Low vitamin B12 usually comes down to one of three problems: you’re not getting enough from food, your body can’t absorb it properly, or a medication is interfering. Absorption problems are the most common culprit, because B12 has one of the most complex absorption pathways of any vitamin. Even people who eat plenty of meat and dairy can end up deficient if something goes wrong along that chain.
How B12 Absorption Actually Works
Understanding why B12 drops starts with understanding how your body takes it in, because this process has several steps that can each break down independently. When you eat B12-rich food, your stomach acid first separates the vitamin from the protein it’s attached to. The freed B12 binds to a protein from your saliva, travels to your small intestine, and gets handed off to a molecule called intrinsic factor, which is produced by specialized cells in your stomach lining. Only after B12 locks onto intrinsic factor can it be absorbed through the wall of the lower small intestine (the ileum) and enter your bloodstream.
This means low stomach acid, damaged stomach lining cells, problems with intrinsic factor, or disease in the lower small intestine can all independently cause B12 to drop. Most other vitamins absorb passively or through simpler channels. B12 is unusually vulnerable to disruption.
Pernicious Anemia: The Autoimmune Cause
Pernicious anemia is one of the most well-known causes of severe B12 deficiency. It’s an autoimmune condition where your immune system produces antibodies that attack either the stomach cells that make intrinsic factor or intrinsic factor itself. Without intrinsic factor, B12 passes straight through your digestive tract without being absorbed, no matter how much you eat.
There are two types of antibodies involved. One type blocks the spot where B12 would normally attach to intrinsic factor. The other targets the receptor in the small intestine where the B12-intrinsic factor complex is supposed to dock. Either way, the result is the same: B12 can’t get into your blood. Over time, the immune attack also causes the stomach lining to thin and shrink (atrophic gastritis), which further reduces acid and intrinsic factor production. Pernicious anemia is diagnosed through blood tests that check for these specific antibodies after a B12 deficiency has been confirmed.
Medications That Lower B12
Two of the most widely prescribed drug categories in the world can quietly drain your B12 over months or years.
Metformin, the standard first-line medication for type 2 diabetes, interferes with B12 absorption through several mechanisms, including disrupting the calcium-dependent step needed for uptake in the small intestine and promoting bacterial overgrowth that competes for the vitamin. About 22% of people on metformin alone develop B12 deficiency, and with long-term use, prevalence can reach as high as 50%.
Proton pump inhibitors (PPIs) like omeprazole and pantoprazole, commonly taken for acid reflux, work by dramatically reducing stomach acid. Since stomach acid is what frees B12 from food protein in the first place, years of PPI use can starve your body of the vitamin. Roughly 26% of people on PPIs alone show deficiency, with some studies reporting rates above 50% for specific PPIs. Taking both metformin and a PPI together pushes deficiency rates to about 34%.
Age-Related Decline
As you get older, your stomach lining gradually thins and produces less acid, a condition called atrophic gastritis. In a study of healthy, independent adults aged 74 to 80, roughly 32% had some degree of atrophic gastritis. Among those with severe thinning, one in four was B12 deficient, compared to fewer than 4% of those with a healthy stomach lining.
This is a slow process. Your liver stores enough B12 to last years, so age-related deficiency doesn’t appear overnight. It typically builds over a long period, which is why it’s often caught incidentally on routine blood work rather than through dramatic symptoms. Adults over 50 are generally advised to get their B12 from fortified foods or supplements, since the synthetic form doesn’t require stomach acid to be released from food protein.
Diet: Vegan and Vegetarian Risk
B12 is found almost exclusively in animal products: meat, fish, eggs, and dairy. If you eat a plant-based diet without supplementing, deficiency is not a risk but a near-certainty given enough time. Studies show roughly 52% of vegan individuals have deficient B12 levels, compared to about 1% of omnivores. Across multiple countries, 50 to 70% of vegetarians and vegans have subnormal B12 status.
Your liver can store between 1 and 5 milligrams of B12, which provides a buffer that can last several years after you stop consuming the vitamin. This delay is deceptive. People who switch to a vegan diet often feel fine for a long time before symptoms appear, which can make the deficiency harder to connect to the dietary change. The recommended daily intake for adults is 2.4 micrograms (2.6 mcg during pregnancy), which is easy to meet through fortified plant milks, nutritional yeast, or a simple supplement.
Surgical and Digestive Causes
Any surgery or disease that alters the stomach or the lower small intestine can disrupt B12 absorption. Gastric bypass surgery (Roux-en-Y) reroutes food past much of the stomach and upper intestine, significantly reducing contact with both stomach acid and intrinsic factor. About 17% of gastric bypass patients develop B12 deficiency within six months, and that rate holds steady at 12 months. Sleeve gastrectomy, which removes part of the stomach but doesn’t reroute the intestine, carries a much lower risk: under 5% at six months and below 1% at one year.
Conditions that inflame or damage the ileum, like Crohn’s disease or celiac disease, can also block absorption. If the section of intestine where B12 is absorbed is scarred or surgically removed, no amount of dietary B12 will compensate, and supplementation by injection becomes necessary.
How B12 Deficiency Is Confirmed
A standard blood test measures serum B12 levels. Values below 200 pg/mL are considered deficient. But B12 blood levels don’t always tell the full story, especially in the borderline range. You can have a “normal” serum level while your cells are still starved of the vitamin.
When results are borderline or symptoms don’t match the numbers, two additional markers help clarify the picture. Methylmalonic acid (MMA) and homocysteine both rise when your body doesn’t have enough B12 to run its normal chemical reactions. Elevated MMA is particularly specific to B12 deficiency, while homocysteine can also rise from low folate. These tests are often ordered together to confirm whether a cellular deficiency is present even when serum B12 looks acceptable.
If deficiency is confirmed and the cause isn’t obviously dietary, antibody testing for pernicious anemia is the next step. Two types of antibodies are checked: one targeting intrinsic factor directly and one targeting the stomach’s acid-producing cells.
Symptoms Worth Recognizing
B12 deficiency can affect almost every system in your body because the vitamin is essential for making red blood cells and maintaining nerve function. Early signs tend to be vague: fatigue, weakness, lightheadedness, and a pale or slightly yellow tint to the skin. These overlap with dozens of other conditions, which is part of why B12 deficiency is frequently missed.
Neurological symptoms are more distinctive and more concerning. Tingling or numbness in the hands and feet, difficulty with balance, memory problems, and mood changes like depression or irritability can all signal that B12 has been low long enough to affect the nervous system. The red blood cells produced during deficiency are abnormally large (a condition called megaloblastic anemia), which shows up on a standard blood count as an elevated mean corpuscular volume above 100 fL. If caught early, most symptoms reverse with supplementation. Nerve damage from prolonged deficiency, however, can be permanent.