Red grains under the microscope
In the 17th century the Dutch naturalists Jan Swammerdam and Antonie van Leeuwenhoek were among the first to see tiny red particles in blood through early microscopes. In the 19th century their colour was traced to haemoglobin, an iron-containing protein, and in 1904 Christian Bohr and colleagues discovered the Bohr effect: haemoglobin releases oxygen more readily in carbon-dioxide-rich tissues. In 1960 Max Perutz used X-ray crystallography to reveal haemoglobin's 3D structure, sharing the 1962 Nobel Prize in Chemistry. Mature human red cells lack a nucleus and mitochondria, so they carry oxygen without using it, and their biconcave shape lets them bend through narrow capillaries.
Production, lifespan and anaemia
Bone marrow makes about two million red cells every second; each circulates for about 120 days before being broken down in the spleen and liver. In 1957 Leon Jacobson and colleagues showed that the kidney senses low oxygen and makes the hormone erythropoietin (EPO) to boost production; cloning the EPO gene in 1985 led to treatments for anaemia in kidney failure — and to doping abuse in sport. The most common cause of anaemia is iron deficiency (iron-deficiency anaemia). In 1926 George Minot and William Murphy treated the once-fatal pernicious anaemia by feeding raw liver; its cause was later found to be vitamin B12 deficiency. Persistent dizziness, breathlessness or pallor warrant a blood test, and whether iron supplements are needed depends on the cause, so consult a doctor.
The first "molecular disease" and gene therapy
In 1949 Linus Pauling and colleagues showed that haemoglobin from sickle-cell patients has different electrical properties, introducing the idea of a "molecular disease" caused by a change in a single protein. A single-base change in the haemoglobin gene makes red cells stiffen into sickles. In 1954 Anthony Allison showed that carrying one copy protects against malaria, explaining through natural selection why the gene is common in parts of Africa. In 2021 a CRISPR therapy that switches fetal haemoglobin back on showed strong results in sickle-cell disease and beta-thalassaemia, and it was approved in 2023. In transfusion, red-cell surface antigens — blood type — must match.
This article is general health information and is not a substitute for diagnosis or treatment. If symptoms persist, see a doctor.
FAQ
- Is a high red blood cell count good?
- Too high can thicken the blood and raise clot risk. Smoking, dehydration, living at altitude or certain diseases can cause it, so discuss out-of-range results with a doctor.
- Why is blood red?
- Because of how iron-containing haem in haemoglobin absorbs light. Oxygenated arterial blood is bright red and deoxygenated venous blood darker red; veins look blue through skin because of light scattering.
Sources reviewed: 2026-10-26
References
- Bohr, C., Hasselbalch, K., & Krogh, A. (1904). Ueber einen in biologischer Beziehung wichtigen Einfluss, den die Kohlensäurespannung des Blutes auf dessen Sauerstoffbindung übt. Skandinavisches Archiv für Physiologie, 16(2), 402–412.
- Minot, G. R., & Murphy, W. P. (1926). Treatment of pernicious anemia by a special diet. JAMA, 87(7), 470–476.
- Pauling, L., Itano, H. A., Singer, S. J., & Wells, I. C. (1949). Sickle cell anemia, a molecular disease. Science, 110(2865), 543–548.
- Allison, A. C. (1954). Protection afforded by sickle-cell trait against subtertian malarial infection. British Medical Journal, 1(4857), 290–294.
- Jacobson, L. O., Goldwasser, E., Fried, W., & Plzak, L. (1957). Role of the kidney in erythropoiesis. Nature, 179(4560), 633–634.
- Perutz, M. F., et al. (1960). Structure of haemoglobin: A three-dimensional Fourier synthesis at 5.5 Å resolution, obtained by X-ray analysis. Nature, 185(4711), 416–422.
- Lin, F.-K., et al. (1985). Cloning and expression of the human erythropoietin gene. PNAS, 82(22), 7580–7584.
- Franco, R. S. (2012). Measurement of red cell lifespan and aging. Transfusion Medicine and Hemotherapy, 39(5), 302–307.
- Frangoul, H., et al. (2021). CRISPR-Cas9 gene editing for sickle cell disease and β-thalassemia. New England Journal of Medicine, 384(3), 252–260.