Fatty liver http://en.wikipedia.org/wiki/Fatty_liver

Fatty liver

Classification and external resources

Micrograph showing a fatty liver (macrovesicular

steatosis), as seen in non-alcoholic fatty liver

disease. Trichrome stain.

ICD-10 K70, K76.0

ICD-9 571.0, 571.8

DiseasesDB 18844

eMedicine med/775 article/170409

MeSH C06.552.241

Different stages of liver damage

Fatty liver, also known as fatty liver disease (FLD), is a reversible condition wherein large vacuoles of

triglyceride fat accumulate in liver cells via the process of steatosis (i.e., abnormal retention of lipids within a

cell). Despite having multiple causes, fatty liver can be considered a single disease that occurs worldwide in

those with excessive alcohol intake and the obese (with or without effects of insulin resistance). The condition

is also associated with other diseases that influence fat metabolism.[1]

It is difficult to distinguish alcoholic FLD

from nonalcoholic FLD, and both show microvesicular and macrovesicular fatty changes at different stages.

Accumulation of fat may also be accompanied by a progressive inflammation of the liver (hepatitis), called

steatohepatitis. By considering the contribution by alcohol, fatty liver may be termed alcoholic steatosis or

nonalcoholic fatty liver disease (NAFLD), and the more severe forms as alcoholic steatohepatitis (part of

alcoholic liver disease) and Non-alcoholic steatohepatitis (NASH).

Causes

Fatty liver (FL) is commonly associated with alcohol or metabolic syndrome (diabetes, hypertension, obesity,

and dyslipidemia), but can also be due to any one of many causes:[2][3]

Metabolic

Abetalipoproteinemia, glycogen storage diseases, Weber-Christian disease, acute fatty liver of

pregnancy, lipodystrophy

Nutritional

Malnutrition, total parenteral nutrition, severe weight loss, refeeding syndrome, jejunoileal bypass,

gastric bypass, jejunal diverticulosis with bacterial overgrowth

Drugs and toxins

Amiodarone, methotrexate, diltiazem, expired tetracycline, highly active antiretroviral therapy,

glucocorticoids, tamoxifen, environmental hepatotoxins (e.g., phosphorus, mushroom poisoning)

Other

Inflammatory bowel disease, HIV, hepatitis C (especially genotype 3), and alpha 1-antitrypsin

deficiency [4]

Pathology

Micrograph of periportal hepatic steatosis, as may be seen due to steroid use, trichrome stain

Fatty change represents the intracytoplasmatic accumulation of triglycerides (neutral fats). At the beginning, the

hepatocytes present small fat vacuoles (liposomes) around the nucleus (microvesicular fatty change). In this

stage, liver cells are filled with multiple fat droplets that do not displace the centrally located nucleus. In the late

stages, the size of the vacuoles increases, pushing the nucleus to the periphery of the cell, giving characteristic

signet ring appearance (macrovesicular fatty change). These vesicles are well-delineated and optically "empty"

because fats dissolve during tissue processing. Large vacuoles may coalesce and produce fatty cysts, which are

irreversible lesions. Macrovesicular steatosis is the most common form and is typically associated with alcohol,

diabetes, obesity, and corticosteroids. Acute fatty liver of pregnancy and Reye's syndrome are examples of

severe liver disease caused by microvesicular fatty change.[5]

The diagnosis of steatosis is made when fat in the

liver exceeds 5–10% by weight.[1][6][7]

Mechanism leading to hepatic steatosis

Defects in fatty acid metabolism are responsible for pathogenesis of FLD, which may be due to imbalance in

energy consumption and its combustion, resulting in lipid storage, or can be a consequence of peripheral

resistance to insulin, whereby the transport of fatty acids from adipose tissue to the liver is increased.[1][8]

Impairment or inhibition of receptor molecules (PPAR-α, PPAR-γ and SREBP1) that control the enzymes

responsible for the oxidation and synthesis of fatty acids appears to contribute to fat accumulation. In addition,

alcoholism is known to damage mitochondria and other cellular structures, further impairing cellular energy

mechanism. On the other hand, nonalcoholic FLD may begin as excess of unmetabolised energy in liver cells.

Hepatic steatosis is considered reversible and to some extent nonprogressive if the underlying cause is reduced

or removed.

Micrograph of inflamed fatty liver (steatohepatitis)

Severe fatty liver is sometimes accompanied by inflammation, a situation referred to as steatohepatitis.

Progression to alcoholic steatohepatitis (ASH) or Non-alcoholic steatohepatitis (NASH) depends on the

persistence or severity of the inciting cause. Pathological lesions in both conditions are similar. However, the

extent of inflammatory response varies widely and does not always correlate with degree of fat accumulation.

Steatosis (retention of lipid) and onset of steatohepatitis may represent successive stages in FLD progression.[9]

Liver disease with extensive inflammation and a high degree of steatosis often progresses to more severe forms

of the disease.[10]

Hepatocyte ballooning and necrosis of varying degrees are often present at this stage. Liver

cell death and inflammatory responses lead to the activation of stellate cells, which play a pivotal role in hepatic

fibrosis. The extent of fibrosis varies widely. Perisinusoidal fibrosis is most common, especially in adults, and

predominates in zone 3 around the terminal hepatic veins.[11]

The progression to cirrhosis may be influenced by the amount of fat and degree of steatohepatitis and by a

variety of other sensitizing factors. In alcoholic FLD, the transition to cirrhosis related to continued alcohol

consumption is well-documented, but the process involved in nonalcoholic FLD is less clear.

Diagnosis

Liver steatosis (fatty liver disease) as seen on CT

Flow chart for diagnosis, modified from[3]

Elevated liver enzyme

Serology to exclude viral hepatitis

Imaging study showing

fatty infiltrate

Excess alcohol intake

Less than two drinks per day‡

More than two drinks per day‡

Nonalcoholic fatty liver disease likely

Alcoholic liver disease likely

‡ Criteria for nonalcoholic fatty liver disease:

consumption of ethanol less than 20 g/day for women and 30 g/day for men[12]

Most individuals are asymptomatic and are usually discovered incidentally because of abnormal liver function

tests or hepatomegaly noted in unrelated medical conditions. Elevated liver biochemistry is found in 50% of

patients with simple steatosis.[13]

The serum alanine transaminase level usually is greater than the aspartate

transaminase level in the nonalcoholic variant and the opposite in alcoholic FLD (AST:ALT more than 2:1).

Imaging studies are often obtained during the evaluation process. Ultrasonography reveals a "bright" liver with

increased echogenicity. Medical imaging can aid in diagnosis of fatty liver; fatty livers have lower density than

spleens on computed tomography (CT), and fat appears bright in T1-weighted magnetic resonance images

(MRIs). No medical imagery, however, is able to distinguish simple steatosis from advanced NASH.

Histological diagnosis by liver biopsy is sought when assessment of severity is indicated.

Treatment

The treatment of fatty liver depends on its cause, and, in general, treating the underlying cause will reverse the

process of steatosis if implemented at an early stage. Two known causes of fatty liver disease are an excess

consumption of alcohol and a prolonged diet containing foods with a high proportion of calories coming from

lipids.[citation needed]

For the patients with non-alcoholic fatty liver disease with pure steatosis and no evidence of

inflammation, a gradual weight loss is often the only recommendation.[2]

In more serious cases, medications that

decrease insulin resistance, hyperlipidemia, and those that induce weight loss have been shown to improve liver

function.[3]

Complication

Up to 10% of cirrhotic alcoholic FLD patients will develop hepatocellular carcinoma. The overall incidence of

liver cancer in nonalcoholic FLD has not yet been quantified, but the association is well-established.[14]

Epidemiology

The prevalence of FLD in the general population ranges from 10% to 24% in various countries.[2]

However, the

condition is observed in up to 75% of obese people, 35% of whom progressing to NAFLD,[15]

despite no

evidence of excessive alcohol consumption. FLD is the most common cause of abnormal liver function tests in

the United States.[2]

"Fatty livers occur in 33% of European-Americans, 45% of Hispanic-Americans, and 24%

of African-Americans."[16]

References 1. ^ Jump up to:

a b c Reddy JK, Rao MS (2006). "Lipid metabolism and liver inflammation. II. Fatty liver disease and fatty acid

oxidation". Am. J. Physiol. Gastrointest. Liver Physiol. 290 (5): G852–8. doi:10.1152/ajpgi.00521.2005. PMID 16603729.

2. ^ Jump up to: a b c d Angulo P (2002). "Nonalcoholic fatty liver disease". N. Engl. J. Med. 346 (16): 1221–31.

doi:10.1056/NEJMra011775. PMID 11961152.

3. ^ Jump up to: a b c Bayard M, Holt J, Boroughs E (2006). "Nonalcoholic fatty liver disease". American Family Physician 73

(11): 1961–8. PMID 16770927.

4. Jump up ^ Valenti L, Dongiovanni P, Piperno A, et al. (October 2006). "Alpha 1-antitrypsin mutations in NAFLD: high

prevalence and association with altered iron metabolism but not with liver damage". Hepatology 44 (4): 857–64.

doi:10.1002/hep.21329. PMID 17006922.

5. Jump up ^ Goldman, Lee (2003). Cecil Textbook of Medicine – 2-Volume Set, Text with Continually Updated Online

Reference. Philadelphia: W.B. Saunders Company. ISBN 0-7216-4563-1.

6. Jump up ^ Adams LA, Lymp JF, St Sauver J, Sanderson SO, Lindor KD, Feldstein A, Angulo P (2005). "The natural history

of nonalcoholic fatty liver disease: a population-based cohort study". Gastroenterology 129 (1): 113–21.

doi:10.1053/j.gastro.2005.04.014. PMID 16012941.

7. Jump up ^ Crabb DW, Galli A, Fischer M, You M (2004). "Molecular mechanisms of alcoholic fatty liver: role of

peroxisome proliferator-activated receptor alpha". Alcohol 34 (1): 35–8. doi:10.1016/j.alcohol.2004.07.005. PMID 15670663.

8. Jump up ^ Medina J, Fernández-Salazar LI, García-Buey L, Moreno-Otero R (2004). "Approach to the pathogenesis and

treatment of Non-alcoholic steatohepatitis". Diabetes Care 27 (8): 2057–66. doi:10.2337/diacare.27.8.2057.

PMID 15277442.

9. Jump up ^ Day CP, James OF (1998). "Steatohepatitis: a tale of two "hits"?". Gastroenterology 114 (4): 842–5.

doi:10.1016/S0016-5085(98)70599-2. PMID 9547102.

10. Jump up ^ Gramlich T, Kleiner DE, McCullough AJ, Matteoni CA, Boparai N, Younossi ZM (2004). "Pathologic features

associated with fibrosis in nonalcoholic fatty liver disease". Hum. Pathol. 35 (2): 196–9. doi:10.1016/j.humpath.2003.09.018.

PMID 14991537.

11. Jump up ^ Zafrani ES (2004). "Non-alcoholic fatty liver disease: an emerging pathological spectrum". Virchows Arch. 444

(1): 3–12. doi:10.1007/s00428-003-0943-7. PMID 14685853.

12. Jump up ^ Adams LA, Angulo P, Lindor KD (2005). "Nonalcoholic fatty liver disease". Canadian Medical Association

Journal 172 (7): 899–905. doi:10.1503/cmaj.045232. PMC 554876. PMID 15795412.

13. Jump up ^ Sleisenger, Marvin (2006). Sleisenger and Fordtran's Gastrointestinal and Liver Disease. Philadelphia: W.B.

Saunders Company. ISBN 1-4160-0245-6.

14. Jump up ^ Qian Y, Fan JG (2005). "Obesity, fatty liver and liver cancer". Hbpd Int 4 (2): 173–7. PMID 15908310.

15. Jump up ^ Hamaguchi M, Kojima T, Takeda N, Nakagawa T, Taniguchi H, Fujii K, Omatsu T, Nakajima T, Sarui H,

Shimazaki M, Kato T, Okuda J, Ida K (2005). "The metabolic syndrome as a predictor of nonalcoholic fatty liver disease".

Ann. Intern. Med. 143 (10): 722–8. PMID 16287793.

16. Jump up ^ Daniel J. DeNoon (September 26, 2008). "Fatty Liver Disease: Genes Affect Risk". WebMD. Retrieved April 6,

2013.

External links American Association for the Study of Liver Diseases

American Liver Foundation

Fatty Liver Disease, Canadian Liver Foundation

00474 at CHORUS

Photo at Atlas of Pathology

NonAlcoholic SteatoHepatitis (NASH) http://digestive.niddk.nih.gov/ddiseases/pubs/nash/

Nonalcoholic steatohepatitis or NASH is a common, often “silent” liver disease. It resembles alcoholic liver

disease, but occurs in people who drink little or no alcohol. The major feature in NASH is fat in the liver, along

with inflammation and damage. Most people with NASH feel well and are not aware that they have a liver

problem. Nevertheless, NASH can be severe and can lead to cirrhosis, in which the liver is permanently

damaged and scarred and no longer able to work properly.

NASH affects 2 to 5 percent of Americans. An additional 10 to 20 percent of Americans have fat in their liver,

but no inflammation or liver damage, a condition called “fatty liver.” Although having fat in the liver is not

normal, by itself it probably causes little harm or permanent damage. If fat is suspected based on blood test

results or scans of the liver, this problem is called nonalcoholic fatty liver disease (NAFLD). If a liver biopsy is

performed in this case, it will show that some people have NASH while others have simple fatty liver.

Both NASH and NAFLD are becoming more common, possibly because of the greater number of Americans

with obesity. In the past 10 years, the rate of obesity has doubled in adults and tripled in children. Obesity also

contributes to diabetes and high blood cholesterol, which can further complicate the health of someone with

NASH. Diabetes and high blood cholesterol are also becoming more common among Americans.

Biliary system.

Diagnosis NASH is usually first suspected in a person who is found to have elevations in liver tests that are included in

routine blood test panels, such as alanine aminotransferase (ALT) or aspartate aminotransferase (AST). When

further evaluation shows no apparent reason for liver disease (such as medications, viral hepatitis, or excessive

use of alcohol) and when x rays or imaging studies of the liver show fat, NASH is suspected. The only means of

proving a diagnosis of NASH and separating it from simple fatty liver is a liver biopsy. For a liver biopsy, a

needle is inserted through the skin to remove a small piece of the liver. NASH is diagnosed when examination

of the tissue with a microscope shows fat along with inflammation and damage to liver cells. If the tissue shows

fat without inflammation and damage, simple fatty liver or NAFLD is diagnosed. An important piece of

information learned from the biopsy is whether scar tissue has developed in the liver. Currently, no blood tests

or scans can reliably provide this information.

Liver biopsy.

Symptoms NASH is usually a silent disease with few or no symptoms. Patients generally feel well in the early stages and

only begin to have symptoms—such as fatigue, weight loss, and weakness—once the disease is more advanced

or cirrhosis develops. The progression of NASH can take years, even decades. The process can stop and, in

some cases, reverse on its own without specific therapy. Or NASH can slowly worsen, causing scarring or

“fibrosis” to appear and accumulate in the liver. As fibrosis worsens, cirrhosis develops; the liver becomes

seriously scarred, hardened, and unable to function normally. Not every person with NASH develops cirrhosis,

but once serious scarring or cirrhosis is present, few treatments can halt the progression. A person with cirrhosis

experiences fluid retention, muscle wasting, bleeding from the intestines, and liver failure. Liver transplantation

is the only treatment for advanced cirrhosis with liver failure, and transplantation is increasingly performed in

people with NASH. NASH ranks as one of the major causes of cirrhosis in America, behind hepatitis C and

alcoholic liver disease.

Stages of liver damage.

Causes Although NASH has become more common, its underlying cause is still not clear. It most often occurs in

persons who are middle-aged and overweight or obese. Many patients with NASH have elevated blood lipids,

such as cholesterol and triglycerides, and many have diabetes or prediabetes, but not every obese person or

every patient with diabetes has NASH. Furthermore, some patients with NASH are not obese, do not have

diabetes, and have normal blood cholesterol and lipids. NASH can occur without any apparent risk factor and

can even occur in children. Thus, NASH is not simply obesity that affects the liver.

While the underlying reason for the liver injury that causes NASH is not known, several factors are possible

candidates:

insulin resistance

release of toxic inflammatory proteins by fat cells (cytokines)

oxidative stress (deterioration of cells) inside liver cells

Treatment Currently, no specific therapies for NASH exist. The most important recommendations given to persons with

this disease are to

reduce their weight (if obese or overweight)

follow a balanced and healthy diet

increase physical activity

avoid alcohol

avoid unnecessary medications

These are standard recommendations, but they can make a difference. They are also helpful for other

conditions, such as heart disease, diabetes, and high cholesterol.

A major attempt should be made to lower body weight into the healthy range. Weight loss can improve liver

tests in patients with NASH and may reverse the disease to some extent. Research at present is focusing on how

much weight loss improves the liver in patients with NASH and whether this improvement lasts over a period of

time.

People with NASH often have other medical conditions, such as diabetes, high blood pressure, or elevated

cholesterol. These conditions should be treated with medication and adequately controlled; having NASH or

elevated liver enzymes should not lead people to avoid treating these other conditions.

Experimental approaches under evaluation in patients with NASH include antioxidants, such as vitamin E,

selenium, and betaine. These medications act by reducing the oxidative stress that appears to increase inside the

liver in patients with NASH. Whether these substances actually help treat the disease is not known, but the

results of clinical trials should become available in the next few years.

Another experimental approach to treating NASH is the use of newer antidiabetic medications—even in persons

without diabetes. Most patients with NASH have insulin resistance, meaning that the insulin normally present in

the bloodstream is less effective for them in controlling blood glucose and fatty acids in the blood than it is for

people who do not have NASH. The newer antidiabetic medications make the body more sensitive to insulin

and may help reduce liver injury in patients with NASH. Studies of these medications—including metformin,

rosiglitazone, and pioglitazone—are being sponsored by the National Institutes of Health and should answer the

question of whether these medications are beneficial in NASH.

Hope through Research What is most needed in the management of NASH is more research to better understand the liver injury found

in this disease. When the pathways that lead to the injury are fully known, safe and effective means can be

developed to reverse these pathways and help patients with NASH. Recent breakthroughs in mapping the

human genome and uncovering the individual steps by which insulin and other hormones regulate blood

glucose and fat could provide the necessary clues.

The National Institute of Diabetes and Digestive and Kidney Diseases funds the NASH Clinical Research

Network, which comprises eight clinical centers located throughout the United States and a coordinating center

at Johns Hopkins University. The NASH network researches the nature and underlying cause of NASH and

conducts clinical studies on prevention and treatment. More information on the NASH Clinical Research

Network and the locations of the clinical centers are available at jhuccs1.us/nash .

Points to Remember Nonalcoholic steatohepatitis (NASH) is fat in the liver, with inflammation and damage.

NASH occurs in people who drink little or no alcohol and affects 2 to 5 percent of Americans,

especially people who are middle-aged and overweight or obese.

NASH can occur in children.

People who have NASH may feel well and may not know that they have a liver disease.

NASH can lead to cirrhosis, a condition in which the liver is permanently damaged and cannot work

properly.

Fatigue can occur at any stage of NASH.

Weight loss and weakness may begin once the disease is advanced or cirrhosis is present.

NASH may be suspected if blood tests show high levels of liver enzymes or if scans show fatty liver.

NASH is diagnosed by examining a small piece of the liver taken through a needle, a procedure

called biopsy.

People who have NASH should reduce their weight, eat a balanced diet, engage in physical activity,

and avoid alcohol and unnecessary medications.

No specific therapies for NASH exist. Experimental therapies being studied include antioxidants and

antidiabetes medications.

For More Information

American Liver Foundation 39 Broadway, Suite 2700

New York, NY 10006

Phone: 1–800–GO–LIVER (1–800–465–4837) or 212–668–1000

Fax: 212–483–8179

Email: info@liverfoundation.org

Internet: www.liverfoundation.org

You may also find additional information about this topic by visiting MedlinePlus at www.medlineplus.gov.

This publication may contain information about medications. When prepared, this publication included the most

current information available. For updates or for questions about any medications, contact the U.S. Food and

Drug Administration toll-free at 1–888–INFO–FDA (1–888–463–6332) or visit www.fda.gov. Consult your

doctor for more information.

National Digestive Diseases Information Clearinghouse 2 Information Way

Bethesda, MD 20892–3570

Phone: 1–800–891–5389

TTY: 1–866–569–1162

Fax: 703–738–4929

Email: nddic@info.niddk.nih.gov

Internet: www.digestive.niddk.nih.gov

The National Digestive Diseases Information Clearinghouse (NDDIC) is a service of the National Institute of

Diabetes and Digestive and Kidney Diseases (NIDDK). The NIDDK is part of the National Institutes of Health

of the U.S. Department of Health and Human Services. Established in 1980, the Clearinghouse provides

information about digestive diseases to people with digestive disorders and to their families, health care

professionals, and the public. The NDDIC answers inquiries, develops and distributes publications, and works

closely with professional and patient organizations and Government agencies to coordinate resources about

digestive diseases.

Publications produced by the Clearinghouse are carefully reviewed by both NIDDK scientists and outside

experts. The original version of this fact sheet was reviewed by Anna Mae Diehl, M.D., Johns Hopkins

University; and Brent Tetre, M.D., St. Louis University.

This publication is not copyrighted. The Clearinghouse encourages users of this publication to duplicate and

distribute as many copies as desired.

NIH Publication No. 07–4921

November 2006

Page last updated April 30, 2012

Nonalcoholic Steatohepatitis (NASH) - Overview http://www.webmd.com/digestive-disorders/tc/nonalcoholic-steatohepatitis-nash-overview

What is nonalcoholic steatohepatitis (NASH)?

Nonalcoholic steatohepatitis (NASH) is liver inflammation caused by a buildup of fat in the liver. Many people

have a buildup of fat in the liver, and for most people it causes no symptoms and no problems. But in some

people, the fat causes inflammation of the liver. Because of the inflammation, the liver doesn’t work as well as

it should.

NASH can get worse and cause scarring of the liver, which leads to cirrhosis. But the disease doesn't always get

worse.

NASH is similar to the kind of liver disease that is caused by long-term, heavy drinking. But NASH occurs in

people who don't abuse alcohol.

What causes NASH?

Experts don't know why some people with a buildup of fat in the liver get NASH and some don't. It could be

that something in the environment triggers the inflammation in those people. Or maybe it runs in their families.

Things that put people at risk for NASH and for liver damage include:

Obesity.

Type 2 diabetes.

High cholesterol and high triglycerides.

Metabolic syndrome.

Most people who have NASH are 40 to 50 years old and have one or more of the problems listed above. But

NASH can happen in people who have none of these risk factors.

What are the symptoms?

You may have 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, you may start to have symptoms 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.

It may take many years for NASH to become severe enough to cause symptoms.

How is NASH diagnosed?

No single test can diagnose NASH. Your doctor will ask you about other health problems you’ve had.

To see if fat is building up in your liver and to rule out other diseases, your doctor may do tests such as:

An abdominal ultrasound.

A CT scan.

An MRI scan.

Your doctor may do a liver biopsy to be sure that you have NASH. In a liver biopsy, your doctor takes a sample

of tissue from your liver and checks it for signs of NASH.

How is it treated?

There is no treatment for NASH. But you may be able to limit damage to your liver by managing conditions

that increase your risk for NASH or make it worse. You can:

Reduce your total cholesterol level.

Reach a healthy weight. If you need to lose weight, be sure to do so slowly (no more than 1 to 2

pounds a week).1 Quick weight loss from crash diets, surgery, or medicine increases inflammation

and scarring in your liver.

Control diabetes.

Stop or cut back on drinking alcohol.

Exercise regularly.

Also, ask your doctor or pharmacist about all the medicines you are taking. Some may harm your liver.

Nonalcoholic Steatohepatitis (NASH) - FAQs What is NASH ?

Nonalcoholic steatohepatitis, or NASH, is inflammation of the liver caused by a buildup of fat in liver cells.

NASH has features similar to alcohol-induced liver disease, but it occurs in people who do not abuse alcohol.

The exact cause of NASH is not known. NASH is part of a group of liver diseases known as nonalcoholic fatty

liver disease (NAFLD). In this group of diseases, fat builds up in the liver and sometimes causes liver damage

that gets worse over time (progressive liver damage). People who get NASH are usually middle-aged and

overweight or obese and often have other conditions such as diabetes. But NASH can occur in a person who has

none of these risk factors.

Many people with NASH have no symptoms and do not know that they have the condition. As NASH gets

worse, symptoms may appear and include being tired all the time and having unexplained weight loss and

general weakness.

There is no standard treatment for NASH. If you do not have symptoms, treatment may not be needed. If your

liver shows scarring (fibrosis), treatment may include reducing cholesterol levels, losing weight, and controlling

diabetes. Treatment may also include stopping the use of medicines that may make symptoms worse. You

should avoid alcohol if your liver is scarred, because alcohol makes damage to the liver worse.

How do I manage my Weight ?

A healthy weight is a weight that lowers your risk for health problems. For most people, body mass index

(BMI) and waist size are good ways to tell if they are at a healthy weight.

But reaching a healthy weight isn't just about reaching a certain number on the scale or a certain BMI. Having

healthy eating and exercise habits is even more important. When you're active and eating well, your body will

settle into a weight that is healthy for you.

If you want to get to a healthy weight and stay there, healthy lifestyle changes will work better than dieting.

Reaching a certain number on the scale is not as important as having a healthy lifestyle.

Why pay attention to your weight? - Staying at a healthy weight is one of the best things you can do for your

health. It can help prevent serious health problems, including:

Heart disease.

Stroke.

High blood pressure.

Type 2 diabetes.

Sleep apnea.

But weight is only one part of your health. Even if you carry some extra weight, eating healthy foods and being

more active can help you feel better, have more energy, and lower your risk for disease.

Why isn't dieting a good idea? - In today's society, there is a lot of pressure to be thin. But being thin has very

little to do with good health. Many of us long to be thin, even though we're already at a healthy weight. So we

get desperate, and we turn to diets for help.

Diets don't work.

o Diets are temporary. When you diet, you're usually not eating the way you will need to eat over the

long term. So when you quit dieting, the extra weight comes back.

o Dieting usually means not letting yourself have many of the foods you love to eat. So when you quit

dieting, you return to eating those foods as much as you used to—or more. And the extra weight

comes back.

o Dieting often means eating so little food that you're hungry all the time and don't have enough

energy. So when you quit dieting, you return to eating as much as you did before—or more. And the

extra weight comes back.

o Most diet programs don't include an increase in activity, which is vital to staying at a healthy weight.

So when you quit dieting, the weight comes back.

Dieting can actually be bad for you.

o After they quit dieting, most people regain the weight they lost—and many gain even more.

Repeatedly losing and gaining weight may be harder on the body than just being overweight.

o Many diets do not include the right balance of foods to keep you healthy.

o Dieting leads to eating disorders in some people.

o Some people feel so defeated after repeatedly failing to lose weight and keep it off that they give up

altogether on healthy eating and being active.

How do I lower my Colesterol ?

Therapeutic Lifestyle Changes (TLC) may help you lower LDL cholesterol. The lifestyle changes include diet,

exercise, weight loss, and other changes. Your doctor will want you to follow TLC even if you are taking

cholesterol-lowering medicine. And medicine will be more effective if you have healthy eating and exercise

habits.

Diet.Diets to lower cholesterol are low in fat—especially saturated fat—and cholesterol. One of the

best things you can do is reduce the amount of saturated fat you eat.

Exercise. You may need to change your exercise habits. Regular exercise, or no exercise, affects

your cholesterol level and your overall heart health. People who have an active lifestyle have a lower

risk for coronary artery disease (CAD) than do people who have a sedentary lifestyle.

Weight loss. Excess weight tends to increase your LDL cholesterol level. Losing just 5 to 10 pounds

(2.3 to 4.5 kilograms) can lower your cholesterol and triglyceride levels. Eating a diet low in

saturated fat and cholesterol, exercising regularly, and cutting calories will help you lose weight.

Other lifestyle changes to think about. There are a number of other lifestyle changes that improve

cholesterol levels, reduce your risk of atherosclerosis, and improve your general health.

o Stop smoking cigarettes. Cigarette smoking is the leading preventable cause of death. Smoking

decreases your HDL ("good") cholesterol. Smoking is believed to change LDL cholesterol to a form

that promotes the buildup of deposits in the walls of your coronary arteries. Smoking significantly

increases your overall chances of developing heart disease, because it damages your heart and blood

vessels.

o Reduce stress. Try to minimize stressful situations as much as possible at work, at home, and

elsewhere. You may also ask your doctor for advice on ways to reduce stress.

How Can I Manage Type-2 Diabetes ?

What is type 2 diabetes? - Type 2 diabetes happens when your body can't use insulin the right way or when the

pancreas can't make enough insulin.

Insulin is a hormone that helps the body's cells use sugar (glucose) for energy. It also helps the body store extra

sugar in muscle, fat, and liver cells. Without insulin, this sugar can't get into your cells to do its work. It stays in

your blood instead. Your blood sugar level then gets too high.

High blood sugar can harm many parts of the body , such as the eyes, heart, blood vessels, nerves, and

kidneys. It can also increase your risk for other health problems (complications).

Type 2 diabetes is different from type 1 diabetes. In type 1 diabetes, the body's immune system destroys the

cells that release insulin, so that over time the body can't produce insulin at all. In type 2 diabetes, the body still

makes some insulin, but it can't use it the right way.

What causes type 2 diabetes? - You can get type 2 diabetes if:

Your body doesn't respond as it should to insulin. This makes it hard for your cells to get sugar from

the blood for energy. This is called insulin resistance.

Your pancreas doesn't make enough insulin.

If you are overweight, get little or no exercise, or have type 2 diabetes in your family, you are more likely to

have problems with the way insulin works in your body. Type 2 diabetes can be prevented or delayed with a

healthy lifestyle, including staying at a healthy weight, making healthy food choices, and getting regular

exercise.

What are the symptoms? - Some people don't have symptoms, especially when diabetes is diagnosed early. This

is because the blood sugar level may rise so slowly that a person may not know that anything is wrong.

The most common symptoms of high blood sugar include:

Feeling very thirsty.

Urinating more often than usual.

Feeling very hungry.

Having blurred vision.

You can get high blood sugar for many reasons, including not taking your diabetes medicines, eating more than

usual (especially sweets), not exercising, or being sick or under a lot of stress.

If you're taking insulin or oral diabetes medicine, you can also have problems with low blood sugar. These

symptoms include:

Sweating.

Feeling weak.

Feeling shaky.

Feeling very hungry.

How is type 2 diabetes diagnosed? - If your doctor thinks that you have type 2 diabetes, he or she will ask you

questions about your medical history, do a physical exam, and order a blood test that measures the amount of

sugar in your blood.

How is it treated? - The key to treating type 2 diabetes is to keep blood sugar levels controlled and in your

target range.

All of the following help to lower blood sugar: Eating healthy foods.

Losing weight, if you are overweight.

Getting regular exercise.

Taking medicines, if you need them.

It's also important to: See your doctor. Regular checkups are important to monitor your health.

Test your blood sugar levels. You have a better chance of keeping your blood sugar in your target

range if you know what your levels are from day to day.

Keep high blood pressure and high cholesterol under control. This can help you lower your risk of

heart and large blood vessel disease.

Quit smoking. This can help you reduce your risk of heart disease and stroke.

It seems like a lot to do—especially at first. You might start with one or two changes. Focus on checking your

blood sugar regularly and being active more often. Work on other tasks as you can.

It can be hard to accept that you have diabetes. It's normal to feel sad or angry. You may even feel grief.

Talking about your feelings can help. Your doctor or other health professionals can help you cope.

Places To Get Help American Liver Foundation (ALF)

39 Broadway, Suite 2700

New York, NY 10006

Phone: 1-800-GO-LIVER (1-800-465-4837)

Fax: (212) 483-8179

Web Address: www.liverfoundation.org

The American Liver Foundation (ALF) funds research and informs the public about liver disease. A nationwide

network of chapters and support groups exists to help people who have liver disease and to help their families.

ALF also sponsors a national organ-donor program to increase public awareness of the continuing need for

organs. You can send an email by completing a form on the contact page on the ALF website:

www.liverfoundation.org/contact.

National Digestive Diseases Information Clearinghouse

2 Information Way

Bethesda, MD 20892-3570

Phone: 1-800-891-5389

Fax: (703) 738-4929

TDD: 1-866-569-1162 toll-free

Email: nddic@info.niddk.nih.gov

Web Address: www.digestive.niddk.nih.gov

This clearinghouse is a service of the U.S. National Institute of Diabetes and Digestive and Kidney Diseases

(NIDDK), part of the U.S. National Institutes of Health. The clearinghouse answers questions; develops,

reviews, and sends out publications; and coordinates information resources about digestive diseases.

Publications produced by the clearinghouse are reviewed carefully for scientific accuracy, content, and

readability.