Anemia happens when your body doesn’t have enough healthy red blood cells to carry oxygen to your tissues. The causes range from simple nutritional gaps to chronic diseases, genetic conditions, and internal bleeding you might not even notice. Globally, anemia affects roughly half a billion women of reproductive age and 269 million young children, making it one of the most common blood disorders in the world.
How Red Blood Cells Work (and Fail)
Your bone marrow constantly produces red blood cells, each packed with hemoglobin, the protein that picks up oxygen in your lungs and delivers it throughout your body. Iron sits at the center of every hemoglobin molecule, which is why iron is so critical to this process. A healthy red blood cell lives about 120 days before it’s broken down, its iron recycled, and a new cell takes its place.
Anemia develops when something disrupts this cycle. Either your body can’t make enough red blood cells, the ones it makes are defective, or red blood cells are being destroyed or lost faster than they can be replaced. Each of these breakdowns has different causes, and they often overlap.
Iron Deficiency: The Most Common Cause
Iron deficiency accounts for roughly half of all anemia cases worldwide. Without enough iron, your bone marrow can’t build functional hemoglobin. The red blood cells it produces end up smaller and paler than normal, carrying less oxygen per cell. This is why iron deficiency anemia tends to creep up gradually: you might feel increasingly tired, short of breath during exercise, or lightheaded before you realize something is wrong.
The iron shortfall itself has several possible sources. Diet is the obvious one, especially for vegetarians or people who eat very little red meat, beans, or fortified grains. But chronic blood loss is just as common and easier to miss. Heavy menstrual periods are a leading cause in premenopausal women. In older adults, slow bleeding from the gastrointestinal tract (peptic ulcers, colon polyps, or even celiac disease damaging the gut lining) can drain iron stores over months without any visible blood in the stool. Celiac disease in particular is worth considering in anyone with unexplained iron deficiency, since it impairs the gut’s ability to absorb iron even when dietary intake is adequate.
Vitamin B12 and Folate Deficiency
Your body also needs vitamin B12 and folate to build red blood cells properly. These vitamins play a different role than iron: they’re essential for DNA synthesis inside developing blood cells. When either is missing, the cells can’t divide normally. Instead, the bone marrow produces oversized, immature red blood cells that don’t function well and die off prematurely.
B12 deficiency is common in older adults because the stomach produces less of the acid needed to absorb B12 from food. It also affects people with autoimmune conditions that attack the stomach lining (a condition historically called pernicious anemia) and people following strict vegan diets, since B12 occurs naturally only in animal products. Folate deficiency tends to show up during pregnancy, when the body’s demand for folate roughly doubles, or in people with poor dietary variety. Alcohol abuse also depletes folate stores.
Chronic Disease and Inflammation
Long-term illnesses like rheumatoid arthritis, lupus, inflammatory bowel disease, cancer, and chronic infections can cause anemia even when your iron intake is perfectly fine. This type, sometimes called anemia of chronic disease, works through a surprisingly clever mechanism your body uses to fight infection.
During prolonged inflammation, your liver ramps up production of a hormone called hepcidin. Hepcidin’s job is to lock down iron. It does this by blocking the protein (ferroportin) that normally shuttles iron out of your gut cells and into your bloodstream. It also traps iron inside the immune cells that recycle old red blood cells. The result: iron gets sequestered inside your tissues, unavailable for making new hemoglobin, even though your total body iron stores may be normal or even high. This is essentially your immune system hoarding iron to starve invading bacteria of a nutrient they need to grow. The trade-off is that your own red blood cell production suffers.
Kidney Disease and Hormone Signals
Your kidneys do far more than filter waste. They’re the sole source of erythropoietin in adults, a hormone that tells your bone marrow to ramp up red blood cell production. As kidney function declines, erythropoietin output drops. Without that signal, the bone marrow slows down. Developing red blood cells don’t mature properly, and the immature ones that do form have shorter lifespans, a process called neocytolysis.
This makes anemia extremely common in chronic kidney disease. It can appear at any stage of kidney decline, not just in advanced failure, and it tends to worsen as kidney function deteriorates further. The fatigue from kidney-related anemia compounds the fatigue from the kidney disease itself, creating a cycle that significantly affects quality of life.
Genetic Conditions That Alter Hemoglobin
Some forms of anemia are inherited. Sickle cell disease is the most well-known example. People with sickle cell disease inherit genes that produce an abnormal form of hemoglobin, causing red blood cells to become rigid and crescent-shaped instead of the flexible, disc-like shape they need to squeeze through tiny blood vessels. These sickle-shaped cells die early, creating a constant shortage of red blood cells. The most severe form (HbSS) involves inheriting the sickle hemoglobin gene from both parents, but other combinations, like inheriting one sickle gene and one gene for hemoglobin C or beta thalassemia, also cause disease.
Thalassemia is another inherited condition where the body produces less hemoglobin than normal because of mutations affecting the protein chains that make up hemoglobin. Depending on how many genes are affected, thalassemia ranges from a mild, barely noticeable drop in hemoglobin to a severe form requiring regular blood transfusions.
Red Blood Cell Destruction
In hemolytic anemias, your bone marrow produces healthy red blood cells, but something destroys them before their normal 120-day lifespan is up. The triggers vary widely. Your immune system can mistakenly target your own red blood cells with antibodies, tagging them for destruction. Certain infections break red blood cells apart directly. Mechanical forces can shear cells physically: artificial heart valves, small blood clots lodged in tiny vessels, or even repeated physical trauma.
Some medications also trigger hemolysis by provoking an immune reaction against red blood cells. Certain antibiotics, anti-inflammatory drugs, and medications used for Parkinson’s disease and urinary tract infections have all been linked to drug-induced hemolytic anemia. The anemia typically resolves once the medication is stopped, but identifying the culprit can take time since the connection isn’t always obvious.
Bone Marrow Failure
In rare cases, the bone marrow itself stops producing enough blood cells. Aplastic anemia occurs when the stem cells in your bone marrow are damaged or destroyed, often by the body’s own immune system turning against them. The trigger for this immune attack can be a viral infection, exposure to certain chemicals (benzene, some pesticides), or a reaction to medications including certain antibiotics, anti-seizure drugs, and anti-inflammatory painkillers. In many cases, no clear trigger is ever identified.
Aplastic anemia affects all blood cell lines, not just red blood cells, so it typically causes low white blood cell counts and low platelet counts alongside anemia. This makes it more dangerous than other forms because it simultaneously increases infection risk and bleeding risk.
Pregnancy and Increased Demand
Pregnancy creates anemia through sheer demand. Your blood volume expands by nearly 50% to support the growing fetus, but red blood cell production doesn’t keep pace with the increase in plasma. This dilution effect is normal to a degree, but it easily tips into true anemia, especially without adequate iron and folate intake. The WHO defines anemia in pregnancy as hemoglobin below 11.0 g/dL in the first and third trimesters, and below 10.5 g/dL in the second trimester (the threshold is slightly lower mid-pregnancy because blood dilution peaks then).
About 37% of pregnant women worldwide are anemic. The consequences extend beyond fatigue: maternal anemia is linked to lower birth weight and higher risk of preterm delivery, which is why iron and folate supplementation is standard in prenatal care.
When Multiple Causes Overlap
In practice, anemia often has more than one cause at the same time. Someone with rheumatoid arthritis may have both inflammation-driven iron trapping and genuine iron deficiency from anti-inflammatory medications irritating the stomach lining. A person with chronic kidney disease may also be deficient in iron or B12. Older adults frequently have a combination of poor dietary intake, chronic disease, and medication effects all contributing to low hemoglobin.
This is why identifying the cause matters more than simply knowing you’re anemic. A blood test showing low hemoglobin is the starting point, but the size and shape of your red blood cells, your iron levels, your B12 and folate levels, and markers of inflammation all help pinpoint what’s driving the problem. Treating iron deficiency when the real issue is chronic inflammation, or vice versa, won’t resolve the anemia and may delay the right diagnosis.