I recently had a lengthy twitter debate with a pair of evolutionists. In the course of that debate, I challenged the evolutionists to produce a beneficial mutation. This article is about one of the answers they produced. The evolutionists insisted that the mutated protein ApoA-1 Milano is an example of a beneficial mutation. This article will examine the protein and what it does, and attempt to answer if it is beneficial or not.
The mutated ApoA-1 Milano protein comes from the apolipoprotein A-1, which is found in humans high-density lipoproteins. A high-density lipoprotein is the good form of human cholesterol. The mutation substitutes a cystine for arginine at a known location on the DNA strand. Unlike most mutations, this substitution still produces readable code. The mutation has the effect of reducing the risk of cardiovascular disease in its carriers. This is in spite of it decreasing the level of good cholesterol and increasing the level of triglycerides, both of which have the effect of increasing heart disease risk. Evolutionists have seized upon this to claim that this is a beneficial mutation.
Interestingly, once the ApoA-1 Milano protein had been identified, major pharmaceutical companies attempted to take it and make cardiovascular drugs. After billions of dollars of research, all attempts, to this point at least, have failed. This has led some researchers to speculate that the original data out of Italy, where the mutation was identified, was either falsified or doctored. Others have speculated that we simply do not know enough how the human body works to make the ApoA-1 Milano mutation successful as a drug. I’m inclined to the latter view. However, that does not mean that the ApoA-1 Milano protein mutation is beneficial. Let us examine what the mutation does.
The ApoA-1 Milano protein mutation changes the protein structure by changing a single nucleotide. This results in a decrease in HDL levels. HDL stands for High-Density Lipoproteins. HDL is otherwise known as cholesterol. There are two types of cholesterol in the human body, with LDL (Low-Density Lipoproteins) being the second type. HDL is good cholesterol. Its role is to take the LDLs, which are the bad cholesterols, to the liver. The liver will then remove them from the bloodstream. By lowering HDL levels, the ApoA-1 Milano protein permits levels of LDLs to increase. Potential consequences of this include gallstones, chest pain, and stroke. Strokes are frequently debilitating and can be fatal. However, this is not the only thing that the ApoA-1 Milano protein mutation can cause.
The mutation that creates the ApoA-1 Milano protein not only lowers levels of High Density Lipoproteins, it increases levels of triglycerides. A triglyceride is the main component of human and animal body fat. They are key components of some types of LDLs. Further, like cholesterol, elevated triglyceride levels can lead to a build-up of plaque in the arteries and veins, a condition referred to as atherosclerosis. This condition is negative. Elevated triglyceride levels also increase stroke risk.
With all that in mind, is the ApoA-1 Milano protein an example of a beneficial mutation? The answer is that it depends. The mutation itself is something of a net neutral. It decreases risk of heart disease, such as atherosclerosis, which is a significant positive. However, it also increases risk of other bad things happening to the body, such as gallstones and strokes. It is a balancing act, part positive, part negative. There is a benefit to having this mutation, but there is also a downside as well. Calling it beneficial seems to be a bit of a stretch, if not simply false.
The ApoA-1 Milano protein mutation, while it carries some benefits, also carries some drawbacks to go along with them. Calling it beneficial merely illustrates how desperate evolutionists are to find evidence to support their theory. They are willing to completely overlook the increased risk of stroke those with this mutation have, in order to trumpet it as evidence for their theory. Such intellectual dishonesty is born of a combination of the knowledge that their theory has no foundation and desperation to avoid the alternative, which is a special creation of an all-knowing Creator. Even if it were to be illustrated that the ApoA-1 Milano protein was completely beneficial, which is unlikely at best, evolutionists need billions of other beneficial mutations to have occurred in order to get from molecules to man. For their theory, this is simply a bridge too far.