Jaundice happens when a yellow pigment called bilirubin builds up in your blood faster than your body can get rid of it. The yellowing of skin and eyes typically becomes visible once bilirubin levels rise above 3 mg/dL, roughly three times the normal upper limit. This buildup can occur for three broad reasons: your body is producing too much bilirubin, your liver can’t process it properly, or something is blocking it from leaving your body through bile.
How Your Body Normally Handles Bilirubin
Bilirubin is a natural byproduct of your body recycling old red blood cells. About 70% of it comes from breaking down hemoglobin, the oxygen-carrying protein in red blood cells that reach the end of their roughly 120-day lifespan. The remaining 30% comes from other sources, including faulty red blood cell production in bone marrow and the breakdown of certain proteins in the liver.
Once released into the bloodstream, this raw (unconjugated) form of bilirubin can’t dissolve in water, so it hitches a ride on a blood protein called albumin to reach the liver. Inside the liver, an enzyme converts it into a water-soluble form. This processed bilirubin then gets pumped into bile, travels through bile ducts to the intestines, and eventually leaves your body in stool. It’s actually what gives stool its brown color. A problem at any point in this chain leads to bilirubin backing up in the blood, and that’s what causes jaundice.
Too Many Red Blood Cells Breaking Down
When red blood cells are destroyed faster than normal, the liver gets flooded with more bilirubin than it can handle. This is called hemolytic jaundice, and it produces a buildup of the raw, unconjugated form. The liver itself is working fine; it’s just overwhelmed by volume.
Many conditions speed up red blood cell destruction. Sickle cell disease and thalassemia produce abnormally shaped cells that break apart early. Hereditary spherocytosis creates fragile, sphere-shaped cells that get trapped and destroyed in the spleen. An enzyme deficiency called G6PD deficiency leaves red blood cells vulnerable to damage from certain foods, infections, or medications. Autoimmune hemolytic anemia causes your immune system to mistakenly attack your own red blood cells.
Infections can also trigger rapid destruction. Malaria is one of the most common causes of hemolytic jaundice worldwide, as the parasite invades and ruptures red blood cells directly. Mismatched blood transfusions, severe burns, and even some snake or spider bites can destroy red blood cells fast enough to cause visible yellowing.
Liver Damage or Dysfunction
When the liver itself is injured or diseased, it loses the ability to process bilirubin efficiently. Both the raw and processed forms accumulate, and this category accounts for many of the most common causes of jaundice in adults.
Viral hepatitis (types A, B, C, and E) inflames liver cells and disrupts their function. Hepatitis A and E typically cause acute illness that resolves, while hepatitis B and C can become chronic and lead to lasting liver damage. Heavy alcohol use damages liver cells over time, progressing from fatty liver to inflammation to cirrhosis, where scar tissue replaces functional liver tissue. Each stage further impairs the liver’s ability to clear bilirubin.
Acetaminophen overdose is one of the most common drug-related causes of liver injury. Even at doses only moderately above the recommended limit, it can overwhelm the liver’s detoxification capacity. NSAIDs like ibuprofen and naproxen can also cause liver damage, though less frequently. Other medications linked to liver injury include certain antibiotics (amoxicillin-clavulanate, erythromycin), statins, birth control pills, anabolic steroids, and the tuberculosis drug isoniazid. Poisoning from wild mushrooms, particularly the death cap variety, can cause severe and rapid liver failure.
Less common liver conditions that cause jaundice include hemochromatosis (iron overload), Wilson disease (copper buildup), and non-alcoholic fatty liver disease that progresses to inflammation.
Blocked Bile Ducts
Even if the liver processes bilirubin correctly, it has nowhere to go if the bile ducts are blocked. This is called obstructive jaundice, and it produces a distinctive set of symptoms beyond just yellow skin.
Gallstones are the most common cause. These hard deposits can slip out of the gallbladder and lodge in the bile duct, blocking the flow of bile. Pancreatic cancer is another major cause, because the pancreas sits right next to the main bile duct and tumors can press against or invade it. Bile duct cancer, liver cancer, and cancers that spread to the area from elsewhere can all create blockages. Scarring from previous surgeries, particularly gallbladder removal, sometimes narrows the ducts enough to obstruct them. Chronic inflammation from conditions like primary sclerosing cholangitis can also gradually close off the ducts.
Obstructive jaundice changes more than just skin color. Because bilirubin can’t reach the intestines, stools turn pale or clay-colored. Instead, the backed-up bilirubin gets filtered through the kidneys, turning urine noticeably dark, sometimes tea or cola-colored. Bile salts that accumulate under the skin often cause intense itching.
Gilbert Syndrome and Genetic Causes
Not all jaundice signals serious illness. Gilbert syndrome is an inherited condition where the liver’s bilirubin-processing enzyme works at reduced capacity. It’s caused by a modified gene, and most people need two copies (one from each parent) to be affected. The condition is common and generally harmless.
People with Gilbert syndrome have mildly elevated bilirubin levels most of the time, but they only turn visibly yellow during certain triggers: fasting, dehydration, illness like a cold or flu, strenuous exercise, stress, or menstruation. The yellowing is temporary and resolves once the trigger passes. Many people with Gilbert syndrome don’t know they have it until a routine blood test reveals elevated bilirubin.
Newborn Jaundice
Jaundice is extremely common in newborns. Studies have found significant jaundice in roughly 10% of full-term infants and 25% of near-term infants, with even higher rates in certain populations. Nearly half of East Asian newborns develop bilirubin levels above 10 mg/dL, compared to about 20% of white infants and 12% of Black infants.
This happens for a straightforward reason: newborns are born with a large supply of red blood cells they no longer need outside the womb, and their immature livers aren’t yet efficient at processing the resulting bilirubin. This physiological jaundice typically appears on the second or third day of life and resolves within one to two weeks as the liver matures. Breastfeeding can sometimes contribute, either because insufficient feeding leads to dehydration and slower bilirubin clearance, or because substances in breast milk delay the liver’s processing.
Pathological jaundice in newborns, which is less common but more serious, appears within the first 24 hours of life or rises to very high levels. Blood type incompatibility between mother and baby, G6PD deficiency, and infections are among the causes. High bilirubin in newborns requires prompt treatment because the unconjugated form can cross into the brain and cause permanent damage.
Signs That Accompany Jaundice
The yellow discoloration usually shows up first in the whites of the eyes before becoming visible in the skin. In people with darker skin tones, checking the eyes, the inside of the mouth, and the palms of the hands is more reliable than looking at the skin surface.
The accompanying symptoms depend on the cause. Hemolytic jaundice often comes with fatigue, shortness of breath, and a rapid heartbeat from anemia. Liver-related jaundice may involve nausea, abdominal pain in the upper right side, and general malaise. Obstructive jaundice tends to produce the classic triad of dark urine, pale stools, and itching. Fever alongside jaundice suggests an infection, whether in the liver, the bile ducts, or elsewhere in the body.
A blood test measuring total and direct bilirubin levels is the starting point for figuring out which part of the pathway is failing. Elevated unconjugated bilirubin points toward excessive red blood cell breakdown or genetic conditions like Gilbert syndrome, while elevated conjugated bilirubin points toward liver disease or obstruction. Imaging of the bile ducts and liver function tests help narrow the cause further.