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Evolution? The Sickle Cell Engima

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The new AITSE newsletter is now available, with interesting entries on “probiotics, evolution, depression, placebos, heroes, self-publishing and a treatment for cancer.” The section on depression is a must-read if you know anyone who suffers it.

For example, “even though 14% of the people taking antidepressants take more than one type, less than half of them have seen a mental health professional in the last year.” Bad news that, because Eeyore himself is not a useful source of information about whether things are going wrong. To him, they always are. But sometimes, they really are, which is why he needs independent monitoring. Meanwhile, …

Evolution?  The Sickle Cell Enigma

In 1954 Dr. Anthony Allison published that people who have one gene for a mutated form of hemoglobin are protected from gettingmalaria, a disease that kills a millionpeople every year. Therefore, this change in the DNA, which leads to sickle cell trait, has been touted as a positive mutation, particularly for people who live in areas where malaria is endemic. It is thought that this beneficial effect is why 40% of Africans and 10% of African Americans have a defective hemoglobin gene. Of course, children born to those individuals, otherwise known as sickle cell carriers, have a one in four chance of having two genes coding for the disease. This means that they will suffer from full blown sickle cell anemia, which is an extremely debilitating disease that decreases average life expectancy to 45 years of age. The mutation somehow renders red blood cells “sticky” so they clog up the blood vessels, leading to pain, breathlessness, fever, stroke, and organ failure. Seems to be a no win situation. If a person has the mutation, they are protected from malaria, but they also run the risk of having offspring who will suffer from a painful and ultimately deadly disease.

A recent article in the Nature magazine reports that researchers have now discovered how the hemoglobin mutation prevents malaria. A bit of cell biology is necessary at this point–please refer to the diagram above, which illustrates one method whereby cells transport their products from the place where they are manufactured (ER) and refined (Golgi) to the cell surface. Basically, the cell builds bridges made of actin, puts the product in a vesicle, and moves the vesicle to the cell surface, where it is released in response to a signal. A simple analogy is a country. Products for export are manufactured and refined inside the country. They may then be loaded into railway cars and trains; the boxcars run along railway tracks to the borders using diesel as fuel. Of course, completion of the export process may require other communication.

So, how does this apply to malaria and sickle cell trait? Apparently, the usual course of infective action is that the parasite will enter a red blood cell and cause it to build a bridge (made out of actin) to transport a sticky substance or protein to the surface of the cells. But, in people with sickle cell trait, the mutant hemoglobin prevents the building of the bridge, so that the vesicles that normally carry the protein to the cell surface float freely within the cell. They never get to the surface. The product is not exported because the railway lines could not be built; there was a pile of rubble in the way. This prevents the red blood cells from becoming sticky and clogging the vessels. Thus, sickle cell carriers are resistant to malaria.

Some would assert that this is an example of evolution in action. After all, the organism has mutated to increase fitness for its particular environment. But, does being a sickle cell carrier, which can be symptomatic in some circumstances and gives a 25% chance of having sick offspring, really increase fitness? And why, in the many, many years that man has been plagued by the malarial parasite, have we not evolved a type of resistance that does not cause illness or has the parasite not evolved a way to overcome these mutations? For an excellent analysis of these and other questions, read The Edge of Evolution by Dr. Michael Behe who, by the way, compared positive mutations to blowing up bridges way back in 2007. Almost prophetic!

5 Replies to “Evolution? The Sickle Cell Engima

  1. 1
    thud says:

    This is sometimes known as the evolutionary arms race. Why haven’t lions evolved to consume everything on the African savannahs? Because their prey have evolved to run faster and live in groups. Why haven’t the lions since starved to death? Because they evolved to run even faster and hunt in teams. And so on, such that they coexist in an equilibrium.

  2. 2
    ScottAndrews2 says:

    This is sometimes known as a post-hoc explanation. Why did prey animals evolve to avoid being entirely wiped out? They didn’t have to. Having all the gazelles wiped out and the remaining lions resort to cannibalism would have been a possibility. How incredibly convenient that the gazelles evolved just enough and the lions did too.

    By the way, when did that equilibrium come about? Are lions and gazelles still getting faster? They don’t seem to have made peace, so is the arms race over? Why did it end? Or if it’s still on, what are the current developments.

    Stories like these sounds great until you scratch for the surface and look for the actual evolution. Exactly what gene varied? What effect did it have? Why was it selected? What happened next? The evolutionary narrative is missing just one thing – evolution.

    I read another case of this lately and it made me laugh.

    Paterson said the discovery showed that anomalocaris had lived in well-lit, clear waters and had developed sophisticated vision extremely rapidly, likely triggering an evolutionary “arms race” among other creatures.
    Spines, poison glands and other defence mechanisms had probably erupted among creatures eager to escape detection by its huge eyes, which protruded from the side of its head on stalks.

    Eager to escape detection, they erupted poison glands and spines. (What does that have to do with escaping detection?) Who cares. They needed spines and poisonous glands, so they just, you know, erupted. Isn’t evolution amazing?

    Paterson is a researcher with the University of New England. I asked earlier whether he speaks for those who understand evolution or whether they would disavow him. No one answered. We’re constantly reminded that we’re IDiots because countless thousands of biologists understand what we don’t. I just want to know if he’s one of them.

  3. 3
    Joe says:

    Why haven’t lions evolved to consume everything on the African savannahs?

    Because they can’t.

    Why haven’t the lions since starved to death?

    Because they are well-designed hunters.

    Next….

  4. 4
    Kurt_Barlow says:

    Joe,

    Because they are well-designed hunters.

    That’s an interesting point, but it does lead me to ask a follow up question.

    If, as we know, 99% of all species that have existed are in fact extinct does that mean that those extinct species were not themselves well designed?

  5. 5
    Jon Garvey says:

    Interesting point. We actually estimate rather than know that 99% of species have gone extinct, on the assumption of evolution. The data of the fossil record, so far, gives us about 250K extinct and maybe 5m current species, which makes 5% extinct. Suggests good design. But believing the fossil record to be incomplete, we can only say that between 5 and 99% of species have become extinct, which doesn’t allow for much theorising at all.

    Of those extinct species we know, most seem to have succumbed to mass extinctions, so we can say they were not well-adapted, or designed, to be hit by asteroids or global freezing.

    Then again, if we assume that today’s species are all descendants of those of the past, one way of viewing it is that they were apparently very well designed to change over time. Nobody says the Model T was badly designed because you can’t order one any more.

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