Alcoholic Liver
Disease

Being in an environment where alcohol use and misuse is encouraged and accepted increase the risk of alcohol dependence and addiction.

Drinking history

Long drinking history increases chance of alcohol dependence

Low self-esteem

Education, high levels of stress

The age someone starts drinking, peer pressure to drink

Participating in binge drinking

Employment factors

People with a higher socio-economic status tend to drink more frequently (Collins, 2016)

People with a low socio-economic status tend to drink larger quantities (Collins, 2016).

Neighborhood disadvantage, personal income, household income, education play a role (Collins, 2016).

Homelessness increases the chance of alcohol use and misuse (Collins, 2016).

Long term inflammation

Alcoholic hepatitis

Scar tissue

Cirrhosis

Jaundice, nausea, abdominal swelling and pain,
pale stool, dark urine, itchy skin, chronic fatigue, etc.

Liver Disease

Pollutants

Lead, mercury, PCB, pesticides, etc.
(American Gastroenterological Association, 2009).

Increases risk for abnormal
liver enzymes

Alcoholism

Lack of Education

Societal Acceptance

Media glorifying drinking

Lack of consequences

high profile celebrities, sports star and local role models promoting alcohol with seemingly no adverse effects

Availability

The higher number of licensed liquor establishments in an area the more likely individuals are to drink

The lower the price of alcohol, it's more likely individuals will drink.

Underage individuals are more likely to drink when alcohol is freely available to them, either by purchasing it directly or when it's available at parties

Advertising/Marketing

Alcohol advertisements creates an environment that suggest alcohol consumption and over-consumption are normal activities.

Liver Disease

Wilson's disease
(Morrison & Kowdley, 2000)

Caused by mutation in
ATP7T gener

Provides instructions to
make copper-transporting ATPase 2

Transports copper from the
liver to other parts of the body

Hemochromatosis (HHC)
(Morrison & Kowdley, 2000)

Iron deposits collect in
liver and other organs

Type 1

Most common, symptoms begin in
adulthood; men between 40-60
and women after menopause,

Mutation in HFE gene
(Genetic Home Reference, 2019)

Produces surface cell marker for liver and intestinal cells that help detect the amount of iron in the body

Type 2

Juvenile onset, if untreated, potential
fatal heart disease is evident by age 30

Mutation in HJV or HAMP gene
(Genetics Home Reference, 2019)

HJV

Makes hemojuvelin protein, helps maintain proper iron levels by regulating hepcidin protein.

HAMP

Makes hepcidin, inhibits iron absorption when iron levels are too high

Type 3

Intermediate between type 1 and
type 2; symptoms usually appear
before the age of 30

Mutation in TFR2 gene
(Genetics Home Reference, 2019)

Makes transferrin receptor 2

Helps iron enter liver cells

Type 4

AKA ferroportin disease

Symptoms begin in adulthood;
men between 40-60 and
women after menopause

Mutation in SLC40A1 gene

Makes ferroportin proteins

Transports iron from food into cells

Alpha 1AT deficiency
(Morrison & Kowdley, 2000)

Mutation in SERPINA1 gene
(Genetics Home Reference, 2020)

Makes alpha 1AT proteins, protects
the body from neutrophil elastase enzyme

Neutrophil elastase released to fight infections, but can attack body tissues when not regulated by alpha 1AT proteins

Alcohol Dependence

Alcohol metabolism genes
(Edinburgh & Foroud, 2013)

ADH1B

ALDH2

Chronic heavy drinking

Alters liver's ability
to metabolize fats

Fat builds
up in the liver