Low hemoglobin means your blood isn’t carrying enough oxygen to your tissues, and the causes fall into three broad categories: you’re losing blood, your body isn’t making enough red blood cells, or your red blood cells are being destroyed faster than they can be replaced. Which category applies to you depends on everything from your diet to your menstrual cycle to underlying conditions you may not know about yet. Understanding the specific reason matters because the fix for one type of low hemoglobin can be completely different from another.
What Counts as Low
Hemoglobin thresholds vary by sex and life stage. For most non-pregnant adults, levels below roughly 12 g/dL in women and 13 g/dL in men are considered anemic. Pregnancy shifts the numbers because blood volume expands significantly: in the first trimester, hemoglobin below 11 g/dL qualifies as anemia, that threshold drops to 10.5 g/dL in the second trimester as blood dilution peaks, then rises back to 11 g/dL in the third trimester. A single low reading doesn’t always mean something is wrong, but it does warrant follow-up to figure out why.
Not Enough Iron, B12, or Folate
The most common reason for low hemoglobin worldwide is a shortage of the raw materials your body needs to build red blood cells. Iron is the mineral at the center of each hemoglobin molecule, so when iron stores run low, your bone marrow simply can’t produce enough functional hemoglobin. This is especially common in people with heavy periods, vegetarians or vegans who don’t supplement, and anyone with poor iron absorption due to gut conditions like celiac disease.
Vitamin B12 and folate work differently. Your body needs both to copy DNA accurately during cell division. Red blood cell precursors in the bone marrow are among the fastest-dividing cells in your body, so they’re hit early and hard when either vitamin is lacking. Without enough B12 or folate, those precursor cells can’t complete normal division. Their outer structure matures on schedule, but the nucleus lags behind with incomplete DNA. Many of these defective cells die before ever leaving the bone marrow. The ones that do make it into circulation are oversized and fewer in number, which drives hemoglobin down.
B12 and folate are also chemically linked. B12 acts as a helper molecule in recycling folate into its active form. When B12 is missing, folate gets trapped in an unusable state, so a B12 deficiency can effectively create a folate deficiency too, even if your folate intake is adequate.
Slow, Hidden Blood Loss
Sometimes hemoglobin drops not because production is impaired but because blood is leaving your body faster than it can be replaced. The obvious causes, like surgery or a major injury, are easy to spot. The sneakier ones are harder to catch. Bleeding in the digestive tract from stomach ulcers, colon polyps, hemorrhoids, or colorectal cancers can be so gradual that you never notice blood in your stool. Over weeks or months, this slow drip depletes your iron stores and pulls hemoglobin steadily downward.
Heavy menstrual periods are another leading cause, particularly in younger women. If you regularly soak through pads or tampons every hour or two, or if your periods last longer than seven days, the cumulative blood loss across cycles can outpace what your bone marrow and diet can keep up with.
How Chronic Illness Blocks Iron
Conditions like rheumatoid arthritis, inflammatory bowel disease, chronic infections, and certain cancers can lower hemoglobin through a mechanism that has nothing to do with diet. When your body is fighting sustained inflammation, immune cells release signaling molecules (particularly one called IL-6) that trigger the liver to produce large amounts of a regulatory protein called hepcidin.
Hepcidin is normally your body’s iron traffic controller. It determines how much iron gets released from storage cells and how much gets absorbed from food. During inflammation, hepcidin levels spike, and it essentially locks iron inside your cells. Iron that’s sitting in storage depots and iron waiting to be absorbed from your gut both get blocked from entering the bloodstream. Your bone marrow is left starved for iron even though your body’s total iron stores may be perfectly normal. This is why blood tests in someone with chronic disease anemia often show low circulating iron alongside normal or even high stored iron, a pattern that looks very different from simple dietary iron deficiency.
Kidney Disease and the Hormone Signal
Your kidneys do more than filter waste. They produce erythropoietin (EPO), the hormone that tells your bone marrow to ramp up red blood cell production. When kidney damage reduces EPO output, your bone marrow doesn’t get the signal to make enough new cells, and hemoglobin drifts lower over time. This is one of the most common complications of chronic kidney disease and often worsens as kidney function declines. It’s a mechanical problem: the factory (bone marrow) works fine, but the order (EPO) never arrives.
Inherited Blood Disorders
Some people are born with genetic changes that affect hemoglobin directly. These conditions fall into two groups: those that reduce the amount of hemoglobin produced, and those that alter its structure.
Thalassemia belongs to the first group. Hemoglobin is built from two types of protein chains (alpha and beta), and thalassemia involves mutations or deletions in the genes for one of those chains. When one chain is underproduced, the imbalance destabilizes red blood cells and shortens their lifespan. Depending on how many genes are affected, thalassemia can range from so mild it never causes symptoms to severe enough to require regular blood transfusions. People with one or two affected genes often have only mildly low hemoglobin that’s frequently mistaken for iron deficiency.
Sickle cell disease is the best-known structural hemoglobin variant. A single gene change causes hemoglobin molecules to clump together under low-oxygen conditions, warping red blood cells into a rigid crescent shape. These misshapen cells get stuck in small blood vessels and are cleared from circulation much faster than normal cells, leading to chronic anemia alongside episodes of severe pain.
Red Blood Cell Destruction
Even without a genetic condition, your body can sometimes destroy its own red blood cells faster than they’re replaced. This is called hemolytic anemia, and it has a range of triggers. Autoimmune reactions can cause your immune system to mistakenly tag red blood cells for destruction. Certain infections, medications, and mechanical forces (like artificial heart valves physically shearing cells apart) can also shorten red blood cell lifespan dramatically. In these cases, hemoglobin drops not from a production problem but from accelerated turnover.
How Low Hemoglobin Feels
Mild drops in hemoglobin often produce no noticeable symptoms at all. As levels fall further, you may notice fatigue, shortness of breath during activities that used to feel easy, dizziness when standing, and a faster-than-normal heartbeat. Your skin, gums, and the inside of your lower eyelids may look paler than usual, though visible pallor typically doesn’t appear until hemoglobin drops below about 7 g/dL.
Iron deficiency specifically can cause a few distinctive signs beyond general anemia symptoms. These include brittle or spoon-shaped nails (where the nail bed curves upward at the edges), cracks at the corners of your mouth, a smooth or sore tongue, and unusual cravings for non-food items like ice, dirt, or starch. These cravings, called pica, are surprisingly common in severe iron deficiency and often resolve once iron levels are restored.
How the Cause Gets Identified
A standard blood count reveals that hemoglobin is low, but it doesn’t explain why. The size and shape of your red blood cells provide the first clue. Small, pale cells point toward iron deficiency or thalassemia. Abnormally large cells suggest B12 or folate deficiency. Normal-sized cells with low hemoglobin often indicate chronic disease, kidney-related anemia, or early blood loss.
From there, additional blood tests narrow the diagnosis. Iron studies measure how much iron is circulating, how much is stored, and how much capacity your blood has to carry more. A reticulocyte count checks whether your bone marrow is responding appropriately by pumping out young red blood cells. If reticulocytes are high, your marrow is working hard to compensate for blood loss or cell destruction. If they’re low, the problem is in production itself. B12 and folate levels, kidney function tests, and inflammatory markers each help rule causes in or out. In some cases, a blood smear examined under a microscope reveals telltale cell shapes, like sickle cells or fragmented cells, that point directly to the underlying condition.
Getting the right diagnosis matters because treatments vary enormously. Iron supplements won’t help if hepcidin is blocking absorption. B12 injections won’t help if the problem is hidden GI bleeding. And treating a nutritional deficiency without investigating why it developed can mean missing something more serious underneath.