Nutritional Anemia in history

The term nutritional anemia refers to a decreased concentration of hemoglobin or a decreased number of red blood cells in the blood that results from the lack of a substance obtained and replenished by ingestion of food stuffs.

Iron, vitamin B12 and folic acid are the primarily requirements for hemoglobin formation. An early study on the composition of blood was conducted by Robert Boyle in 1864.

Vincenzo Mengini a chemist and physician in Italy, demonstrated in 1747 that particles of dried, powdered blood were attracted to a lodestone, suggesting the existence of iron in blood.

The relationship among hookworm infection, iron deficiency and poor growth an cognition in children were describe in the 19th century and early part of the 20th century.

In 1824, James Scarth Combe described a pernicious anemia, a fatal nutritional anemia and suggested it could be related to a disorder of the digestive tract.

The understanding toward the etiology of pernicious anemia did not come until 1926 when George Minot and William Murphy, physician from Boston found that lightly cooked liver, which the prominent hematologist G. H Whipple had found to accelerate the regeneration of blood in dogs made anemic by exsanguinations, was highly effective as therapy for the disease.

Whipple, Minot and Murphy received the Nobel Prize in Physiology or Medicine in 1934 for their discovery that liver treated pernicious anemia.
Nutritional Anemia in history

History of iron deficiency anemia

The Papyrus Ebers, and Egyptian manual of therapeutics from 1500 BC, describes a disease characterized by pallor, dyspnea and edema that may have been iron deficiency anemia. This ancient disease possibly was due to chronic hookworm infestation.

In 1554, a disorder called chlorosis – derived from the Greek word for green, was first described; this was probably a type of iron deficiency anemia. It was describe by 16th and 17th century physicians as a disorder most prevalent in adolescent girl who has inadequate dietary intake of iron and high requirement for iron due to increased loss from menses.

In 1825, the red coloring matter of blood was reported to have an iron content of 0.35% a value very close to that calculated by modern methods. About the same time, anemia was recognized as being due to low levels of iron in the blood and as reduction in the number of red cells.

In the late 1920s and early 1930s another form of iron deficiency anemia was recognized, ‘chronic hypochromic’ anemia.

Iron is incorporated into a large number of cellular proteins. Many are involved in enzyme catalysis and electron transport, whereas others are involved in carrying oxygen or storing and transporting iron itself.

It may also result from inadequate dietary iron intake, malabsorption, blood loss or rarely intravascular hemolysis with hemoglobinuria.

The clinical manifestations of chronic iron deficiency anemia include fatigue, anorexia, headache, lassitude, tachycardia, neurologic disorders, pallor of the skin and mucosae and koilonychia.

The value of dietary iron has been known for centuries It is said that Persian physician Melampus in 4000 BC gave iron supplements to sailors who led in battle.

Other account of iron as therapy date to ancient Egypt and Rome. Hippocrates, used iron to cure chlorosis. Iron continued to be used to treat various illness during the following centuries, but without any real understanding of its function.

The role of iron became apparent in the 17th century when iron therapy was used as a ‘cure’ for chlorosis, or ‘green sickness’, in France. Thomas Sydenham, recognized as the father do English medicine, recommended iron or steel fillings, steeped in cold Rhine wine.

There were a studies at that time that the presence of iron in blood and that blood iron levels could be increased by the feeding of iron-rich foods.
History of iron deficiency anemia

Short History of Sickle Cell Anemia

Sickle cell anemia is a blood disease. The genetic basis of sickle cell anemia is central to the history of medical genetics.

No one knows exactly when sickle cell anemia was first reported. Ancient people did not now the cause of sickle cell anemia. However, they saw children suffering from painful disease.

Sickle cell anemia is more common in Africa than on any other continent.

The existence of sickle anemia has long been suspected in ancient Egypt among mummies with severe anemia. DNA was extracted form dental samples (of Egyptian Predynastic mummies 3200 BC), indicating the presence of sickle cell anemia.

The first account of sickle cell disease in Western medical literature is attributed to James Herrick, a prominent American cardiologist from Chicago.

In 1910 he observed sickle shape red cells in the blood of a dental student, Clement Noel a 20 years old from Grenada who suffered from chronic hemolytic anemia.

The student complaint was complex: shortness of breath, dizziness, headaches, leg ulcers, severe stomach pain and anemia. Dr. Herrick had never seen a case like it before.

The red blood cells in the blood sample were obviously abnormal. Instead of their ordinary disk-like shape, they were distorted into long, sickle shaped structure.

In 1940s. scientists labeled sickle cell anemia as the first ‘molecular disease’.

The researchers learned more details about sickle cell anemia and how to it distorted red blood cell but cure failed to appear. By early 1970s, sickle cell anemia was called “the neglected diseases.”

In 1947 James V. Neel, scientist from University of Rochester, concluded that with respect to the mode of inheritance sickle cell anemia was a homozygous state and sickle cell trait the heterozygous state for a genetic character that had yet to be define.

Linus Pauling proposed that sickling reflected an abnormality of the hemoglobin molecule, based on the observation of Irving Sherman, then a medical student, that under the polarizing microscope sickle cells, induced by deoxygenation, exhibited birefringence.
Short History of Sickle Cell Anemia