Out of the three billion or so base pairs that make up human DNA, there is a single gene with a big job.
This gene codes for hemoglobin, the protein in red blood cells responsible for carrying oxygen to every cell in the body. Just one change, just one mutation at a single point in the gene results in a defective version of hemoglobin.
Healthy red blood cells have a characteristic biconcave shape, perfect for squeezing into the tiniest of blood vessels to deliver the oxygen payload carried by hemoglobin.
Defective hemoglobin changes the shape of a red blood cell. Instead of smooth and biconcave, the cells are hard and sticky and are C-shaped, like a crescent or sickle.
We have two copies of every gene – one from mom, one from dad. If one copy of the hemoglobin gene is operational, enough functioning red blood cells are made to keep a person healthy. A carrier of a defective hemoglobin gene may never know it or may only have occasional problems.
British physician Anthony Allison grew up in the Rift Valley of Kenya. Allison returned to Africa in the 1950s with the intent of studying the A-B-O blood groups in East African people, but he changed course when he observed a curious phenomenon.
Almost forty percent of the population in equatorial Africa were carriers of the defective hemoglobin gene, and most carriers were clustered in warm coastal areas.
Allison knew that the warm, wet areas of Kenya were breeding grounds for the mosquito that carries the deadly malaria parasite.
Was there a connection between carriers of the defective hemoglobin gene and malaria? Allyson wanted to know.
Thousands of blood samples and a massive study later, Allison had his answer: carriers of the defective form of hemoglobin are resistant to malaria.
Carriers produce just enough defective hemoglobin to make their blood cells inhospitable to the malaria parasite. The parasites have a hard time entering sickled cells.
To advocates of the intelligent design version of creationism, human DNA bears the mark of design. “Intelligent design” says that random mutations only break things. Important mutations, mutations that confer benefit, cannot arise randomly and therefore must have been directed, micromanaged by an intelligent designer.
Mosquitos kill, but a mutation in one gene confers malaria resistance. A good thing, right? A dandy design! With a tweak at just the right spot in the DNA, the designer heroically saves lives.
Not so fast.
It is not a surprise that a gene that provides malaria resistance would take off in a population. But with a high frequency of a single gene, it won’t be long before two carriers have children. If both parents are carriers, chances are ONE IN FOUR that a child will inherit not one, but TWO copies of the defective hemoglobin gene.
Children who inherit two copies of the gene are resistant to malaria, yes, but at a terrific cost: sickle cell disease.
In sickle cell disease, red blood cells stick and clump together and block blood vessels. The result is excruciating pain and often stroke. Sickled cells are short-lived, so sufferers are anemic, exhausted, and prone to serious infections and kidney failure.
Before modern medicine, children with sickle cell disease usually died in early childhood. Many still do.
The malaria resistance afforded to those with one copy of the gene fuels its spread.
Crediting the malaria-resistance mutation to a loving choice by an intelligent designer demands consideration of the other side of the coin: the 300,000 children born each year with sickle-cell disease.
Janet K. Ray 