Iron levels drop when your body loses more iron than it takes in, absorbs less from food, or locks iron away where it can’t be used. The causes range from everyday dietary habits and normal biology to medications and chronic health conditions. Understanding which factors apply to you can help you figure out why your levels might be low and what to do about it.
Foods and Drinks That Block Iron Absorption
What you eat alongside iron-rich foods matters as much as the iron itself. Several common compounds in food and beverages interfere with your body’s ability to absorb iron from your gut.
Tea, coffee, and other tannin-rich drinks are among the strongest inhibitors. Black tea consumed with a meal can reduce iron absorption by 60 to 90% compared to water. Even a single cup of tea dropped iron bioavailability from about 18% down to 7% in one study, and doubling the amount of tea didn’t make it much worse. The plant compounds responsible, called tannins and polyphenols, bind to iron in your digestive tract and make it harder for your intestines to absorb. Oregano and other herbs with high tannin content have a similar effect.
Phytic acid, found in whole grains, legumes, nuts, and seeds, is another major blocker. Cereal-based foods can have strikingly low iron absorption rates: as little as 0.33% from oat porridge and 0.99% from wheat porridge in studies where phytic acid was left intact. When researchers broke down the phytic acid before feeding participants the same foods, absorption jumped dramatically, to nearly 3% from oats and over 11% from wheat. Soaking, sprouting, and fermenting grains and legumes are traditional preparation methods that partially break down phytic acid and improve iron uptake.
Calcium competes directly with iron for absorption. Doses of 1,000 mg or more of calcium reduced non-heme iron absorption by about 50% in one study, and 800 mg was enough to cut heme iron absorption by nearly 38%. This is worth knowing if you take calcium supplements or drink a lot of milk with meals. Spacing calcium-heavy foods or supplements away from your iron-rich meals by a couple of hours helps avoid the conflict.
Menstruation and Blood Loss
Monthly blood loss is the single most common reason premenopausal women have lower iron stores than men. A typical menstrual cycle costs the body about 1 mg of iron. That sounds small, but it adds up over months and years, especially if your diet doesn’t consistently replace it.
Heavy periods change the math dramatically. Women with heavy menstrual bleeding lose a median of 5.2 mg of iron per cycle, roughly five to six times the normal amount. At that rate, dietary intake alone often can’t keep up, and iron stores steadily decline. Any other source of chronic blood loss, such as a bleeding ulcer, frequent blood donation, or regular use of blood-thinning medications, creates the same problem.
Pregnancy’s Rising Iron Demand
Pregnancy doesn’t lower iron through loss. It lowers iron by massively increasing how much your body needs. In the first trimester, daily iron requirements sit around 0.8 mg, similar to a non-pregnant state. By the second trimester, that jumps to 4 to 5 mg per day. In the third trimester, the requirement exceeds 6 mg daily to support the expanding blood volume, the growing placenta, and fetal development. Most women can’t meet that demand through food alone, which is why iron stores commonly drop during pregnancy even with a good diet.
Medications That Reduce Iron Absorption
Proton pump inhibitors (PPIs), commonly taken for acid reflux and heartburn, lower iron levels by reducing stomach acid. Your body needs that acid to convert the form of iron found in plant foods, grains, and vegetables into a form your intestines can actually absorb. PPIs suppress acid production at the source, raising the pH in your stomach and leaving much of the iron in your food in an unusable state. Over months or years of regular PPI use, this can lead to measurable iron deficiency.
Antacids work through a similar mechanism, though their effect is shorter-lived. Other medications that can interfere with iron include certain antibiotics and drugs that bind to minerals in the gut.
Chronic Inflammation and Iron Trapping
One of the less intuitive ways iron levels drop is through inflammation. When your body fights a chronic infection, autoimmune disease, or other ongoing inflammatory condition, it deliberately pulls iron out of circulation and locks it away. This is actually a defense mechanism: many bacteria need iron to grow, so your body hides it.
The process works through a hormone called hepcidin, produced in the liver. Inflammatory signals, particularly a molecule called IL-6, ramp up hepcidin production. Hepcidin then destroys the channels that cells use to release iron into the bloodstream. The result is iron trapped inside immune cells and the cells lining your intestines, unable to reach your blood where it’s needed to make red blood cells. Your total body iron may actually be normal or even high, but the iron available for use is functionally low. This pattern, sometimes called anemia of chronic disease, shows up in conditions like rheumatoid arthritis, inflammatory bowel disease, chronic kidney disease, and some cancers.
Gut Conditions That Block Absorption
Iron is primarily absorbed in the upper part of the small intestine. Any condition that damages or inflames that area can drastically reduce how much iron gets through. Celiac disease is a classic example: the immune reaction to gluten flattens the intestinal lining and destroys the surface area needed for nutrient absorption. Crohn’s disease, particularly when it affects the upper small intestine, has a similar effect.
Gastric bypass and other weight-loss surgeries that reroute or remove portions of the stomach and upper intestine also reduce iron absorption permanently. People who’ve had these procedures typically need lifelong monitoring and supplementation.
Exercise and Athletic Training
Intense exercise lowers iron through multiple pathways at once. Runners are especially susceptible to something called foot-strike hemolysis: the repeated impact of feet hitting the ground physically ruptures red blood cells in the blood vessels of the feet. The iron from those destroyed cells has to be recycled, and some is lost in the process.
Beyond mechanical damage, heavy exercise causes iron loss through sweat, minor gastrointestinal bleeding, and even small amounts of blood in urine. On top of all that, the inflammation triggered by hard training raises hepcidin levels, which temporarily reduces iron absorption from the gut and blocks the recycling of iron from old red blood cells. For endurance athletes training daily, these small losses compound. Iron deficiency is one of the most common nutritional deficiencies in competitive runners, swimmers, and cyclists.
How Iron Deficiency Is Detected
A standard blood test measuring ferritin, the protein that stores iron, is the most common way to check iron status. The World Health Organization sets the threshold for iron deficiency at below 15 micrograms per liter for non-pregnant women and below 12 for young children. However, recent multinational research suggests these cutoffs may be too low. Hemoglobin levels, which reflect your body’s ability to carry oxygen, start declining when ferritin drops below about 25 micrograms per liter in women and 22 in children. In other words, functional consequences may begin well before you hit the traditional diagnostic threshold.
If inflammation is present, ferritin can appear falsely normal or even elevated because it rises as part of the inflammatory response. In those cases, additional markers like transferrin saturation or soluble transferrin receptor help clarify whether a true iron deficit exists underneath the inflammation.