Editing the Human Genome, Bioethics, and Human Life

It is election time, and that, of course, brings a lot of debate, media articles, and (to be straightforward) distraction from other important issues going on in the world. Now, I am not saying politics is not important, but I am saying that sometimes we can get so caught up in candidates, debates, and primaries that we miss other events going on in our world that have equally profound and far-reaching ramifications for humanity (if not surpassing importance).

Such an event has been largely missed by the popular media, and I would argue that is has the potential to affect the human race in a way that far out-weighs any single election in the United States. It is that the Human Fertilisation and Embryology Authority (HFEA) in the UK has given the Francis Crick Institute the green light to use a gene editing technique called CRISPR to conduct experiments that modify the genome of human embryos.

Yes, you read that correctly: the Francis Crick Institute is going to begin modifying the genome of human embryos with the expressed goal of "understanding the process by which embryos develop... that will help identify causes of miscarriage and infertility." Proponents of the research say that it could help scientists to understand why there is a such a high rate miscarriages, how to eliminate certain diseases, and how to treat infertility more effectively. So, you might ask, "Why is that an issue? Who could be against that?" Well, when we are talking about tampering with the human genome itself, such an endeavor has far-reaching implications that provide quite good reasons to be against it.

I am, of course, not the first person to point this out. In fact, there has been a widespread outcry against these efforts by scientists across the world, calling for a worldwide moratorium on the engineering of the human genome. In an open letter by the Center for Genetics and Society, dozens of scientists across the globe call for such research to be stopped before it does irreparable damage to the human race:

Some suggest that germline modification be allowed for therapeutic purposes but not for “enhancement.”  But the distinction between these applications is subjective and would be difficult or impossible to implement as policy. Permitting germline intervention for any intended purpose would open the door to an era of high-tech consumer eugenics in which affluent parents seek to choose socially preferred qualities for their children. At a time when economic inequality is surging worldwide, heritable genetic modification could inscribe new forms of inequality and discrimination onto the human genome.  

For these reasons, several dozen countries, including most of those with highly developed biotechnology sectors, have explicitly banned human germline modification. The Council of Europe’s binding 1997 Convention on Human Rights and Biomedicine also prohibits it. Numerous opinion surveys show that the great majority of Americans and others worldwide believe that heritable genetic modification should be prohibited. 

While we are encouraged by efforts on the part of scientific bodies to move the process of deliberation about acceptable uses of gene editing forward, we are concerned that much of the focus has been on technical issues of safety (implying that if it were safe it would be acceptable), rather than on broader ethical and social implications. We strongly believe that the National Academies’ initiative and international meeting should be considered a very early step of a broadly inclusive program of public discussion. Any recommendations emerging from the meeting or the initiative should make this clear. 

In sum, there is no justification for, and many arguments against, human germline modification for reproductive purposes. We call for a prohibition on such germline modification and a robust and broadly inclusive discussion on the socially responsible uses of this and other emerging genetic technologies. (Emphasis added...)

Check out the open letter yourself to look at the signatures and who is arguing that this is far too dangerous for the human race to attempt. It is not just me or other Christians (and we will get into my reasons in a moment) but scientists from many religious worldviews across the globe. Here we have a group of scientists who understand that just because we have the technology and ability to do something does not mean we should do it. We must think about the implications of our scientific research and weigh that against what good (if any) it might accomplish. In an imperfect world like ours, there are times when we must not pursue some scientific research because whatever good it might accomplish cannot be justified and is far outweighed by the loss of human life, the destruction of human dignity, the unknown affects on the human race, and the implications for human society.

As I alluded above, many Christians have also discussed the ethics and dangers of such an endeavor. In this article, Church and Culture discusses some of the ethical implications of such research. In this one, Anjeanette "AJ" Roberts of Reasons to Believe discusses the implications the image of God has on such research as well as the unknown effects on humanity that such tampering could have. Both of them are worth reading along with the open letter mentioned above, but I would like to add another ethical implication that I have yet to hear discussed: the ethical implications of the process of this scientific research itself.

In a nutshell, this process of research will "deactivate genes in leftover embryos from IVF clinics to see if it hinders development." Basically, using CRISPR, the scientists will deactivate genes, allow the embryo to develop, and then see what happens--how the deactivation of that gene helps or hinders the overall development of the human embyro. (Currently, the growth process of the embryo will take place in a lab because it is not yet legal to insert a genetically modified embryo in a human host. Not yet, but that is the next step.) They must use this process because at our current level of technology, it is possible to isolate certain genes that affect or contribute to certain diseases, defects, or developmental stages, but it is generally not known how those genes function in the overall development of a human or affect the overall development of our genome (i.e. genetic makeup). Genes are not so isolated that one gene only has one function. How particular genes contribute to the overall gene expression of a being is largely unpredictable. So, just because a research group might know what genes affect certain developmental outcomes, they do not necessarily know how those genes affect the development of the entire genome of the individual. That means this research must proceed by making targeted changes to the genome of an embryo and then seeing whether or not the embryo develops properly with the desired outcome.

Now, think about that process as a whole: they will deactivate genes, allow the human embryo to develop (i.e. grow), and see what happens. What we are talking about here is taking a human life (a human person from conception, as I argue here), modifying its genome, and then seeing if it dies or not, develops healthily or not, develops unforeseen side effects or not, etc. It is akin to taking a baby, cutting off its leg, and then saying, "Now, let's what happens as it grows." This research goes even beyond current embryonic stem cell research (which is also a deplorable destruction of human life) because it doesn't just take cells from an embryo killing it in the process; it modifies the embryo and allows it to live on just to see how the modification affects its life. This is slavery at its worst, the likes of which our world, unfortunately, has seen in the past. Perhaps a few historical examples will help put some perspective on this research.

During WWII, the Nazi's conducted experiments on Jews at many of their concentration camps, but the majority were performed at Auschwitz and Ravensbrueck. If you have not read about these experiments, they are not for the faint of heart. Nazi doctors performed all sorts of horrific experiments on those who were considered "untermensch" ("sub-human") to see what would happen and/or to see if they could develop medical treatments that would be beneficial to German soldiers. And, after WWII, at the International Military Tribunal at Nuremberg, these doctors were tried and convicted of war crimes against humanity. What they did was absolutely deplorable and deserved to be tried as crimes against humanity, but it is not ethically different from what HFEA has just granted the Francis Crick Institute permission to do: experiment on humans to see what will happen and/or try to development medical treatments that will be beneficial for other humans. Just because these humans are less developed physically they the rest of us, just because they do not have a voice to cry out for help, just because they do not have the ability to try to flee the scientists does not mean they are any less human than you or me (cf. the SLED test for more detail on this).

Perhaps one more example from America history will help. Have you ever heard of the Tuskegee syphilis experiment? American physicians studied about 600 black males in Alabama who had syphilis, and they told the men that they were getting "free medical care." What these doctors were really doing was refusing to treat their syphilis so that the doctors could study the progression of untreated syphilis in humans. They let these men suffer and die just to see what would happen--to see how syphilis would progress when untreated. This also was a gross and deplorable misuse of scientific research that cost the lives of hundreds of men, but, again, it is not ethically different from what HFEA has just granted the Francis Crick Institute permission to do.

If the Francis Crick Institute is allowed to continue its research or if others follow suit, then these "left over" human embryos from IVF will become a slave class in our world, kept alive simply for experimentation not unlike what the Nazis did in WWII or what happened in Tuskegee, AL. Yes, the researchers are trying to do good with their experiments, but that does not justify the process. The end does not justify the means--developing treatments for humans by taking human life or, indeed, altering human life and allowing it to develop to see what happens is unacceptable. The end of this research may have profound implications on the human race in the future that we cannot predict, as the above articles and letters show, but even the process of this research itself should be condemned by us.

I hope and pray the outcry of scientists across the globe will bring this research to an end soon, and perhaps this blog post will help in that process. May God have mercy on us for how we treat His images.

By His Grace,
Taylor

Much Ado About Nothing: More Adam and Eve Genetic Discussion

"If we take into account that, again, the difference is calibration, this result is compatible with all the other results that have been generated with regard to the y-chromosome data, and that data, I believe, supports a biblical understanding of human origins. So, I don't see this study as a challenge to our model or a challenge to the previous work that has been done. So, this is 'much ado about nothing,' in my opinion, all due to differences in clock calibration." ~ Dr. Fazale "Fuz" Rana

You may have seen articles like "African-American's Y chromosome sparks shift in evolutionary timetable" or "Don't call him 'Adam': South Carolina man’s genes help date first man" in the popular news in the past few days. These articles discuss some recent research based on the y-chromosome (y-c) of a South Carolina man, which appears to be genetically very different from the y-c's of most other men in the world. The difference of his y-c from the rest of ours pushes the date for modern humans back more than 200,000 years earlier than all previous studies have estimated. At least, that is what the researchers claim in their report on their findings.

Since I have written about the genetic research with regard to Adam and Eve in past articles (here and here) and argued for the historicity of the biblical account, I had planned to get the journal article on which these news articles are based and check out the data myself. However, a scientist whom I greatly respect--Dr. Fazale "Fuz" Rana--and who works for Reasons to Believe has already reviewed the data and reported his take on it in this podcast. I just finished listening to his evaluation of the research, and I think it is sound. I probably could not improve on it, so I recommend you go listen to what he has to say about it (the podcast is about 27 minutes long).

In sum, the crux of the whole issue is how these researchers calibrated their molecular clock analysis. (I have explained how molecular clocks work, and also discussed their failings, here.) They used a different calibration from every other bit genetic research that has ever been done. As a result, their research and date look significantly different from everyone else's. In addition, their date does not match the evidence from the fossil record, which is also a significant strike against them. If they had used the same calibration that everyone else uses, their date would have turned out to be slightly older than all previous research (and the fossil record evidence), but it would have agreed with all previous research within acceptable margins of experimental error. They argue that their calibration is superior, but they have no basis for making that assertion since there is no benchmark against which to measure molecular clock analysis except the fossil record, with which their date does not agree. What they have done is analogous to changing the calibration of your speedometer in your car and then trying to tell a police officer that you were not speeding based on your calibration. Neither he nor a judge is going to accept that your calibration is more reliable without hard, proven evidence. We should not accept this research unless it can show sufficient reason for overturning all previous research and the superiority of their calibration. Listen to Dr. Rana's podcast for a much more detailed explanation. It will be worth your time.

So, as Dr. Rana states above, this is really just "much ado about nothing." Until these researchers can prove with much more data the superiority of their calibration of molecular clocks, they have not overthrown the more generally accepted dates for Adam and Eve. Now, of course, evolutionists will say that those dates do not prove Adam and Eve at all, but I have argued elsewhere that the scientific data can be validly interpreted within a biblical framework that supports the historicity of the Genesis 1-3 account of human origins. No appeal to evolution is necessary to maintain a consistent view of the data, and this result does not change that.

By His Grace,
Taylor

Redefining the Chemistry of Life? Followup

In January 2011, I wrote a blog post on a (media-hyped) discovery of a strain of bacteria that appeared to be using arsenic instead of phosphorus in its biochemistry. In the post, I argued that this organism does not at all "redefine the chemistry of life" or find "arsenic tasty," as the study and media commentary suggested. I concluded that (at best) this organism is a facultative arsenophile, which means it seems that it can use arsenic in its biochemistry when necessary but prefers phosphorus and needs it to thrive.

In the most recent issue of Science (the journal in which the original study was published), two more papers have been published by teams who did independent research on the bacteria in question (GFAJ-1), and their findings refute the contention that GFAJ-1 is using arsenic at all. One shows that there is no evidence for arsenates being incorporated into the bacteria's nucleic acids. The other argues that GFAJ-1 is really an arsenic-resistant bacteria (a possibility I noted in my original post) that still needs phosphates to survive and thrive.

If you want my take on the research, the original post I wrote on the topic is still relevant. My original conclusion, which appears to still be valid, was as follows:

It is not an organism that has a "redefining" biochemistry, it is not an "arsenic-base" organism, it does not find "arsenic tasty"; at best it an extremophile that can possibly make use of arsenic when it is the only thing available in the environment but its preference would be phosphate.

Before I wrap this post up, I want to comment on one more thing that I quoted from Dr. Rana above. It has been suggested that this type of organism could represent an alternate way that life could emerge. Sorry, but this kind of organism does not provide a different possible pathway for life to originate. The reason why Dr. Rana says that, and I agree, is because this type of organism not only has the biochemistry of normal bacteria but has extra mechanisms that allow it to live under the harsh condition of excess arsenic. In short, it is an organism that is significantly more complex than normal bacteria that is based on phosphates alone. Arsenate is unstable, so unless you already have in place mechanisms that could stabilize the arsenates, there is no way life could form with arsenates. Origin of life in an arsenate system (vs. a phosphate system) is a significantly more complex pathway and even more improbable than the existing, phosphate-based origin of life scenarios. The same is true for all extremophiles. In fact, there have been papers written by other biologists arguing this point.

So, after time for further research and peer-review, life is still CHNOPS-based (see the original post for explanation on that) and no other alternate pathway for the origins of life is evidenced by this study. Life is still as delicate and complicated as science has consistently shown and requires an Intelligent Designer for its existence.

By His Grace,
Taylor

Adam and Eve: A Tale of Two Cases

A couple of months ago I wrote a blog post about the historicity of Adam and Eve called "Who Was Adam?". In it I posted an excerpt from a blog of a friend of a friend and my response to her post where I showed that it is not the scientific data that calls into question the historicity of Adam and Eve but an evolutionary interpretation of the data. Since then, my post has been published on The Aquila Report, a Reformed news service, and I have talked about the issue at length with many people. I wanted to follow that post up with some clarification on the issue and further defend the biblical view. When the pertinent data is looked at from the two points (an evolutionary or biblical) of view we get a "tale of two cases".

First, I think we need to clarify a few things when it comes to the use of terms that one might hear thrown around when this issue is talked about. There have been several Christian scientists who deny the historicity of Adam and Eve because they claim that it "would be against all the genomics evidence that we’ve assembled over the last 20 years, so not likely at all..." (Dennis Venema, Trinity Western University) Some have flat out said that, "genetics convincingly shows that there was never a time when there were just two persons." (Darrel Falk and Kathryn Applegate, BioLogos) Francis Collins of the Human Genome Project says, "Adam and Eve as the literal first couple and ancestors of all humans do not fit the evidence." But what do they mean when they say, "genetics convincingly shows" or "against all genomics evidence"? What genetic evidence are they referring to? This is a very important question because a lot is riding on this evidence.

The problem with this generalized claim is that genetic evidence has four components to it. There are four types of DNA that gets lumped into the phrase "genetic evidence" and some of it makes the interpretation of Collins, Venema, et al. very uncertain (we will get to why that is below). The four types of DNA are as follows:

• Autosomal DNA -- This is the DNA that makes up most of your genome and is a random combination of both of your parent's DNA. Since this autosomal DNA (atDNA) is a random combination of your parent's DNA (and their's is a random combination of their parents, ad infinitum) everyone's is completely unique. (This may also be referred to as "nuclear DNA" but that term is less precise.) For a good explanation of this type of DNA see this video.
• Chromosomal DNA Types -- At the genetic level, what determines our sex is our chromosomes. Males have a X and a Y chromosome. Females have two X chromosomes. Each contains DNA: 
• X Chromosomal DNA -- This is the DNA that makes up your X chromosome (X-c) that you get from your mother. It is a random combination of her two X chromosomes, so, like the autosomal DNA, it is unique, though it does not change as quickly as autosomal DNA. For a good explanation of this type of DNA see this video. 
• Y Chromosomal DNA -- This is the DNA that makes up the male Y chromosome (Y-c) and it is only passed from fathers to sons. Since there is only one Y-c, there is no random recombination of genes so the only thing that can cause change in the Y-c is mutation. This means it often not unique and changes very, very slowly. For a good explanation of this type of DNA see this video.
• Mitochondrial DNA -- This final form of DNA comes from the mitochondrial of your cells and it only comes from your mother. Male or female, it does not matter, your mitochondrial DNA (mtDNA) only comes from your mother. So, like the Y-c, there is no recombination of genes so the only thing that can cause change in the mtDNA is mutation. This also means, like the Y-c, it is often not unique and changes very, very slowly. For a good explanation of this type of DNA see this video.

We need to demand specificity from anyone making the claim that "genetic evidence" shows something. What kind of genetic evidence are they referring to? This will become important below.

Another term that gets used by scientists that often confuses people is "human". Now, you might think should be simple but it is not. An evolutionary biologist will use the term "human" to refer to any type of hominid from the homo genus like homo erectus or homo rudolfensis, not just homo sapiens (the taxonomic name for what species you and I are). This confuses the matter because scientists may refer to an ancient "human" fossil, footprint, or gene and they may not be referring to our species at all. This term also gives rise to the phrase "ancient modern human" used to refer to a homo sapien that lived in pre-historic times. This phrase not a contradiction in terms, but a further specification biologists use to refer to homo sapiens--a modern human species that lived long ago. I say this to make sure you aware of what is really being talked about when you read a science article in the popular news. If they say "human" they may not mean the species that you and I belong to and it may require more investigation on your part to figure out what they are really referring to. You can be sure that when I use the term "human" I mean a human like you and me, not any kind of animal that may have walked erect.

Second, we need to clarify that data that is being referred to by these scientists quoted above and that I will refer to below. There are two important types of data that come into play. The first I have already talked about in my previous post on this subject, and it is the mtDNA and Y-c data that shows that the entire human race can be traced back to one single mtDNA sequence for females and one Y-c sequence for males, a single pair of humans. (For a more detailed explanation of this see my first post on the subject.) As I just mentioned above, the mtDNA and Y-c change very slowly because the only mechanism for change is mutation. Therefore, scientist can trace the mutations of DNA take from all types of people throughout the globe back to a single first sequence for males and females. It is the single method of change--mutation--and the slow rate of change that makes this possible. (This would be impossible with atDNA, which is why it is important to know what kind of DNA someone is referring to!) The second type of data looks at the genetic diversity of humanity in the atDNA in humans. This data is drawn from mathematical models and attempts to take the present diversity of human atDNA and calculate how long it would take to get to the present state of diversity. These models have showed that in order for humanity to get to its present state of genetic diversity, it would have to have started out from a small population of humans (on the order of thousands) and not a single pair. These two sets of data appear to be in conflict, which is where our tale of two cases begins.

There are two possible ways of looking at this data. In these two interpretations different types of genetic data are given priority, which, again, is why it is important to know what genetic data someone is referring to when they say, "the genetic evidence says...".

Case #1 -- The Interpretation of Venema, Collins, et al.:
The mathematical modeling from the atDNA is given priority and it is assumed that humanity could not have originated from a single pair. This assumption is then imposed on the data that comes from the mtDNA and the Y-c. The question is then asked, "How could we have one ancient modern human mtDNA sequence and one Y-c sequence for all of us when humanity did not arise from a single pair?" Their answer is the "one lucky mother" hypothesis. They hold that there was originally thousands of mtDNA sequences and Y-c sequences in the first ancient modern humans but somewhere along the way all lines of these types of DNA died off except the one mtDNA and one Y-c that exist today in the present population. These sequences were from the "lucky" man and woman whose DNA was passed on while all other lines of DNA died out.

Case #2 -- The Biblical Interpretation:
In this case, the mtDNA and Y-c evidence is given priority because of the faults in the mathematical modeling and because of highly improbably "one lucky mother" hypothesis. In this case, the model is assumed to be incomplete (see below) and so it cannot be given the weight of mtDNA and Y-c tracking (which, remember, is a much slower process and much easier to trace backward). These ancient sequences are taken to actually point to a single man and single woman who were the progenitors of the entire human race. No special hypothesis is necessary for this interpretation, simply an acknowledgement of the limits of mathematical modeling with atDNA.

So, which of these cases seems more likely? It should be obvious by now that I choose case #2. Why? Well, I would like to expound upon the faults in the mathematical modeling and the "one lucky mother" hypothesis that I mentioned above:

• First, the mathematical models, while sophisticated, do not take into account very important data and therefore the results are unreliable. Remember, with atDNA, there is a random recombination of parental genes so there are many more things coming into play than just mutations--many things which the model leaves out. For one, it assumes that environmental factors do not drive genetic diversity. Environmental factors are things like location, food supply, isolation, diseases, and anything else that can drive a population to change. Recent studies (like this one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1766376/) have shown this this is a dangerous assumption and can greatly skew the data. These models also assume monogamy throughout human history, and we all know that this is not a valid assumption. Now, before you think the scientists are just being sloppy, consider how difficult it would be to include these factors into a model. How many sexual partners do you assume each human has? How do you know what environmental pressures were on an ancient human population for which we have no historical record? You cannot and so these models cannot realistically include these things. However, this just goes to show that their results should be used with great reservation. 
• Second, the "one lucky mother" hypothesis has a critical flaw in it. If one assumes that ancient humanity began with a small population of thousands, then for this hypothesis to work one has to find a catastrophic yet very selective mechanism that will kill off all genetic lines except for one male's and one female's. It must be catastrophic enough to kill off thousands of lines and all their progeny and yet it must also be selective enough to kill off all but one for the females and one for the males. What event or process could be so terrible that it would kill off all genetic lines and yet also so selective that it would leave one and only one genetic line for each sex? Even theorizing about such a mechanism is nearly impossible. 

So, we must choose between case #1 and case #2. Case #1 puts more weight on mathematical models that are incomplete (see above) and must come up with a complicated mechanism for killing of all genetic lines but those of one male and one female. Case #2 acknowledges the issues with mathematical modeling and takes the mtDNA and Y-c data at face value without having to postulate extraordinary events to explain the data. If Ockham's razor means anything at all any more, we must acknowledge that case #2 is likely the correct explanation of the data.

What would keep intelligent men like the ones mentioned above from acknowledging that case #2 is more likely the correct explanation of the data? Presuppositions. We must remember that all of us look at this data with our bias that we bring to the table. I look at the data having faith that what Scripture says is historical and theologically important and therefore I choose case #2. Theistic evolutionists, like the Christians mentioned above, look at the data already believing that evolution is a fact and therefore choose case #1 because it fits that presupposition better. Am I any different from them in this regard? No, I readily admit that my bias influences my decision, but the point is that case #2 is 1) an equally valid interpretation of the data and 2) fits the data well with fewer complications and less reliance on incomplete modeling.

Scripture is my highest priority and I make no apologies for that, but it is also true that the data itself does not go against Scripture. It actually fits quite well with Scripture. This is what we should expect if we truly believe that God is the author of all truth, whether it comes from the infallible authority of Scripture or the scientific realm. For, as Paul says in Romans 11:36, "from Him and through Him and to Him are all things. To Him be glory forever. Amen."

By His Grace,
Taylor

Who Was Adam?

"Collectively, the consensus that emerges from this work indicates that humanity originated recently (about 100,000 years ago) from East Africa (near the location theologians ascribed to the Garden of Eden) from a small population. Amazingly, studies using mitochondrial and Y chromosomal DNA markers trace humanity’s origin back to a single man and woman." ~ Dr. Fazale ("Fuz") Rana, "A Burgoo of Human Origin Discoveries"

Today I responded to a post on the blog of a friend of a friend: Reflections on God's Word. In this post the author, Maria, talks about the move by some Christians, Francis Collins in this case, to dismiss Adam and Eve as historical figures. Dr. Collins, of the Human Genome Project, has looked at the genetic data and concluded that he believes Adam and Eve were not historical. Maria proceeds to flesh out the biblical implications of this in her post and points out why a historical Adam and Eve are important to orthodox Christian doctrine. Here is a portion of what she said:

...Collins has concluded from this study, as reported in a book he recently co-authored (The Language of Science and Faith), that “Adam & Eve as the literal first couple and ancestors of all humans do not fit the evidence”.

This assumption is disturbing on two accounts: First of all, those who support the findings and support theistic evolution minimize the impact of their assertions.  Second and more fraught with potential harm, is the implication for much of Biblical Theology and directly the trustworthiness of the Bible.  I will address the second of these issues.

The author of the “Christianity Today” article, Richard Ostling, correctly articulates what is at stake:

• Humans’ unique status as image bearers of God

• The doctrine of original sin and the fall

• The genealogy of Jesus in Luke 3

• Jesus’ teaching that all of the Old Testament points to Him (Luke 24)

• Paul’s teaching that links the historical Adam with redemption through Christ

This issue is different from the debate among evangelical Christians who argue Old Earth vs. Young Earth.  In that arena, it is clearer that there are at least two possible interpretations.  The Bible refers to days (yowm) spent in creating the world.  In Hebrew ‘yowm/Strongs H3117’ can mean 24 hours, a year or a long period of time.  So the creation account is open to discussion without raising the trustworthiness of the Bible as an issue.

But if there is not a literal and historical Adam, then here are the implications:

• God did NOT decide as a Trinitarian unit to make man in His image, male and female (Gen 1:27)

• God did NOT have a conversation with Adam in Gen 2:16-17

• Eve did NOT talk with Satan as serpent in Gen 3:1-5

• Eve did NOT sin in Gen 3:6

• No sudden guilt, shame and cover-up happened in Gen 3:7

• No face-to-face encounter between God and the first couple took place in Gen 3:8-9

• Adam & Eve did not try to pass the buck, playing the blame game in Gen 3:11-13

• Gospel Hope was not first preached in Gen 3:15

• No penalty for sin was announced in Gen 3:16-19, thereby explaining what is wrong with our world

...

You should go read the rest of her post here. It is a good biblical and philosophical defense of the trustworthiness of God's Word and Adam as a historical figure. Go ahead, go read it and then come back here..........

Now that you are back, I would like to share with you how I responded to her post. I thought it appropriate and necessary to respond from the scientific side of things as well. I wanted Maria, and all her readers, to know that it is Dr. Collins' interpretation of the data that is against a historical Adam, but his interpretation is not the only valid interpretation (as my quote in the beginning points out). Here is what I said:

Great article, I was directed here by a mutual friend–Adam Powers. I do not want to minimize the great points you made above but I also wanted to give a little perspective on Dr. Collins’ statement/opinion. I hope that this will encourage you in that you not only make a good Biblical and philosophical argument but that the scientific data are not against you.

Dr. Collins is truly a Christian, I believe, though I disagree with him about theistic evolution. One thing we must keep in mind with people like Collins who look at the genetic evidence is that they are looking at it with evolutionary presuppositions already in mind.

There are many studies that have emerged recently (like these: http://www.nature.com/nature/journal/v451/n7181/abs/nature06611.html, http://www.sciencemag.org/content/319/5866/1100.abstract, http://www.sciencemag.org/content/277/5323/176.short) that indicate the mitochondrial DNA (mtDNA) of all humans can be traced back to one single sequence on the order of about 100,000 years ago. (We all get our mtDNA from our mothers only so even though I am a male my mtDNA still came from only my mother.) Other work done on the Y chromosome (Y-c) shows that all males can be traced back to a single Y-c (studies like this one: http://www.nature.com/nature/journal/v378/n6555/abs/378379a0.html) on the order of about 60,000 years ago.

Collins looks at this data and, because of his evolutionary presuppositions, thinks that this one sequence was just the “one lucky mother” whose DNA was passed on, while all the other DNA from the first “evolved” females died out. He interprets the Y-c data the same way. However, there is no evidence to favor this interpretation over one that looks at the data and says, “All humanity can be traced back to a single man and a single woman.” The second interpretation is simply much more difficult for Collins to fit into his evolutionary presuppositions, so he chooses the first. It is not the data that demands Christians throw out the idea of a historical Adam, it is Collins’ interpretation of it based on his presuppositions. The data equally support a historical Adam and Eve interpretation.

One might look at the dates and think, “Wait, how could the historical Eve be 100,000 years ago and the historical Adam be 60,000 years ago?” Scientists have asked a similar question. You might hear a geneticist say, “Did Adam know Eve?” and by that he means, “Did the woman who we get our mtDNA from know the man we get our Y-c from?” I think the Bible can easily fit well with this data. For us men, biblically who is the oldest male ancestor we could possibly trace our lineage back to? You might be tempted to say, “Adam” but is that really right? Actually, the oldest male we could possibly trace the Y-c back to is Noah. Why? Because of what is called a “population bottle neck”–the world’s population dropped to 8 people and then started over again. Noah and his three sons all had the same Y-c so there is no way to trace the Y-c beyond Noah farther back to anyone else. However, since it is reasonable to assume that Noah’s wife and his sons' three wives came from four different lineages, geneticists can trace the mtDNA beyond Noah. So, of course the dates would be different. In fact, the Bible (indirectly) predicts that these dates would be different!

Now, I am not trying to start an argument on your blog about the length of creation days (as you said, that can be debated without questioning the trustworthiness of the Bible) or whether or not the biblical genealogies are complete (which I also think can be debated without questioning the trustworthiness of the Bible). What I am trying to do is show that Collins’ interpretation of the data is not the only valid interpretation. It is equally valid, and I think more supportable, to say that human origins can be traced back to one man and one woman–Adam and Eve. So, far from ruling out a historical Adam, the genetic evidence supports it as one of the valid interpretations of the data.

I would like to suggest a book to those who would like to do more research on this topic: Who Was Adam? by Dr. Hugh Ross and Dr. Frazale Rana. It is an excellent resource by two men whose intellect far exceeds my own that dives deep into the scientific data and shows how modern discoveries do not discount and actually support a historical Adam (contra Dr. Collins).

By His Grace,
Taylor

Redefining the Chemistry of Life?

"The way I like to think about this organism is that it's an extremophile. They've discovered a new extremophile... This is an organism that they have discovered that would prefer phosphorus but can make use of arsenic if it is present... Just because life exists under extreme conditions doesn't mean that it is more likely to originate under those conditions than more moderate conditions... Whether... high temperature, high acid, high alkalinity, high salinity, or high radiation environments, all those circumstances... will actually disrupt pre-biotic chemistry needed to generate life and this would be the same situation. Just because it exists under high arsenate conditions does not mean it could originate under those conditions." ~ Dr. Fazale "Fuz" Rana

Last month there were a bunch of headlines floating around touting a discovery made by NASA astrobiology research fellow Felisa Wolfe-Simon ("Fe Lisa" or "Iron Lisa") that she and her team published in Science. A few popular headlines were "Arsenic-eating microbe may redefine chemistry of life", "Microbe Finds Arsenic Tasty; Redefines Life", or (my favorite) "Arsenic-Eating Bacteria Opens New Possibilities for Alien Life". A few of you out there have asked me about this privately and I have given some short answers, but I have wanted to write up a more detailed comment on this work for the last month. Because December was so busy, as I am sure it was for all of you, I have not gotten to it until now. Of course, that might be a good thing because I have now had the chance to read the paper and look at some peer criticism of how this was communicated to the public. But, now that I have a little time, here it goes...

Before we get into the actual paper and discovery, I would like to talk a little about the history of thought in chemistry and biology that led to this research and Dr. Wolfe-Simon's discovery. This is going to get a little bit technical but I will do my best to explain it clearly and it is necessary to talk about this discovery.

Life as we know it has six major elements that are crucial for it: carbon, hydrogen, nitrogen, oxygen, phosphorus, and sulfur. You might see these abbreviated as CHNOPS because they are commonly talked about as a group in reference to life. These particular elements are among the most abundant in the universe and have unique chemical properties that allow them to assemble into complex, stable molecules that can then further aggregate into complex, stable super-systems (DNA and RNA would be examples of these) to create an organism. Most scientists today believe that life must have these elements to exist. There are, however, a few that believe life could possibly be built on an alternative biochemistry. For example, it has been suggested that silicon could replace carbon or, in the case of this discovery, arsenic could replace phosphorus.

Why these particular replacements? Well that has to do with the chemistry of the elements in the Periodic Table (PT). The PT is one of the greatest achievements of science (I say that even though I am a physicist, not a chemist) and one of the reasons I say that is because of its construction. One can look at the PT and get a lot of information about the elements just by the position of those elements in the table. For example, elements in the same column have similar chemical properties. The closer they are, the more similar the chemistry. That is what is important for our purposes here. Take a look at the cutout from the PT on the left. Carbon's chemical symbol is C, silicon's is Si, and silicon is right below carbon in the PT, which shows us that there are chemically similar. Phosphorus' chemical symbol is P, arsenic's chemical symbol is As, and arsenic is right below phosphorus in the PT, which, again, tells us that they too are chemically similar. Some scientists think that the chemistry may be similar enough to represent possibilities for alternate biochemistries other than CHNOPS. Perhaps one could replace Si for C, thus the biochemistry would be SiHNOPS or perhaps As could replace P creating a CHNOAsS biochemistry. It is this kind of thinking that motivated the study.

Before we go further to the pertinent study, a few words need to be said about phosphorus and arsenic since they are the important elements for this particular discovery. In nature phosphorus primarily exists as phosphates (an ion with four oxygen atoms bound to a phosphorus atom). In this form, phosphorus plays an extremely important role in biochemistry. It is crucial to a number of biochemical functions (like regulating protein activity and the formation of the cell membrane) and biomolecules (like DNA, RNA, and metabolites). It has been generally thought that it is phosphorus' unique qualities that allow it to play an integral role in all of these functions but, as described above, arsenic is chemically very similar to phosphorus. Could arsenates (similar to phosphates) serve the above functions?

Arsenic does form into arsenates (an ion with four oxygen atoms bound to an arsenic atom) but they are toxic. Since arsenates are so similar to phosphates, organisms can incorporate them into biomolecules but since they are different from phosphates, the bonds in those biomolecules created with arsenates (instead of phosphates) will become unstable and break down, creating havoc in the metabolic system of the organism. So arsenate is similar enough to phosphate to be allowed into the cell but dissimilar enough that, once incorporated, the cell starts to break down. If this happens on a large enough scale the organism will die. So, life should not be capable of existing in an arsenate system.

This brings us to this discovery by Dr. Wolfe-Simon and her team. First, I would like to say that this is very impressive work. These scientists should be commended for this discovery and they should be proud of themselves for opening up the door to what will probably be years of fascinating research on this organism and others like it. That being said, the discovery as portrayed to the media and the general public is overblown. This newly discovered organism is not an "arsenic-based" organism, it does not find "arsenic tasty", and it is not really as "alien" as it is made out to be.

So, what did they discover? Well, Dr. Wolfe-Simon and her team went to Mono Lake in CA to search for bacteria that use arsenic. They chose Mono Lake because it has an extraordinarily high phosphorus and arsenic content so any bacteria found there would at least have to be able to deal with arsenic. They discovered a strain of bacteria, that they labeled GFAJ-1, which appears to be able to use arsenates and phosphates to grow. They then wanted to see if it could survive only with arsenates. In order to test this, they took GFAJ-1 from the lake (where the environment has high levels of phosphorus and arsenic) into their lab and put it in an environment with no phosphates and lots of arsenates. They did this to try to force the bacteria to use only arsenates, if it could, since phosphates were not available at all. They found that GFAJ-1 did survive and appeared to be incorporating arsenates into its biochemistry. Now, since the bacteria was formed in the lake with phosphorus and arsenic, they have not yet proven that it can completely substitute arsenates for phosphates because the bacteria still had plenty of phosphates to run critical systems. They did, however, show that it appears that at least some of the cells functions were using arsenates instead of phosphates, which was thought to be impossible. Through a process known as fractionation they found evidence that the arsenates were being used by GFAJ-1 in proteins, nucleic acids (DNA and RNA), and metabolites. The bacteria was even able to grow and reproduce under these conditions. Conventional biochemical knowledge says that GFAJ-1 should have died because the arsenates should have destabilized almost its entire metabolic system. With all this data, however, the conclusion that this bacteria appears to be able to do what was thought impossible--incorporate arsenates into its biochemistry, stabilize the arsenates (through a yet-to-be-determined mechanism), and survive--seems plausible (though it is also possible that this bacteria could simply be strongly resistant to arsenates).

Did they show that this life is "alien" or discover something that "redefines" the chemistry of life? No, they did not. Let me explain why. Assuming they are right that GFAJ-1 really is incorporating arsenates into its biochemistry: 

• First, even though the organism was able to survive under the extreme arsenate-rich and phosphate-poor environment, it was far from thriving like it did in Mono Lake where phosphate was readily available. The bacteria grew very slowly, reproduced at a proverbial snail's pace, and had a very distorted growth morphology. What is going on here is not completely clear yet, but these issues in the growth of the bacteria show that it probably has some kind of machinery in place to stabilize arsenates yet would prefer phosphates. So while the bacteria can survive in an arsenate-rich environment, it certainly prefers phosphates and will only thrive with phosphates.
• Second, there has been no long-term experiment done to see how long this bacteria can survive under these conditions. The bacteria began with phosphates since it was taken from Mono Lake. As it reproduced in the lab those phosphates were divided up to run critical systems. It is highly possible, as some critics has suggested, that colony could die off after it has spread its phosphate supply too thin. 
• Third, this finding is not proof that there is any bacteria naturally doing this. It only shows that it this bacteria seems to have a mechanism that allows it to use arsenate when it has to. It could potentially do it naturally (no one is sure how long it can) but this is certainly not proof that there are lifeforms regularly doing this.
• Fourth, the team had to create an arsenic-rich, phosphorus-poor environment. Finding a natural environment like this where biochemistry would have to be completely redefined is highly unlikely. Why? Because phosphorus is much more abundant in our universe than arsenic. In the earth's crust there is 667 times more phosphorus than arsenic. In the rest of our known universe there is 2500 times for phosphorus than arsenic. These abundances show that it is highly improbable that there would ever be a naturally occurring environment anywhere in the universe with all arsenic and no phosphorus that would cause life's chemistry to be redefined in a way similar to GFAJ-1.

What is the bottom-line? If it is not "alien" and does not "redefine" life's chemistry, what kind of organism is it? As I quoted from Dr. Rana above, it is (at best) an extremophile--organisms that can grow and survive under extreme conditions like high temperatures, high acidity, or, in this case, environments with high amounts of toxic arsenates. To get a little more specific, it could be a facultative arsenophile, which means it seems that it can use arsenic when necessary. Organisms are either obligatory or facultative. The former means they require a particular set of conditions to live. The latter means that the organism can make use of something if it is present under extreme conditions but do not prefer it. For example, e. coli is a facultative anaerobe, meaning that it would prefer an environment with oxygen but can, if necessary, survive in an oxygen-poor environment. In this case, GFAJ-1 being a facultative arsenophile means that it seems to make use of arsenic under extreme conditions. It is not an organism that has a "redefining" biochemistry, it is not an "arsenic-base" organism, it does not find "arsenic tasty;" at best it an extremophile that can possibly make use of arsenic when it is the only thing available in the environment but its preference would be phosphate.

Before I wrap this post up, I want to comment on one more thing that I quoted from Dr. Rana above. It has been suggested that this type of organism could represent an alternate way that life could emerge. Sorry, but this kind of organism does not provide a different possible pathway for life to originate. The reason why Dr. Rana says that, and I agree, is because this type of organism not only has the biochemistry of normal bacteria but has extra mechanisms that allow it to live under the harsh condition of excess arsenic. In short, it is an organism that is significantly more complex than normal bacteria that is based on phosphates alone. Arsenate is unstable, so unless you already have in place mechanisms that could stabilize the arsenates, there is no way life could form with arsenates. Origin of life in an arsenate system (vs. a phosphate system) is a significantly more complex pathway and even more improbable than the existing, phosphate-based origin of life scenarios. The same is true for all extremophiles. In fact, there have been papers written by other biologists arguing this point.

So what has Dr. Wolfe-Simon's done? She and her team have done some excellent research and made a fascinating discovery but they have not redefined anything or discovered something alien. What they have done is open the door for much more research in this area. There are still a lot of questions to be answered about this bacteria. Is GFAJ-1 really using the arsenates or just surviving as best it can in such an environment? If so, how are the arsenates stabilized? What do the molecules that incorporate arsenate look like? Could a DNA molecule with arsenate instead of phosphate be made in the lab?

By His Grace,
Taylor

99% Chimp... but also 35% Daffodil?

"In the context of a 35% similarity to a daffodil, the 99.44% of the DNA of human to chimp doesn’t seem so remarkable. After all, humans are obviously a heck of a lot more similar to chimpanzees than to daffodils. More than that, to say that humans are over one-third daffodil is more ludicrous than profound. There are hardly any comparisons you can make to a daffodil in which humans are 33% similar." ~ Dr. Jonathan Marks, What it Means to be 95% Chimpanzee: Apes, People, and their Genes

You have probably heard it before, "Humans are 99% chimp!" The percentage number of genetic similarity reported ranges from 90-99% (the actual number is probably closer to 90% when one takes into account indels--insertions and deletions in the DNA sequences--but that is not really important for our purposes here). This statement is based on work done by Mary-Claire King and A. C. Wilson in 1975. Their work showed several human and chimpanzee proteins display a 99% agreement in amino acid sequence. This indicated that humans and chimpanzees are closer genetic relatives than anyone at that time had thought. Soon popular evolutionary news caught wind of this and the field has never been the same since. It seems like compelling evidence for an Darwinian paradigm. Is it?

Not really, actually. As Dr. Marks states above, we could also say that humans are 35% daffodil based on this method of comparison, which is absurd. Comparisons based on the percent similarity of genetic sequences is basically meaningless. It being meaningless has led others, like Science correspondent Jon Cohen, to write, "Now it’s totally clear that it’s [the 99% genetic similarity] more a hindrance for understanding than a help." Most of the scientific community that supports naturalistic evolution has largely abandoned this comparison since it has no value. Yet, this icon of evolution is still floating around in popular media and text books.

Why does this comparison have little value? Well, let me try to explain it using an example. Assume that you and I each have a box of colored pencils. Each of our boxes contains 100 pencils. When we compare the boxes we find that 99 of our colors are the same and we each have one color the other does not have. If we each start to draw are we going to come up with pictures that are 99% similar? No, of course not. Why? Because the pictures depend not so much on the colored pencils we use but on the way we express ourselves in our drawings, how the colored pencils are used functionally. We may be using the same supplies but we would use them in vastly different ways. Well, genes are like that. Genetic similarity in organisms counts for nothing, it is how the genes are expressed that really matters. Having similar genes means nothing because functionally they operate very differently in different organisms.

Recent work on the FOXP2 gene creates a great example of this. (This is going to get a little technical but I think it is very helpful in illustrating my point above with an important, real-life example.) This gene has gotten a lot of attention lately because of its importance to language capability. This gene codes for a DNA-binding protein, which are proteins used in differential gene regulation--the controlling of activity in genes much like a volume control. They can turn genes "on" or "off" or regulate their activeness anywhere in between. The FOXP2 gene plays this role in humans and other organisms, like chimpanzees.

In humans this gene is critical for language capability. A study done by the Max Plank Institute (published in Nature in 2001) showed that any modification of this gene in humans cripples language capability. It not only disables the ability of the humans to make the sounds necessary for language but it also disables their ability to comprehend language completely. In this study they also looked at the amino acids that make up the protein that this gene produces--the FOXP2 protein--in chimps, mice, and humans. Out of the 715 amino acids that make up the protein in chimps, mice, and humans, the mouse and human protein differed by only three amino acids and the chimp human protein differed by only two amino acids (that is about a 0.3% difference).

In a recent paper also published in Nature, a team of scientists from several universities reported on an analysis they did of how this difference in the FOXP2 gene for humans and chimps affected biological development. In order to study the effect they culture two sets of neurons that had the FOXP2 gene removed from them. (They did this so they could have the same starting point for each gene they were studying.) In one set they introduced the human FOXP2 gene and in another set they introduced the chimp FOXP2 gene. They then observed how the neurons were affected by the different genes. What they found was profound. In the set of neurons with the human gene there were 60 other genes that were up-regulated (more active) by this protein compared to the chimp neurons and there were 50 other genes that were down-regulated (less active) by this protein compared to the chimp neurons. So, the introduction of one human gene that is 99.7% similar to the chimp version of the gene had a profound affect on 110 other genes in development! A two-out-of-715 amino acid difference had significant biological consequences.

This study illustrates how a 90-99% genetic similarity between humans and chimps really means nothing. Even if one were to grant that the similarity is 99% (as I briefly mentioned above, the number is closer to 90%), that 1% genetic difference has profound implications when it comes to gene expression in each species. Gene similarity is meaningless. Gene expression is what is important.

By His Grace,
Taylor

Synthetic Life and the Delicateness of Life

"It shows you how accurate it has to be, one letter out of a million..." ~ Dr. Craig Venter

Many of you heard about the very impressive step that Craig Venter and his team at the J. Craig Venter Institute have made in the quest to create artificial life. It was in the headlines about two months ago. If you did not hear about it, just do a Google search for "A step to artificial life: Manmade DNA powers cell" and a good number of results from many different news agencies will come up. I have wanted to write about this incredible scientific advance for a while but have not been able to find the time until now.

The above statement by Dr. Venter, I think, has great implications for the design debate going on in the scientific community (though he probably did not mean for it to). I will get into that, but first I would like to summarize what he and his team did because it is very impressive work that should be applauded for it has almost limitless potential for possible agricultural, commercial, biomedical, and environmental applications.

First things first: what did Venter and his team do? They truly have created a cell completely powered by synthetic DNA and it was an achievement he and his team have been working on for the past fifteen years. What did they do? For the details one would have to have read the paper that was published in the journal Science, so allow me to break it down for you as best I can.

Let me start with a basic overview. In this research they were working with two different kinds of bacteria, Mycoplasma mycoides (M. mycoides) and Mycoplasma capricolum (M. capricolum). They chose these bacteria because of their relatively small genome size (about one million genetic letters which is about 1,000 genes) and the rapid growth rate of M. capricolum (less time wasted growing bacteria). First, they sequenced the entire genome of M. mycoides. A genome consists of many DNA molecules and the DNA molecules are a collection of genetic letters (abbreviated A, G, C, and T), which hold the genetic information about the organism. Sequencing a genome means determining the order of all the genetic letters, thus creating the "blueprint" for the organism. Second, they synthesized/created a synthetic version of the M. mycoides genome starting with the four basic chemicals of DNA (corresponding to the genetic letters). Third, they implanted the synthetic M. mycoides genome into a M. capricolum bacterium. That genome replaced the host's native genome and took over the operation of the bacterium, essentially changing the M. capricolum bacterium into a (synthetic) M. mycoides bacterium.

Even though I only described three major steps, the process is not simple at all. Allow me elaborate on some of the difficult points.

• Sequencing the entire genome of M. mycoides, even a small genome like this one, is very difficult. They had to take the genome and fragment it (separate it into chunks) and then take each fragment and further fragment them until the whole genome was broken down into its individual letters. (A recent advance in graphene could potentially speed up this process considerably.)
• Synthesizing the genome is even more difficult. They essentially did the above process in reverse. They created small fragments (about 1,000 genetic letters) of the genome, took those fragments and put them together to make larger fragments, then took those larger fragments, and so forth until they had a complete genome. To do this they needed a very good strategy. They looked at the entire sequence (all one million letters), determined the best points to break it up into 1,000-letter fragments, made sure the fragments overlapped slightly (so they could piece them together), and then started creating the fragments and assembling them. To assemble the fragments they used yeast as a kind of "factory" to combine sets of ten 1,000-letter fragments into fragments of 10,000 genetic letters, then combine those 10,000-letter fragments into 100,000-letter fragments, and then, finally, combine those into the one million-letter genome. (Using the yeast as a "factory" is far more complicated than what I just explained because they had to incorporate DNA sequences that caused the yeast to recognize the DNA as its own and they had to do this without altering the M. mycoides genome. They also had to introduce DNA sequences to allow them to do quality control checks after every step to make sure each stage was executed without error.) This is an incredibly ingenious, complicated, and delicate strategy for synthesizing DNA sequences.
• Their strategy for implanting the synthetic genome into a M. capricolum bacterium was equally ingenious and difficult. One of the big hurdles were enzymes known as restriction endonucleases (RE). These are enzymes found in bacteria and archaea that serve as a defense mechanism against the introduction foreign DNA into the cells of the organism (which is exactly what Venter's team was trying to do). These enzymes cleave to specific locations of the DNA helix and cut the DNA at those locations, destroying the foreign DNA. One might then ask, "What about the natural DNA in the host organism? Why is it not destroyed?" Well, natural DNA has a protection system against the RE called the methylase system. This system "methylates" the host's natural DNA by adding a modification enzyme to the RE cleavage sites, which protects it from the RE. In order to get around this, Venter's team developed a strain of M. capricolum with the RE disabled, thus making the M. capricolum susceptible to the (foreign) M. mycoides genome they needed to implant. Then, after implanting it, the synthetic M. mycoides genome produced its own RE that destroyed the host's M. capricolum genome, thus allowing the M. mycoides genome to take over the operation of the M. capricolum bacterium completely. This transformed the M. capricolum bacterium into a synthetic M. mycoides bacterium, which was able to grow into a whole colony of synthetic bacteria.

Even if you got lost in the above explanation, you probably are beginning to realize now how incredibly complicated and difficult this scientific advance was. It took dozens of scientists fifteen years to be able to get this far and there were many setbacks along the way. One setback, the one Venter was commenting on in the above quote, was the result of a mutation (a "typo") that altered one genetic letter out of the million-letter genome. This typo set them back several weeks and completely disabled their synthetic M. capricolum bacterium. The mutation of one genetic letter out of a million caused the organism to be unable to operate and die.

What does mean for the design debate (I mentioned this in the very beginning of this post)? 

1. This advancement shows how complicated and delicate life is and that the work of an incredibly intelligent mind (or a team of incredibly intelligent minds, in this case) is required in order for life to originate. It has shown empirically that to transform life (representing the evolutionary process) or to create life from scratch (representing the origins of life process) requires the intervention of an intelligent agent (if one genetic letter is wrong, as mentioned above, the whole genome is useless). Work like this does not eliminate a need for God; quite the opposite, for it demonstrates how precarious life is and that God is required for life. 
2. This work also demonstrates life's minimum complexity and shows that, even in its lowest possible state, life is extremely complex (far more complex than any naturalistic evolutionary model can account for). 
3. This work creates a completely new category of arguments for design in the universe. The already existing categories of arguments made by scientists that support design are the following: 1) inference to the best explanation, which basically looks at all the models that could account for life and seeks to show that the naturalistic evolutionary models are inferior in their explanation of the facts and 2) argument from design, which basically looks at the apparent design in the universe, notes the similarities to independent human designs, and then argues by analogy that life must be designed. This work introduces a third form of argumentation, which argues that we know now from empirical experience that the making of life requires intelligent ingenuity.

From my Christian point of view this work is very exciting not only because is it just really cool science, not only because it opens up science to a not-too-far-off world of possible applications (bacteria that can create hydrogen for clean fuel, bacteria that can create cheap pharmaceuticals, or even bacteria that can consume oil), but also because it shows in a compelling way, I think, that life requires a Mind--Intelligent Designer--to exist and cannot be the result of random, natural processes. 

By His Grace,

Taylor

Measuring Time From DNA

"As we develop better molecular methods, people would like it if the molecular dates reconciled with the fossil record. Then everybody would be happy, but instead the gap is getting wider, and in the end, that might actually be interesting." ~ Michael Donoghue

Michael Donoghue endorsed a paper titled "An uncorrelated relaxed-clock analysis suggests an earlier origin for flowering plants" about the origins of angiosperms (flowering plants) that was recently published in the Proceedings of the National Academy of Sciences by a team of researchers from Yale University and The National Evolutionary Synthesis Center. In this paper the researchers talk a lot about a technique known as "molecular clock analysis." This technique is a way that evolutionary biologists attempt to understand the relationships between organisms and the time frames where the organisms (presuming an evolutionary model) diverged from each other on the evolutionary track. Evolutionary biologists will compare DNA sequences from organism that exist today, use that information to attempt to build evolutionary trees, and then use molecular clocks to determine when the organisms diverged from each other on the evolutionary tree.

Let me attempt to explain how molecular clocks work. DNA has genetic "letters," which are abbreviated A, G, C, and T. The linear sequence of these letters contains genetic information (much like a word in language contains information because of its definition). The letters build genetic "words," which harbor the genetic information of the DNA molecule. Mutations can alter the sequence of genetic "letters" (much like a misspelling in a word) and molecular clock analysis attempts to measure the rate of these "misspellings" from mutations. If you compare two different DNA sequences which come from organisms that (presuming an evolutionary model) have a common ancestor and you know the rate of change/mutation of the DNA then you can extrapolate the time frame in which the organisms diverged from each other.

The problem with molecular clock analysis is that you have to make assumptions about the rate of change/mutation of the genetic "letters" in the DNA. Evolutionary biologists will attempt to calibrate the rate of change in the clock by going to the fossil record, looking at when certain organisms appeared in the record (organisms that are assumed to be evolutionary relatives), and then correlating the lapses in time with the changes in DNA to create a rate. They then take this calibrated rate and apply it to the entire evolutionary tree they have built to attempt to determine when organisms may have diverged from each other. The problems with this are: 1) it is notoriously difficult to do and 2) the results achieved by the analysis most often do not agree with what is seen in the fossil record. These researchers (from the teams mentioned above) attempt to get around these problems by varying the rate of mutation over time. They "relaxed" the clock. They vary the rate (often times by a lot and with rates too rapid for an evolutionary model) in order to get molecular clock analysis to match up with the fossil record.

Often times molecular clocks are used as a very important tools in molecular biology and cited as evidence for evolution. I like Donoghue's quote above because he seems to recognize the inconsistency in using molecular clocks to validate evolution. The fact that the "gap is getting wider" is "interesting" because it then either invalidates naturalistic evolution or invalidates the molecular clock method itself. This study shows us how flawed this technique actually is. It shows that there is generally no agreement between molecular clocks and the fossil record and that in order to get agreement researchers are rigging their inputs (relaxing the clock) until they get something that agrees with the fossil record. I am sorry, but this is not the way to do science. You can say that the rates may change over time (as rates often do) but you cannot just assume whatever rate(s) you want in order to get the results you are looking for. You have to have criteria that justifies 1) differing rates over time and 2) the specific rates you are using. What justifies using these different rates? For a scientist to do this they must have objective reasons for doing it. Playing with the data until you get the results you were looking for is not a reason. This hurts the case for molecular clocks being support for evolution. If you play with the data until you get the results you want (for the naturalistic evolution model) you cannot then turn around and say it is evidence for the evolutionary paradigm and this study highlights that particular problem. This paper shows that either molecular clock analysis (as it stands right now) is very flawed, the naturalistic evolution models are flawed, or both.

By His Grace,
Taylor