A-I Milano mutation—evidence for evolution?
Published: 3 February 2006 (GMT+10)
21 February 2003
This week’s selected feedback from J.R. is about another claimed beneficial mutation, since many people have an idea that this would disprove creation. Despite the rule against URLs in feedbacks, in this case it was unavoidable, and we thought that Dr Don Batten’s Biblical and scientific perspective would be helpful. Once again, the key is that evolution requires information-increasing mutations, while even the rare beneficial ones do not help evolution because they are losses of information. J.R. responded to the original answer with appreciation, showing that Dr Batten’s explanation was helpful in clearing up this common misunderstanding.
I really hope [your ministry] does an article or report on this. So far, I haven’t found a creationist group that will report anything on this complex. Seeing as how [CMI] reported on the fruit fly issue, with the evolutionists claiming this A-I Milano complex as vastly more important evidence than the fruit fly stuff, I hope to see a [CMI] report soon.
Here are two URLs:
Site #1)The Milano Mutation: A Rare Protein Mutation Offers New Hope for Heart Disease Patients1
Site #2)‘Defective’ but beneficial gene may bring about novel ways to clear arterial plaque buildup2
I have checked these, and they work as of Feb 04, 2003.
Thanks for the good communication.
It would appear that the questioner is under the mistaken impression that beneficial mutations are a problem for creationists. Some creationists make this unfortunate error. The mutations Q&A section of our Web site clearly teaches that the issue is not whether the mutation is beneficial but if it adds new genetic information (specified complexity). So it would have been clear that the A-I Milano mutation is not evidence for microbe-to-man evolution.
What has happened? One amino acid has been replaced with a cysteine residue in a protein that normally assembles high density lipoproteins (HDLs), which are involved in removing ‘bad’ cholesterol from arteries. The mutant form of the protein is less effective at what it is supposed to do, but it does act as an antioxidant, which seems to prevent atherosclerosis (hardening of arteries). In fact, because of the added -SH on the cysteine, 70% of the proteins manufactured bind together in pairs (called dimers), restricting their usefulness. The 30% remaining do the job as an antioxidant. Because the protein is cleverly designed to target ‘hot spots’ in arteries and this targeting is preserved in the mutant form, the antioxidant activity is delivered to the same sites as the cholesterol-transporting HDLs. In other words, specificity of the antioxidant activity (for lipids) does not lie with the mutation itself, but with the protein structure, which already existed, in which the mutation occurred. The specificity already existed in the wild-type A-I protein before the mutation occurred.
Now in gaining an anti-oxidant activity, the protein has lost a lot of activity for making HDLs. So the mutant protein has sacrificed specificity. Since antioxidant activity is not a very specific activity (a great variety of simple chemicals will act as antioxidants), it would seem that the result of this mutation has been a net loss of specificity, or, in other words, information. This is exactly as we would expect with a random change.
Note that quantifying the amount of information is not as easy as just counting the number of functions or even the number of base pairs (‘letters’) in a gene. This is simplistic reasoning. It is firstly, but not only, a question of specificity. For example, if I said, ‘Fix the Porsche,’ this conveys more information than ‘Fix the automobile,’ although the latter has more letters. If I said, ‘Fix the car and the truck,’ we now have two ‘functions’ in this sentence, but does it contain more information than ‘Fix the Porsche’? We are now comparing a command with two ‘functions,’ but both of low specificity, with a command with one function and high specificity. In this case deciding which has the most information is not simple. This illustrates the importance of context and purpose (teleology). For example, if there were only one car to fix, a Porsche, ‘Fix the automobile’ would carry as much information as ‘Fix the Porsche.’ But if there were dozens of possible cars or trucks to fix, ‘Fix the Porsche’ would contain much more useful information than ‘Fix the car and truck.’ Dr Werner Gitt explores these issues in detail in his incisive In the Beginning Was Information.
For more information on defining information mathematically, see How is information content measured? (somewhat technical). However, mathematical definitions of information only work in certain contexts (e.g. substrate specificity of enzymes).
It would also be useful to study the article Is antibiotic resistance really due to increase in information? and the explanations about information content accompanied by Dr Lee Spetner’ graphs of the activity of the enzyme ribitol dehydrogenase. The Milano mutation seems to parallel the mutant enzyme, with a lower peak and broader spectrum, i.e. towards lower specificity hence lower information.
Of course it remains to be seen if this mutation is completely beneficial. The fact that the persons with it are unable to produce normal levels of HDLs, which are known to perform a valuable role in moving ‘bad’ cholesterol, suggests that there could be a health down side to this mutation (as there is with sickle-cell anemia).
Apparently this mutation has only been seen in heterozygotes. That is, all those who have the mutation have a normal gene pairing the mutant gene. The homozygous state (both genes the same) could be lethal. This would then parallel sickle-cell anemia, which evolutionists often put up as an example of evolution in action. Here the heterozygote has an advantage, but the homozygote is lethal. This cannot be an example of upward evolutionary progression since the mutant form can never take over the population; it will always be limited to a small percentage of individuals in the population.
However, with the A-I Milano mutation, there are not yet many people with the mutation, so the chances of two people with the mutation marrying and having children so that a homozygote could be produced (1 in 4 of the children) would be very low—it probably has not happened yet. The ‘jury remains out’ on whether a homozygote would be viable.3
Needless to say, if someone follows a healthy lifestyle, eats the right things (something like the food pyramid as recently revised by Harvard Medical School, although this could be improved further), exercises, maintains a healthy weight and does not abuse their body by smoking, the A-I Milano mutation will likely be of no use. Epidemiological studies show that heart disease can probably be avoided.
For the original paper, see: Bielicki, J.K., Oda, M.N., Apolipoprotein A-I (Milano) and apolipoprotein A-I(Paris) exhibit an antioxidant activity distinct from that of wild-type apolipoprotein A-I, Biochemistry 41(6):2089-96, 2002.
References and Note
- <www.science.doe.gov/Science_News/feature_articles_2002/May/Milano_Mutation/Milano%20Mutation.htm> [Return to text.]
- <www.eurekalert.org/pub_releases/2000-02/CMC-bbgm-1502100.php> [Return to text.]
- Mice have been created by genetic engineering to have a human A-I Milano mutant allele paired with a mouse gene that has been inactivated. Such mice appear to be viable, which suggests that a homozygote human could be viable. See Guido Franceschini, G. et al., Increased cholesterol efflux potential of sera from ApoA-IMilano carriers and transgenic mice, Arteriosclerosis, Thrombosis, and Vascular Biology 19:1257–1262, 1999. [Return to text.]