|email - December 2019|
Here is our answer to the evolutionists’ “beneficial mutations” argument about ApoA-1 Milano.
We are grateful to Aiden for sending us this email:
Hi Science Against Evolution. Name is Aiden. Love your website and certainly your responses in debunking evolutionists. Recently though I asked a very simple question to see what answers I could get from evolutionists. “Can any evolutionist give a beneficial mutation that results in brand new genetic information?” is all I asked. Finally an evolutionist gave a response. “ApoA-1 Milano? That’s one beneficial mutation.” And of course the evolutionist had to end his comment with an insult stating “I know very well that you are simply too scared to even google it.” FYI. I did google it.
Anyway, I’m an educated layman not a PhD scientist so understanding this mutation (as in the scientific terms surrounding it) and how this directly relates to information-increasing mutations is difficult for me. Mind explaining it as simple as possible and why this mutation doesn’t support evolution? Thank you!
Our immediate knee-jerk reaction was, “Why is this evolutionist talking about ApoA-1 Milano instead of sickle-cell disease?” As long as I can remember, the sickle-cell argument has been the evolutionists’ go-to argument for beneficial mutations. Since you may have heard the more common sickle-cell argument, let’s address that one first before we address ApoA-1 Milano.
The impact of sickle cell trait on malaria immunity illustrates some evolutionary trade-offs that have occurred because of endemic malaria. Sickle cell trait causes a change in the hemoglobin molecule in the blood. Normally, red blood cells have a very flexible, biconcave shape that allows them to move through narrow capillaries; however, when the modified hemoglobin S molecules are exposed to low amounts of oxygen, or crowd together due to dehydration, they can stick together forming strands that cause the cell to sickle or distort into a curved shape. In these strands the molecule is not as effective in taking or releasing oxygen, and the cell is not flexible enough to circulate freely. In the early stages of malaria, the parasite can cause infected red cells to sickle, and so they are removed from circulation sooner. This reduces the frequency with which malaria parasites complete their life cycle in the cell. Individuals who are homozygous (with two copies of the abnormal hemoglobin beta allele) have sickle-cell anaemia, while those who are heterozygous (with one abnormal allele and one normal allele) experience resistance to malaria without severe anemia. Although the shorter life expectancy for those with the homozygous condition would tend to disfavor the trait's survival, the trait is preserved in malaria-prone regions because of the benefits provided by the heterozygous form. 1
The saying, “It’s an ill wind (that blows no good)” suggests that even when something bad happens, someone else will get an advantage from it. When interest rates go up, it is bad for borrowers—but good for lenders. Although it is bad to suffer from sickle-cell disease, if it keeps you from getting malaria, it might be worth it. That was the evolutionists’ traditional example of beneficial mutations.
People with sickle-cell disease have a shorter life expectancy, so it is hard to argue its benefits. Perhaps evolutionists have moved on to the ApoA-1 Milano argument because the sickle-cell mutation isn’t beneficial enough to be a compelling argument.
The problem evolutionists have with the ApoA-1 Milano argument is that it is complicated. But, consistent with the notion that every negative might be a positive, if the evolutionists’ ApoA-1 Milano argument is too difficult to understand, people might just accept it without question. The disadvantage of being hard to understand might actually be a benefit to evolutionists!
Aiden is not someone who accepts something just because it is hard to understand. That’s why Aiden wrote,
Anyway, I’m an educated layman not a PhD scientist so understanding this mutation (as in the scientific terms surrounding it) and how this directly relates to information-increasing mutations is difficult for me. Mind explaining it as simple as possible and why this mutation doesn’t support evolution?
We will try to explain what this has (or doesn’t have) to do with increasing information as simply as possible.
The ApoA-1 Milano argument has to do with HDL cholesterol.
There are several types of lipoproteins in the blood. In order of increasing density, they are chylomicrons, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Lower protein/lipid ratios make for less dense lipoproteins. Cholesterol within different lipoproteins is identical, although some is carried as its native "free" alcohol form (the cholesterol-OH group facing the water surrounding the particles), while others as fatty acyl esters, known also as cholesterol esters, within the particles. 2
In 2016, the United States Department of Agriculture Dietary Guidelines Advisory Committee recommended that Americans eat as little dietary cholesterol as possible. Increased dietary intake of industrial trans fats is associated with an increased risk in all-cause mortality and cardiovascular diseases. Trans fats have been shown to correlate with reduced levels of HDL and increased levels of LDL. Based on this evidence, along with other claims implicating low HDL and high LDL levels in cardiovascular disease, many health authorities advocate reducing LDL-cholesterol through changes in diet in addition to other lifestyle modifications. 3
Low levels of HDL are “bad,” but higher levels of HDL are “good.” This is why HDL is called “good cholesterol” and LDL is called “bad cholesterol.”
HDL particles are thought to transport cholesterol back to the liver, either for excretion or for other tissues that synthesize hormones, in a process known as reverse cholesterol transport (RCT). Large numbers of HDL particles correlates with better health outcomes, whereas low numbers of HDL particles is associated with atheromatous disease progression in the arteries. 4
ApoA-1 Milano is found in mutated HDL, which does a better job of transporting cholesterol to the liver than normal HDL (even though there is less of it) and reduces heart disease.
Apolipoprotein A-1 Milano (also ETC-216, now MDCO-216) is a naturally occurring mutated variant of the apolipoprotein A1 protein found in human HDL, the lipoprotein particle that carries cholesterol from tissues to the liver and is associated with protection against cardiovascular disease. ApoA1 Milano was first identified by Dr. Cesare Sirtori in Milan, who also demonstrated that its presence significantly reduced cardiovascular disease, even though it caused a reduction in HDL levels and an increase in triglyceride levels. … The mutation was traced to one man, Giovanni Pomarelli, who was born in the village in 1780 and passed it on to his offspring. 5
ApoA-1 Milano is a beneficial mutation with no apparent downsides, which might be why evolutionists prefer it over the sickle-cell argument; but it doesn’t address Aiden’s question.
“Can any evolutionist give a beneficial mutation that results in brand new genetic information?”
ApoA-1 Milano mutated HDL doesn’t contain any more information than ordinary HDL. It doesn’t perform any different function. It just performs the same function better. It is simply a variation, like being stronger or more sexually attractive.
Darwin based his theory upon the observation that not all offspring are identical. There are small differences. That is undeniable. He believed that those differences might provide a survival advantage, and that is probably true—to some extent. It certainly tips the scale a little, which might be significant in some cases. But it isn’t necessarily the slowest gazelle that wanders too close to the lion crouching in the tall grass. Sometimes survival of the fittest isn’t as important as survival of the luckiest.
Even though evolutionists sometimes debate the importance of natural selection, there is some effect, no matter how small it might be. In most cases, a mutation causes a survival disadvantage, and natural selection is the chlorine in the gene pool which removes the mutation in a generation or two. Natural selection tends to prevent evolution more than cause it.
I haven’t noticed it recently, but when I was young, the TV commercials for laundry detergents often claimed to be “new and improved.” Of course, they could not be any better if they weren’t changed—but change doesn’t necessarily result in improvement.
Even if they did really work better, they still did nothing more than remove dirt. They didn’t repair tears in the clothes, or connect your clothes to the Internet so your phone would tell you when they needed to be washed. The detergents didn’t provide any new functionality. They just performed the same function, presumably better, which might have caused consumers to buy it. Getting clothes cleaner might have improved sales more than another brand’s “fresh, clean scent,” or catchy jingle that a competitive detergent’s commercial used.
We are belaboring this point because there is an important distinction between beneficial mutations and creative mutations. Beneficial mutations perform the same function better. Creative mutations (if they existed) would perform new functions. Aiden’s question about increased information has to do with new functionality, not a marginal improvement in existing functionality.
If people bred reindeer the way they breed horses, then larger, or faster, or stronger reindeer might “evolve” over several generations. Size, speed, and strength are existing reindeer characteristics which selective breeding can increase, up to a limit. Santa can’t breed flying reindeer because that would require a creative mutation which increases genetic information.
For a reptile to evolve into a mammal, it has to evolve mammary glands by accident. Reptiles don’t have poor mammary glands which were improved slightly by a mutation to create mammals. They would need new genetic information to evolve functioning breasts.
The ApoA-1 Milano argument depends upon the assumption that the ApoA-1 Milano variant is a new innovation. That isn’t necessarily true.
Every time a DNA molecule gets copied, there is a chance for a mistake. If that mistake is fatal, the organism dies. If it is merely harmful, natural selection will eliminate it in a generation or two. When a mistake is merely suboptimal, natural selection might not be powerful enough to eliminate it. By chance, it might become dominant in the population.
There is a chance that a subsequent mistake might undo the original mistake. Perhaps ApoA-1 Milano was the original version, and the common form of HDL is actually a suboptimal mutation which somehow established itself in the population centuries ago. Perhaps Giovanni Pomarelli was simply a guy who accidentally had a mutation that changed his HDL cholesterol back to the original, uncorrupted form!
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