Y-Adam, mito-Eve and all that

Our regular commenter pngarrison let me know he has just posted a piece on his own blog, explaining the actual genetic situation regarding those often confused concepts of Y-chromosome “Adam”, mitochondrial “Eve”, population bottlenecks and so on. His training is in biochemistry, but with good of experience in genetics too.

I think it’s the clearest explanation I’ve read that actually gives some of the meaty scientific details, so I’d recommend it even to those non-biologists amongst us who find the concepts opaque. You should end up with a better grasp by the end.

The article also ends with some useful reflections on the theological significance, or non-significance, of these findings to the biblical account of Adam and Eve, in a way that (unlike some treatments) doesn’t simply shrug off the existence of Adam and say “Genetics can’t lie.” YECs may not be persuaded, but it gives the rest of us plenty to consider.

You should find the piece here.

Jon Garvey

About Jon Garvey

Training in medicine (which was my career), social psychology and theology. Interests in most things, but especially the science-faith interface. The rest of my time, though, is spent writing, playing and recording music.
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6 Responses to Y-Adam, mito-Eve and all that

  1. GD GD says:

    I guess my previous remarks may be mistakenly taken to mean that I am stridently opposed to ideas derived from Darwinian evolutionary thinking, such as common descent. Perhaps I may contribute to a fruitful exchange by commenting on this article by png. I have read it out of interest on science and faith, and do not offer an opinion as a professional scientist, and again I restate my main interest in these discussions is to better understand the harmony between faith and science.

    Png makes a clear and easy to understand presentation of the topic. The first point that I noted was a description of a mechanism that I assume forms the basis for the idea of the sequences that are used in determining ancestry. I do not claim any expertise here and I have looked at one paper (that I recall) recently that provided details of such mechanisms, and I was impressed (perhaps astonished) at the elegance and reproducibility of what was discussed. Inevitably I asked myself, how can this be caused by random processes? I understand this question is mundane, but when one considers the basis for Darwin is random variations, due to various changes (often termed mutations), it is extremely difficult to reconcile the elegance and precision of this mechanism with random aspects that so profoundly determine the changes leading to different species. I am not suggesting another mechanism should be postulated – my point is what I simply state – can we link randomness as the basis for Darwin, with such mechanistic observations? As to a law of natural selection in this context – I shall allow my silence to speak for itself.

    The second point was that the aspects of variations in the human race and related matters were initially drawn from data obtained from living human beings. This is the strongest (and imo the most important) item in this paper/blog by png. It is also noteworthy that the past is obtained from archaeological data and I assume remains that may be found dating back to 10’s of thousand years. I also think data that may go back to 40,000 years may be rationalised in this way, and this model appears to provide similar insights to the Monte Carlo model I have referred to previously. However going back further leaves me feeling less confident – and the data used to argue for 100’s of million years and species seems far less convincing – and I would regard this to be speculation (as I have defined the term previously).

    And finally to a common ancestor (which I think is the main point). From my reading of some papers, and thinking about Darwin’s tree of life, I cannot see how anyone can get past the ‘trunk’ of that tree, or what is termed the Universal Common Ancestor. My sense of humour kicks in here – I propose the theory of ‘the grand blob’, which was formed by ancient virus, fungi, bacterial and the half-replicating things, which conspired to form the mighty blob, which somehow existed long enough, not only to produce many other blobs, but also remained, or formed itself, into the truck from which all other species sprang. And as for the many branches derived from the ‘grand blob’ – well I think I have said enough.

    I hope no one takes offense at this lighter treatment of the subject, but it does raise a serious question, just how would such an event fit in with any theory, be it Darwinian or otherwise. One answer is that it does not, but many would speculate that it may somehow – but then, so what!

    My hope is this post will be the last from me on matters such as common descent – I cannot see any theologically significant item would be found, let alone identify areas for controversy and heat, from these matters. Nor would I advocate other approaches to research into these areas – however we need to understand when and why speculation takes place in science.

  2. Jon Garvey Jon Garvey says:

    GD

    Your discussion goes well beyond the purpose (as I see it) of png’s article, though that’s certainly fine by me in the broad context of The Hump. As I see it, his overall aims are (a) to explain the current wisdom on early human populations fairly simply and (b) to show that the data doesn’t seem to sit well with a single original couple in recent millennia as the sole biological progenitors of the whole human race.

    Let me extrapolate from there a little to the more general questions of evolution from the viewpoint of the solidity of our epistemological foundations.

    The genetic data from both current population and ancient DNA is strongly suggestive of a tree structure over time, hence giving weight to the out of Africa hypothesis.

    The details of that hypothesis, to an extent, depend on a model of predictable rates of mutation, which might well turn out to be in error, which could significantly impact the date of these events and the postulated size of any population bottleneck.

    This could alter the science, but as pngarrison discusses, shouldn’t alter the theology. Suppose, for example, new models showed the possibility of a single originating couple for Homo sapiens say a million years ago. There would, in fact, be good biblical and archaeological reasons for such a couple not being Adam and Eve: wrong time, wrong place, wrong culture, wrong genalogies, wrong likelihood of story being preserved that long.

    So if one’s theology allows for some process of transformation of species or evolution, these things are of interest but not necessarily of theological importance.

    As for natural selection, as I understand it the variations used for plotting these changes over time are useful because they are considered not to be particularly subject to selection. If, in fact, they are, that’s one possible source of significant error… but again, affects no theological issues.

    And so we’re back to randomness which, we agree, is a key issue in the big evolutionary picture, in relationship to God’s oversight. But randomness is an assumption, not data. With reference to the subject of png’s piece, I guess changes to mito-DNA or the Y-chromosome are treated as random in the sense that it is their lack of evident purpose and their clock-like character that form the useful model.

    But just as the changing frequency of letters in a language might be used as some kind of clock, there is nothing to suggest that the changes are meaningless. Frivolously, God might well keep nucleotides ticking over at a steady rate to give us a clock … or more likely, there are better reasons that don’t concern us at all.

    The Grand Blob theory sounds a winner to me: the estimated time of LUCA actually gives us a bottleneck at which the rampant horizontal gene transfer that led to the blob finally slowed and evolution as we know it started. Somewhere in the world the Blob may exist as a fossil, but like all those transitional species it’s more likely to have perished. You know it makes sense.

  3. Hanan says:

    I think you would all really enjoy reading this piece. I shared it once on BioLogos, but here it is again.

    http://drmsh.com/2012/07/26/genesis-13-face-compatible-genome-research/

  4. Jon Garvey Jon Garvey says:

    Hi Hanan

    Thanks for the link. Much of what Heiser says is, I think, what the text says (and, in common with others including Walton and even many in the past) was what it was always intended to say. That is that the narratives of Genesis 1-2.4 and 2-3 tell different stories with different purposes, and that Adam is a specific individual within the human race.

    My main difference with Heiser is that I see the archetypal nature of Adam (and hence the interpretation of Romans 5) as more fundamental than he does – I don’t believe than sin was inevitable for all humans in this world, and that Adam did introduce transgression and death (cf specific biblical meaning of “death” in this post). But one can dispute the theology within a general biblical framwork that, in my view (and I suspect png’s too, not to put words in his mouth) needs to be understood on its own terms, and not by favourable or unfavourable comparisons to the agenda and findings of contemporary science.

  5. pngarrison says:

    On selection in regards to the Y and mtDNA, there doesn’t appear to be much selection on the vast majority of variants on the Y. Variants in the few genes can decrease male fertility, and there appear to be some unidentified variants that predispose to heart disease or prostate cancer in rare families. If these occurred at a post-reproductive age, they wouldn’t affect selection. Genealogy people talk about specific Y sub-haplogroups that seem to have higher or lower mutation rates, but there’s no scientific work confirming that, and I suspect they’re just seeing the tails of the bell curve which tends to get our attention.

    A much larger fraction of the mtDNA is occupied by genes (9 in humans) and regulatory sequences, and as a consequence variants are much more likely to experience selection, most often negative, but occasionally positive. There are a large number of mtDNA variants that cause diseases of varying severity, and some haplogroups seem to have increased energy metabolism. H is the most common mtDNA major haplogroup in Europe, and it has been reported that Hg H mitochondria give higher values than some other haplogroups in test tube measurements of energy metabolism. Of course Europeans have been reproductively quite successful in the last few thousand years – I think it is an open question whether mitochondrial gene variants contributed anything to that. Mitochondrial metabolism cuts both ways – the mitochondrion generates most of the ATP, but that metabolism also produces superoxide and hydrogen peroxide as side products that cause damage to DNA, proteins and other molecules, and mitochondria are integral to one of the main pathways of programmed cell death and thus to cancer responses to a cell becoming cancerous. Our somatic mtDNA accumulates copies with substantial deletions as we age, and that may be one of the factors in normal aging.

    There have been attempts to adjust the estimated mutation rate of mtDNA for the effects of selection, although I haven’t looked at them carefully. I would expect that it would adjust the observed rate up some, to account for the fact that lineages with mutations that have a large functional inhibition would be lost quickly so we wouldn’t observe them.

  6. pngarrison says:

    My memory failed me. There are 14 protein coding genes and 24 RNA coding genes on human mtDNA.

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