-3
4. Losing even 5–10% of total body weight can be
PUFA in NAFLD was published in 2006 by Capanni et
sufficient to create a significant improvement in
al (33). Both biochemical (ALT, GGT) and ultrasound
NAFLD and metabolic syndrome in general.
improvement in NAFLD was shown in the 42 patients
5. Avoid excessively rapid weight loss (>1.6 kg/week),
who received 1 gm n-3 PUFA daily over a period of 12
as it may increase the progression of NAFLD.
months. Another larger study evaluated a total of 134
6. Careful attention to the management of the accom-
patients randomized to a control group (which received
panying metabolic syndrome—hyperlipidemia, heart
a calorie restricted diet and placebo) and a study group
(which received the recommended diet and 2 gm thrice
7. Morbidly obese patients (BMI >40 or BMI >35 with
daily of n-3 PUFA). The authors showed a 53% reduc-
co-morbidities) should be considered for referral forbariatric surgery.
tion in fatty liver in those patients receiving n-3 PUFA
8. n-3 PUFA appear to be encouraging as potential
compared to 35% in patients receiving dietary manage-
treatment for NAFLD, but further studies are needed
ment alone (34). Similar biochemical and imaging
improvement in NAFLD was seen in two more studies
9. Trial of orlistat in patients failing diet therapy.
using n-3 PUFA (35,36). No adverse events were
10. Avoid foods with HFCS and trans-fats.
reported in any of these studies. n-3 PUFA may have arole in the management of NAFLD, but more studiesare needed to confirm its benefit and define dosing andduration of administration.
isocaloric diet for 7 days, showed an increase in hepaticfat deposition as assessed by MR spectroscopy (40).
Trans-fatty acids (TFA) have been shown to be
HIGH FRUCTOSE CORN SYRUP
associated with obesity, insulin resistance and coro-
AND TRANS-FATTY ACIDS IN NAFLD
nary artery disease (41). Animal studies have docu-
High fructose corn syrup (HFCS) is a common sweet-
mented the role of TFA in the pathogenesis of NAFLD
ener in soft drinks and fruit drinks. Currently the aver-
and NASH (42,43). However, no human studies look-
age American consumes 12% of the total energy intake
ing at the association of NAFLD and trans-fats have
as fructose, primarily as HFCS (38). Porikos et al
showed transaminase elevations in healthy people con-suming 25% of their calories in the form of sucrosewhich contains 50% fructose (37). A recent study com-
ROLE OF BARIATRIC SURGERY
paring the dietary patterns of 49 patients with NAFLD
IN PATIENTS WITH NAFLD
to 24 control patients with other types of chronic liver
The most studied intervention in obese patients for
disease, found a two fold higher consumption of HFCS
weight loss is the use of bariatric surgery. The National
in patients with NAFLD (365 kcal vs. 170 kcal) (39).
Institutes of Health (NIH) guidelines recommend
Another crossover study with 16 healthy males (with
bariatric surgery for obese patients with a BMI >40
history of diabetes in parents) and 8 controls who
kg/m2 or >35 kg/m2 for patients with significant co-
received either a high calorie and high fructose diet or a
morbidities such as heart disease, diabetes or obstruc-
PRACTICAL GASTROENTEROLOGY • FEBRUARY 2010 Nutritional Recommendations for Patients NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #82
tive sleep apnea (44). Currently, the common bariatric
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STATE OF LOUISIANA COURT OF APPEAL, THIRD CIRCUIT WCA 13-534 RHONDA POWELL VERSUS THE OPELOUSAS HOUSING AUTHORITY OFFICE OF WORKERS‟ COMPENSATION - Number 4 ADAM C. JOHNSON, WORKERS‟ COMPENSATION JUDGE BILLY HOWARD EZELL Court composed of Sylvia R. Cooks, Marc T. Amy, and Billy Howard Ezell, Judges. AFFIRMED. Gloria A. Angus Angus Law Firm, LLC P. O. B
j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / s c h r e sIs there an affective working memory deficit in patients with chronic schizophrenia?Nicola Mammarella ,, Beth Fairfield Valeria De Leonardis , Barbara Carretti , Erika Borella Elisa Frisullo Alberto Di Domenico a Department of Neuroscience and Imaging, University of Chieti, Italyb Department of Gene