Gallstones form when substances in bile, a digestive fluid stored in your gallbladder, become too concentrated and crystallize into solid deposits. About 20 million American adults have gallstones, with women affected roughly twice as often as men. Most stones develop gradually over months or years, and the process depends on the type of stone, your genetics, your hormones, and how well your gallbladder contracts.
What Bile Is and Why It Matters
Your liver continuously produces bile, a greenish fluid that helps digest fats. Bile contains cholesterol, bile salts (which act like detergent to dissolve fat), and bilirubin (a waste product from the breakdown of old red blood cells). Between meals, bile collects and concentrates in your gallbladder. When you eat, the gallbladder squeezes bile into your small intestine.
Normally, bile salts keep cholesterol dissolved in a liquid state. Problems start when the balance tips: too much cholesterol, too much bilirubin, or not enough bile salts. Once bile becomes oversaturated with one of these substances, solid crystals can begin to form.
How Cholesterol Stones Form
Cholesterol stones are the most common type, making up the majority of gallstones in Western countries. They form through a predictable sequence of events.
First, the liver secretes more cholesterol into bile than the bile salts can keep dissolved. This creates what’s called supersaturated bile. Supersaturation alone isn’t enough to cause stones, though. Many people have mildly supersaturated bile and never develop problems. The next step is nucleation: tiny cholesterol crystals begin to cluster together around microscopic particles like calcium salts or proteins. In people who form stones, this crystal formation happens faster than normal.
The gallbladder then plays a critical role. In stone-formers, the gallbladder tends to contract sluggishly, a condition called hypomotility. A sluggish gallbladder doesn’t empty completely after meals, so concentrated bile sits in the gallbladder longer, giving crystals more time to grow. Meanwhile, the gallbladder lining produces excess mucin, a gel-like substance that traps the tiny crystals and helps them clump into larger stones. Over months, those clumps harden into pebble-like deposits ranging from a grain of sand to a golf ball in size.
How Pigment Stones Form
Pigment stones are made primarily from bilirubin rather than cholesterol, and they come in two varieties with different causes.
Black pigment stones form when bile becomes oversaturated with a calcium-bilirubin compound. This usually happens when the body breaks down red blood cells faster than normal, a process called hemolysis. Conditions like sickle cell disease and certain blood disorders flood the liver with bilirubin, which ends up in bile. Unlike cholesterol stones, black pigment stones don’t require a sluggish gallbladder to develop.
Brown pigment stones have a completely different origin. They typically form in the bile ducts rather than the gallbladder itself, and they’re driven by bacterial infection or parasitic infestation of the biliary system. Bacteria break down fats and other compounds in bile, releasing substances that combine with calcium and precipitate into soft, muddy stones. These stones are more common in parts of East Asia and are also seen in people who’ve had previous surgery on the bile ducts.
Why Women Are at Higher Risk
Estrogen is a major driver of gallstone formation. It increases the amount of cholesterol the liver secretes into bile while simultaneously reducing bile salt concentrations, pushing bile toward that critical oversaturated state. This is why gallstone prevalence is higher in women than in men at every age and in every population studied.
Pregnancy amplifies this effect. Estrogen levels rise steadily throughout pregnancy, and the risk of gallstone formation climbs with them, peaking during the third trimester. Progesterone, which also rises during pregnancy, further slows gallbladder contractions, adding stasis to the equation. Birth control pills and hormone replacement therapy carry the same mechanism on a smaller scale, because both deliver supplemental estrogen.
Genetics and Ethnicity
Your genes play a meaningful role in gallstone risk. One of the best-studied genetic links involves the ABCG8 gene, which controls a transporter protein in liver cells that pumps cholesterol into bile. Certain common variants of this gene produce a transporter that’s overly active, flooding bile with more cholesterol than it can hold dissolved. People who carry these variants face a higher baseline risk of cholesterol stones regardless of their diet or weight.
Ethnicity reflects this genetic influence. Mexican American women have the highest gallstone prevalence in the United States, at roughly 27%, compared to about 17% for non-Hispanic white women and 14% for non-Hispanic Black women. Among men, the pattern is similar but overall prevalence is lower: around 9% for Mexican American and non-Hispanic white men, and about 5% for non-Hispanic Black men. Native American populations, particularly the Pima tribe, also carry elevated genetic risk.
Other Major Risk Factors
Obesity is one of the strongest modifiable risk factors. Excess body fat increases cholesterol synthesis in the liver, which raises bile cholesterol levels. Ironically, rapid weight loss is also risky. When you lose weight very quickly, especially on very low calorie diets or after bariatric surgery, the liver mobilizes stored cholesterol rapidly, dumping it into bile faster than bile salts can handle. At the same time, the gallbladder may contract less often because you’re eating less fat, creating the perfect combination of supersaturation and stasis.
Age matters too. Gallstones become increasingly common after 40, as bile composition shifts over time and gallbladder motility naturally declines. Diabetes, metabolic syndrome, and conditions that affect the gut’s ability to reabsorb bile salts (like Crohn’s disease affecting the lower small intestine) also raise risk by altering the cholesterol-to-bile-salt ratio.
What Gallstones Feel Like
Most gallstones cause no symptoms at all. Many people discover them incidentally during an ultrasound or CT scan done for something else. Asymptomatic stones generally don’t require treatment.
When a stone does cause trouble, it’s usually because it temporarily blocks the duct that drains the gallbladder. This produces biliary colic: a sudden, intense pain in the upper right abdomen that can radiate to the right shoulder or between the shoulder blades. Despite the name “colic,” the pain is typically steady rather than coming in waves, and it lasts up to three hours. It often strikes after a fatty meal, which triggers the gallbladder to squeeze. If pain persists beyond three hours, it may indicate that the blockage has caused the gallbladder wall to become inflamed, a more serious condition that usually requires prompt medical attention.
Reducing Your Risk
Diet is one of the most practical levers you can pull. Dietary fiber has a consistently protective effect. A large analysis of U.S. adults found that every additional 5 grams of fiber per day was associated with an 11% lower prevalence of gallstones. People eating more than 25 grams of fiber daily had about a third lower risk compared to those eating the least fiber. Fiber likely helps by binding bile salts in the gut and altering the cholesterol content of bile.
Maintaining a stable, healthy weight reduces risk by keeping liver cholesterol output in check. If you do need to lose weight, a moderate pace of 1 to 2 pounds per week is safer for your gallbladder than crash dieting. Regular physical activity appears protective independently of weight, possibly because it improves gallbladder motility. Healthy fats in moderation, like those in nuts, olive oil, and fish, stimulate regular gallbladder contractions and prevent the stasis that encourages crystal formation.