Answer by Diane Eager
What is Sickle Cell Anaemia?
Anaemia is a decrease in the number of red blood cells, or in the total amount of haemoglobin in the blood. Haemoglobin is the protein in red blood cells that carries oxygen, and anaemic condition results in tiredness and other problems. Sickle cell anaemia is a blood disease which renders blood cells inefficient due to a mutation in a gene for haemoglobin.
Red blood cells are normally round and flexible. In sickle cell anaemia the abnormal haemoglobin distorts the shape of the red blood cells until they become spiked and bent like an old fashioned sickle, and have a tendency to fall apart (a problem known as haemolysis). Sickle cells do not live as long as normal cells and the bone marrow cannot make enough new ones to maintain the blood’s normal number. They also become rigid and stick to the walls of small blood vessels where they cause inflammation and blockages of blood vessels. As a result people who have this disease suffer from chronic pain and tiredness, along with damage to their bones, lungs, brain and kidneys, and are prone to infections and strokes.
Because humans inherit two copies of the haemoglobin genes that is involved in sickle cell anaemia, it is possible to inherit one sickle cell gene and one normal gene. These people are able to make normal haemoglobin as well as sickle cell haemoglobin, and are described as having “sickle cell trait”. They may not experience many problems from sickle cell haemoglobin except in conditions of low oxygen, e.g. at high altitudes. People who inherit two copies of the mutated gene have the full blown life threatening disease that damages body organs and bones, and soon kills them unless they have access to good long term medical treatment.
Sickle Cells and Malaria
Because it is true that people with sickle cell anaemia and sickle cell trait have some resistance to a deadly form of malaria caused by a parasite named Plasmodium falciparum, the claim has been made that sickle cell mutation has an evolutionary survival advantage. A recent study reported in Science vol. 334 pp. 1283-1286, 2 December 2011 DOI: 10.1126/science.1213775 has revealed how this form of malaria resistance works.
Malaria is caused by single-celled parasites that don’t just float around in blood – they take up residence inside red blood cells. Scientists at Heidelberg University in Germany and the Biomedical Research Centre Pietro Annigoni in Ouagadougou, Burkina Faso studied red blood cells infected with Plasmodium falciparum malaria parasites, and compared how they function in normal cells compared to their behaviour in the cells of people who carry one sickle cell gene.
After the parasites invade healthy red blood cell they take a protein named actin and use it to transport another protein, named adhesin, made by the parasite, to the cell surface. Actin normally sits just under the cell membrane and helps keep the cells pliable so they can squeeze through narrow capillaries (microscopic blood vessels) without harming the vessel walls. The parasite uses the actin protein to make “bridges” within the cell to transport the adhesion protein. Once on the surface, the adhesin makes the cells sticky, and causes them to adhere to each other and to the blood vessel walls, causing widespread inflammation of small blood vessels. However, in cells containing mutant haemoglobin, malarial parasites are hindered from using actin to transport the adhesion protein because the sickle cell haemoglobin molecules become unstable, and form a degraded molecule named ferryl haemoglobin, which interferes with the bridge-building process.
So resistance to malaria in people with the sickle cell gene is the result of two different disease processes colliding with each other. In other words, the mutant blood is so bad not even malarial bugs can do well in it.
Sickle cell malarial resistance is never complete, and people can still get infected by malaria, but they are less likely to die from it, and therefore, may live to pass the sickle cell gene onto the next generation. As a result, the gene for sickle cell haemoglobin remains at a relatively high level in the population of those who live in regions infested with malaria. The persistence of sickle cell genes in populations who live in some malaria prone regions combined with its apparent resistance properties are the reason it is claimed to be an example of evolution.
Is it evolution?
Evolution requires the addition of new functional genes that will add new features to a living organism, or changes in genes that improve the function of already existing features, so that a living thing can fit better into its environment. The sickle cell mutation is a change to a human gene that results in a change in the way the body responds to the environment, but it is not evolution. In sickle cell anaemia all that has happed is a fully functional gene that already existed has been damaged by a mutation, and is now a less functional gene. This is degeneration, i.e. the opposite of evolution. Those who benefit from the resistance to malaria can only live to enjoy it because they are able to make some normal haemoglobin to keep their red blood cells functioning. Furthermore, the prevalence of the sickle cells gene in a population also means many children inherit two sickle cell genes, get full blown sickle cell disease and die from sickle cell disease instead of malaria.
The change from a normal gene to a mutant sickle cell gene is not caused by the malaria, so it cannot be called an adaptation. The gene is most common in people in sub-Saharan Africa, the Middle East and India, where malaria is endemic. However, malaria also found in southern USA, Central America, tropical regions of South America, south-east Asia, Melanesia and northern Australia. Yet the gene for sickle cell does not in these places unless people have migrated, or have ancestors, from Africa or India. It is also interesting to note that with increasing migration of human populations the gene has also spread into many areas of the world, including places that do not have malaria, and where it has no “benefit”. In places that have large numbers of people with African or Indian ancestry it causes considerable health problems because the gene continues to be passed on through the generations. It is estimated that approximately 8% of African Americans carry the gene. No evolution is involved here – just normal inheritance.
In summary, human resistance to malaria via the sickle cell gene is not an example of evolution, but an example of what can happen when two different disease processes collide. Both these diseases serve as a reminder that the world is degenerating, i.e. going downhill rather the evolving upwards.
Sickle Cells, Malaria and Creation
Adam and Eve lived in a created world where all creatures ate plants (Genesis 1:30), so mosquitos wouldn’t have bitten people. In fact, mosquitoes still suck plant juices and nectar to give them energy, and male mosquitos live on these exclusively. Female mosquitoes need extra iron and protein to lay their eggs, so when they cannot get enough from plants they look to other easily accessible sources, such as human blood.
Recent research has shown that not all mosquitos transmit malaria. In order to spread the disease the malaria parasites have to move from the mosquito’s gut to their salivary glands. Mosquitos only spread disease when their own immune systems are compromised, and they cannot resist invasion by microbes. Most mosquitos are able to keep the parasites under control, and not let them get beyond their gut. (See Science, vol. 312, p514, 28 April 2006, and our report here)
Malaria is a reminder of the degeneration of the world that began when Adam sinned, and first produced recognizable diseases by the days of Job, not because bugs were evolving, but because man, bugs and the environment have all degenerated. Mutations are often claimed to be a source of new and improved living organisms, but the sickle cell mutation does the opposite – it only results in badly functioning haemoglobin. People with the sickle cell trait, who carry one sickle cell gene only benefit from their increased resistance to malaria because they also have a haemoglobin normal gene to keep their red blood cells functioning, but every one of them would rather have normal haemoglobin genes and normal blood, and be spared the anxiety about passing the sickle cell gene to the next generation. An article from the Institute for Creation Research issues this challenge: “If a Darwinist wants to say that a harmful mutation in the oxygen-carrying capacity of the blood is “good”—they’re welcome to do so. But one has to wonder how many evolutionists would willingly subject themselves to this mutation (if it were possible)—as they prepared to go to a malaria zone.” (Reference: http://www.icr.org/article/905/) Those who have two sickle cell genes get no benefit at all because the sickle cell disease will kill them in the end, usually before they can reproduce.
Overall, sickle cell disease and its interaction with malaria is evidence for an original good creation followed by degeneration, as described in Genesis, rather than evolution from simple to complex life forms.
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