Mendelian inheritance and evolution. Part II

The modern evolutionary synthesis reconciled what Mendel had showed about the discrete nature of inheritance (or so it was thought), and what Darwin had insisted on was the major gradual, more or less continuous, nature of the variation in traits and their evolution.

A lot of things contributed to this reconciliation.  Many experiments, largely stimulated by the 1900 rediscovery of Mendel's 1866 work, began to find mutations that were not grotesque, but had small effects, and were perfectly viable for the organism.  Big bad mutations did still arise and had been obvious and easy to see, but now the majority of mutations seemed to be of the lesser type.

Quantitative traits like stature varied gradually rather than by discrete jumps (such as between yellow and green peas).  Darwin's distant cousin Francis Galton had shown formally what had been obvious, that even for quantitative traits relatives resembled each other--indeed, they did so more than they might for traits with strong dominance (yellow peas did not resemble their green-pea ancestors in that trait).  A variety of investigators, most notably the statistical geneticist RA Fisher (in 1918) recognized how the two types of inheritance could be brought under the same umbrella.  If complex or quantitative traits were caused by the effects of many different genes, each making a small contribution, then the resemblance among relatives, the quantitative variation, and Mendelian inheritance were all consistent.

If that was so, then Darwinian gradual evolution was possible even with Mendelian inheritance as the basic fact of life.  That's what the modern synthesis showed.  It seemed wholly legitimate, indeed perhaps strikingly insightful, and it became the core theory of biology (and in many eyes, we think somewhat erroneously in ways similar to the adherence to Mendelism as the ground-state of inheritance, it still is).  The formal theory of evolution or, to many, of life was the mathematical theory called population genetics.  Well, Isaac Newton said something to the effect that if it can't be expressed mathematically it can't be a law of Nature, so we needed something real, not soft for biology!

It is strange for a central theory in a serious science to say nothing whatever about actual traits of the entities--organisms--that it purports to explain, but that's what population genetics does.  It says only that variation is comprised of discrete Mendelian (that is, discretely transmitted) units of inheritance ('genes' has been the word for them), and that by chance and mainly by the systematic force of natural selection, changes in the frequency of genetic variants were responsible for variation among organisms and among species.  Surprisingly, this theory became accepted even before there was any real theory of what a 'gene' is!  That means it was such a blanket view, so mathematically rigorous, that it could be universally applied to entities that hadn't even been discovered.  Reconciling this theory with actual traits has only come in recent decades under rubrics like EvoDevo (the evolution of development).  Our book, Mermaid's Tale, deals with these issues extensively, and we try to show that there has been far too much stress in biology that rested on the Competition-among-clearcut-units-is-almost-everything worldview of the modern synthesis.

The dogma became that Mendelism and Darwinism are compatible.

But in a real sense, we think, this is fundamentally wrong.  The modern synthesis essentially was possible only because Mendelian inheritance was itself wrong!

Wicked smart apes

I tried to hate it. I really did.

But despite all the Hollywood violence; despite its (inadvertent but dangerous) glorification of the life of a pet chimp and of having one; despite the digital movements that weren’t always quite right… I still enjoyed Rise of the Planet of the Apes.

[If you’re worried about spoilers, (A) Don’t read the title of the movie, and (B) Don’t read any further until you’ve seen it. But to be honest, I'm not sure I reveal anything that wasn't already revealed in the trailers.]

I can't control how apologetic I feel for liking this flick so much. As a human I care deeply what other humans think of me and my movie tastes. And in a weird way I care what chimps, bonobos, gorillas and orangutans would think of me liking it. I guess I shouldn't apologize for being human and I can't easily stop being such a dork.

Perhaps it was the near-future sci-fi possibility of it. Perhaps it was all the sneaky little throwbacks to the original flick. Perhaps it was the attempt to tackle issues of personal bias, emotions, and capitalistic greed in the world of science. Perhaps it was the way James Franco wore that little white lab coat. Perhaps it was my adoration of apes overpowering the fact that these were mere digitized computer actor-humans. Perhaps it was the triumph of the apes! Perhaps it was impossible to go anywhere but up from my subterranean expectations. Perhaps I’m just a human and we humans love our big loud, manipulative blockbuster movies, especially ones that ask, “What does it mean to be human?”

The shows were all sold out on Sunday in West Warwick, so I’m betting most of my students will see this movie—if not this summer, then soon. And I’m sure to be fielding the questions they’re bound to have after watching it. You may have to field the same ones.

I may even use the movie as a teaching tool to help with topics like gene therapy, virus biology and therapeutic use, non-human disease models and test subjects, transgenic lab animals, and inheritance.

Although I’ve worked with custom-engineered virus vectors to modify and to shut down specified protein synthesis in epithelial cells, my experience stops there. And to help me try to make sense of this movie, I asked Ken and Anne to answer some questions that movie goers are bound to wonder.

Ken and Anne: Fire away.

Holly: In the movie Rise of the Planet of the Apes, a scientist invents a possible treatment for Alzheimer’s that regenerates neurons and they test it on chimpanzees in a fantastic lab (and the scientist also administers it to his father at home). The delivery system for the treatment is a virus vector injected into the bloodstream (for humans) or administered through a gas mask (for the lab chimps) that changes known genes associated with Alzheimer’s in humans (not chimps!). When a chimpanzee (who does not have Alzheimer's) is infected with the virus she becomes significantly more intelligent.

1. How does one test a cure for a human disease in non-affected non-humans?

Ken: We've not seen the movie but here are some guesses at your questions. In principle (far from practice at the moment), one could get such a vector into a person that could target the particular gene in cells, and replace it with a gene the vector carries. (If this were incorporated in the germ line of the mother or father, it would be passed on to their kids as part of their genome.) Testing simply would be taking a DNA sample (any cells--blood, cheek swab, etc) and looking for the sequence of the inserted gene. This is what is done to make transgenic mice (but the gene is inserted into an egg, not breathed in by an adult).

Anne: There are 2 things that normally would need to be tested in developing gene therapy; the system for delivering the genetic modification, and the efficacy of that modification. In principle they could/should be tested separately, so the delivery system would be tested on normal subjects before the efficacy of the cure is tested, so that, if it doesn't work, the researcher knows it's not because of the delivery system. Testing of many pharmaceutical products is done in similar stages -- first determine whether it's safe on normal people, then whether it actually cures. The first stage is often done on 'professional guinea pigs', people who make their living volunteering to test drug safety. But you're right, it's not the cure that's being tested on people without the disease, it's the efficacy or safety of the procedure.

2. The Alzheimer's (AD) cure not only heals neural degeneration (as evident in the human test case), but it improves cognition too and when both humans and normal chimps are infected their intelligence increases literally over night. Could that be possible? How?

Ken: It could (in principle) fix damaged neurons in the patient (this is at the moment largely fantasy but by now there may be some precedents--we're not up to date on what claims may be being made.) If the person's inherited genes that led to AD also led to poor cognition, and if changing the gene once their brain is developed could goose up the neurons' activities, then this, too, could occur in principle. Suppose for example that the problem were a neurotransmitter receptor that was somehow not very efficient, and this were replaced so that signals traveled between synapses more rapidly. Again this is all 'suppose' at present!

Anne: If intelligence is due to synapse speed, say, one could imagine that could be upgraded quickly. It's harder to imagine that the biochemistry underlying chimp intelligence is the same as that that causes dementia, and that therefore they'd have the same fix!

3. Also—and this is the real question I’m interested in discussing especially considering the recent Mendel-Wasn’t-Right theme here on the MT!—A female chimp who has been infected actually passes the positive genetic affects onto her offspring. They even remark how her son is intelligent because it's "in his genes." How could this be possible?

Ken & Anne: In the same way as related to #1 above, the offspring would inherit the faster-firing receptor gene and would be smarter.

All of this assumes that one gene change would work across genomic background variation, with no side effects, and all that. But the dream of real gene therapy has been to do what you're describing (again, we didn't see the movie). A good example would be replacing sickle cell hemoglobin (the beta globin gene) with a normal version, or replacing the mutant Tay Sachs or Cystic Fibrosis gene with normal sequences. But to be inherited it has to involve the germ line cells.

There are some known mechanisms that illustrate how such a dream scenario could be plausible. Cells have receptors that bring what binds to them into the cell (usually, this is for some normal cell response to the environment). A virus could be engineered to be taken into some specific cell, like a neuron, in this way. The virus could be designed so that genes it carries are made into RNA corresponding to the 'good' gene version, along with code for a protein like reverse transcriptase that turns RNA into DNA and inserts it into chromosomes could be used. The latter is how viruses currently incorporate into DNA and cause trouble; our genomes are littered with such inserted elements. The difference is that they insert only occasionally and even then into random places in the genome, or places of their choosing.

To get this into places of our choosing, we would have to engineer the system to recognize some sequence of the target gene area and insert the virus's passenger gene at that place, excising the current (bad) gene there.

In any cell in which this occurred, the transgene would have replaced the normal gene, and the job would be done for that cell. If in a sperm or egg precursor, then that would be transmitted to (half of) the person's offspring.

There are versions of each of these transgenic techniques already in practice, but in every case there are limits relative to the desired outcome, and they mainly work in mice that have already been prepared for the experiment by manipulating mouse egg cells. We use such transgenic mice in our own work here on craniofacially relevant genes.

There used to be a lot of hope for such gene therapy, but failures have led many if not most companies to give up the effort. Mostly what is still being tried (I think) is and has always been to administer something to a patient and change his or her genes, or insert a compensatory gene, in affected cells. Injections of such things into muscle to alleviate muscular dystrophy, or by inhaler to alleviate CF, or to fix immune system problems have been tried and probably some at least are still under test.

That still leaves movie goers wondering how someone, like Caesar-the-chimp’s mother in the movie, could contract a virus orally or through the bloodstream which somehow finds its way to the eggs or sperm and then inserts its DNA into those cells and modifies them. That’s the only way the modified DNA sequence could be inherited by future generations, like Caesar, but it's not outside the realm of plausibility. Just think of the evolutionary possibilities!

Arsenic bacteria on trial

The arsenic bacteria story has taken a new turn.  First, Wolfe-Simon et al. published a paper in Science in December of last year, accompanied by much hoopla, reporting that they'd grown bacteria in a low phosphorus environment, and that the bacteria were able to incorporate arsenic in place of the missing phosphorus in their DNA.  The research was funded by NASA, so much of the hoopla had to do with these results proving that extraterrestrial life was possible.

We, as many others, blogged about the story at the time, and a few times since, including here.  We were skeptical, but not nearly as skeptical or vociferous as many other critics.  And we were skeptical not about the biochemistry, though it seems we should have been -- our excuse is that it's not our field -- but about whether the results, if true, meant what was being claimed they meant about evolution.  We thought not. 

We didn't follow all the online discussion, and there was a lot of it, but perhaps the most meticulous critic was Rosie Redfield, a microbiologist at the University of British Columbia.  Almost immediately upon publication of the Wolfe-Simon paper she went into much detail on her blog about what was missing, not controlled for, or misinterpreted by Wolfe-Simon et al., and she and Wolfe-Simon had a back and forth, also on her blog, addressing some of Redfield's questions.  The basic issues were that there was enough phosphorus in the growth medium, even if limited, to allow bacteria to grow, and that Wolfe-Simon et al. hadn't conclusively demonstrated that arsenic in fact had been incorporated into the bacterial DNA, much less that life could exist on it alone.  Redfield also questioned the purity of Wolfe-Simon's samples.

In May, Science published eight technical comments about the original paper, to which the original authors responded.  Redfield was one of those eight.  Wolfe-Simon offered to send samples of her GFAJ-1 bacteria to anyone who wanted to test her results, and Redfield said she might be interested. 

And she was.  She is now replicating the original experiments, but correcting the numerous errors she pointed out in her critiques.  And, she's blogging her experience and her results as they come.  So far, she has grown the bacteria in a phosphorus-deficient medium, without added arsenic, and found that they do grow, albeit slowly, apparently contradicting Wolfe-Simon et al.  She has confirmed through sequencing that she's working with the same GFAJ-1 bacteria as in the original experiment.  Her next step is to add arsenic to the growth medium and see if that improves growth. 

Replicating -- or not -- results such as these is important practice, especially when the rigor of the original experiments is so widely questioned.  This is out of our technical area, but seems to show the positive side of scientific confirmation, a core part of scientific epistemology, at its best.

Unfortunately, this kind of replication is often impossible in genetics or evolution, because we can't replicate others' samples or see evolution at work over millions of past years.  Even new samples, on evolutionary grounds, cannot be assumed to be 'replicates' of other samples, because of the amount of genetic variation, environmental effects, and so on, that is inevitably involved.  So the fact that the arsenic experiment can be redone so elegantly is a thing of beauty -- and envy, to geneticists. 

Of course, even if Redfield demonstrates to most people's satisfaction that her bacteria do not incorporate arsenic into their DNA, that doesn't show that it couldn't happen.  Nor that it hasn't happened (see our original post on this issue with respect to what it might mean if it had, as reported in 1980).  Nor even, in principle at least, that it couldn't happen.  Those are biochemical issues.  The important issue in the context of the original spacey claims is that evolution works with what is at hand.  Whether something can occur under earthly conditions, using bacteria that have 4 billion years of ancestry on this Earth and its environments, has absolutely no bearing on whether it might have occurred on some other planet.

More to the point, it has no bearing whatever on whether 'life' much less 'intelligent life' exists on other planets.  NASA is pulling the wool over your eyes if you don't see that.   We've posted on the life-in-space issue a couple of months ago.

So let's keep the issues separated.  Can earth-like life, after 4 billion years, survive without phosphorous?  Was the arsenic-life report reliable?  Is there life elsewhere, and if so, what might it be like?

Mendelian Inheritance and evolution. Part I

We recently discussed problems with the idea of Mendelian inheritance, and the way that assuming that was a mode of trait inheritance has been so misleading and, we think for that reason incorrect.  (Here's the first of the five posts in that series.)  We'd now like to consider some of the implications of our point of view, when it comes to evolution.  We think this in fact reinforces that point of view, as we'll try to show.

Some traits do seem clearly to 'segregate' (be distributed) among family members in a present or absent mode, associated with a single allele (variant) at a gene, and if one allele is more likely to prevail that is called 'dominant'.

We pointed out that Mendel chose traits that 'worked'--that provided clear-cut material that allowed him to understand the nature of 'inheritance.'  That word is actually somewhat off, because Mendel was interested in the nature of hybridization (inheritance in a mixed cross between strains), and there was the confusion that still widely reigns, between inheritance of traits and inheritance of genes.  By pragmatically equating the two, because that wasn't too far off in his chosen model situation, Mendel got his result.  Even he knew that most traits didn't work that way (and even some traits that should, in some species he later studied, didn't).

For many decades after Mendel, it was thought that such traits had two important properties:  they were stable, and they made clear-cut qualitative trait differences.  If either wasn't true, then Mendel's rules wouldn't work, hybridization wouldn't work as expected, and how inheritance worked would remain obscure.

And, when Darwin's and Wallace's ideas came along, it was clear that evolution wouldn't work, either!  The most one might expect would be that one of the alleles would replace the other over time, by natural selection.   But this was not satisfactory, because evolution clearly involved smaller, gradual changes more than big dramatic ones.  And evolution, even by Darwin's mistaken genetic ideas, would continually generate new variation for selection to screen.  That was a big problem, because the observed new alleles, traits in offspring that were not present in their ancestors, seemed mainly to be grotesquely harmful, not material that selection could work with to adapt to changing circumstances.

Darwin was aware of much of this, too, in fact.  He could not see how immutable traits, like the dominant/recessive ones, could evolve and also he felt that evolution simply had to be gradual and more or less continuous. Among his reasons were his erroneous largely Lamarckian notion of the physical basis of inheritance, and the fear that without gradualism traits or species might arise suddenly....requiring explanations for their origin.

As a result, for decades leading biologists, realizing that Darwin's gradual inheritance theory (that he called 'pangenesis') was fundamentally wrong, were not convinced that natural selection could account for adaptive evolution or, in particular, that this had anything to do with the known mechanisms of inheritance.

The solution that was widely accepted and prevails (not always accurately) to today, was worked out in the 1930s and later, based on some theory and data from earlier in the 1900s.  This solution was known by names like the 'modern evolutionary synthesis.'   It reconciled Mendelian inheritance with gradual evolution in ways that were consistent with variation within and between species, and with the fossil record.

There are many things to dispute about the modern synthesis, and we'll point them out (and have mentioned them before here on MT).  But one thing that is important, but so far as we know hardly if at all recognized, was that the modern synthesis was possible only if Mendel was wrong, in ways we tried to outline in our recent previous series.

We'll elaborate on these thoughts in the next installment.....so stay tuned!

Mammography and breast cancer mortality: correlation is not causation

Breast cancer mortality has been declining in the industrialized world over the last several decades.  At the same time, mammographic screening has become the norm in most of Europe, Australia and North America.  Does early detection explain the reduced mortality? A paper in the Aug 1 British Medical Journal concludes that it does not.

The study looked at three country pairs (Northern Ireland vs the Republic of Ireland, the Netherlands vs Belgium and Flanders, and Sweden vs Norway), in which breast cancer screening was introduced at different time periods.  The paper points out that it would not be unprecedented for screening to lead to lower death rates because that's exactly what happened with cervical cancer mortality, which quickly decreased in the countries in which it was first introduced, with a lag time as others adopted the practice. That seems clearly because early detection led to curative treatment.

Thus, the researchers decided to test the idea that mortality from breast cancer fell first in countries that first had high screening rates (for the purposes of this study, over 70%).  So, they looked at breast cancer mortality in these neighboring pairs of countries, which happened to have implemented screening many years apart, and they controlled for confounding factors that might have influenced mortality risk.

All data were population data: breast cancer death rates for each country were drawn from a World Health Organization mortality database, and confounding variables (obesity, age at first birth and total fertility, all of which have been shown to affect risk of breast cancer) from nation-wide statistics on these, by age.  Data on breast cancer management was also population-based; they looked at expenditures on anticancer drugs, the 'uptake of new anticancer drugs in general...after their introduction in the country, and the uptake of trastuzumab [a recently introduced cancer medication that is effective against a subset of breast tumors]...after its introduction in the country.'

National organized screening was first introduced in Sweden in1986, and by 1990 90% of Swedish women had been offered a screening.  Screening rates there are among the highest in any country.  In Norway, in contrast, organized screening wasn't introduced until 1996 as a pilot project, and was gradually expanded until in 2005 the program was nationwide.  Breast cancer mortality fell by 16% in Sweden and by 24% in Norway between 1989 and 2006. 

Mammography screening and mortality, Sweden and Norway

Trends are similar in the Netherlands and Belgium, with organized screening beginning in 1989 in the former, and not until 2001 in the latter, with only 59% of Belgian women undergoing screening by 2005.  Breast cancer mortality fell by 25% in the Netherlands from 1989 to 2006, and by 19.9% in Belgium, but  by 24.6% in Flanders.

Finally, screening began in the 1990s in Northern Ireland, but was first introduced in the Republic of Ireland in 2000, and it wasn't until 2008 that more than 70% of women over 50 were screened.  Breast cancer mortality decreased by 29.6% in Northern Ireland and by 26.7% in the Republic of Ireland between 1989 and 2006.

The authors report that, at the population level, obesity levels and reproductive variables didn't differ significantly between countries, and cancer treatment, measured by drug expenditures, didn't differ significantly between countries, though uptake of recent drugs seemed to be slower in Norther Ireland than other countries.

This is a population-based study, which means that confounding variables can't be linked to individuals.  Thus, for example, it's possible that obesity rates differ significantly among women who undergo mammography and those who don't.  Given this limitation, the study concludes

The contrast between the timing of breast cancer screening being implemented and the similarity in mortality reduction between the country pairs do not suggest that a large proportion of the mortality reduction after 1990 can be attributed to mammography screening. Improvements in treatment and in the efficiency of healthcare systems may be more plausible explanations. Our study adds further population data to the evidence of studies that have used various designs and found that mammography screening by itself has little detectable impact on mortality due to breast cancer.

Given that there is a small, perhaps even undetectable, increase in risk of breast cancer due to exposure to the screening process itself, this study is another that gives pause to the idea that all women over either 40 or 50, depending on who is doing the recommending, would benefit from routine annual, or biannual, mammography.  X-ray screening for breast cancer is, however, a practice by now considered by many to be state-of-the-art medical care for women in many countries, and previous attempts to recommend that its use be curtailed, based on similar findings in 2009, met with loud and widespread disapproval.

There is the other fact that mammography leads to early diagnosis and intervention, but that means (1) higher rates of reported cases and (2) morbidity and trauma (including psychological) due to the treatment of the detected tumors.  But evidence we discussed in earlier posts (here and here) showed that many of those tumors would have resolved on their own, needing no treatment. So even if lifestyles are responsible for the overall reduction in cases, screening has the potential negative effect of over-diagnosis.

The fact that mammography is big business can't be ignored here.  Just as DNA sequencing is big business, and it's in the interest of sequencing manufacturers for science to find more uses for their machines, the makers of mammographic equipment, as well as mammography clinics, can't take kindly to the idea that women might need less screening.

But even if we don't throw the complicating factor of vested interests into the mix, as with other health issues that are studied on the population level, it's difficult to know how to apply these results to individuals.  Population-level data lead to population-level recommendations.  That is the job of public health, of course, so the problem is not simple.  In 2009, much of the negative reaction to the recommendations for less screening came from women who testified that mammography saved their life.  Surely there are such instances, but given the vagaries of tumor type, stage at which it's found, speed of growth, response to chemotherapy and so forth, which they are is hard, if not impossible to determine.  And certainly impossible to predict.

August CoE

The August Carnival of Evolution is up.  Links to 60 different posts on evolution, on a wide variety of blogs.  Check it out.

And, if you blog on evolution related themes, submit your posts for the September CoE here.

Large eyes evolved to allow people to see better at higher latitudes? Just so.

People whose ancestors long lived at higher latitudes have larger eyes and larger brains than the rest of us, and a new paper, reported here, tells us why.

People who live at higher latitudes have larger eyes and more processing power in their brains to deal with visual information compared with those living nearer the equator, a study suggests.

"As you move away from the equator, there's less and less light available, so humans have had to evolve bigger and bigger eyes," said Eiluned Pearce from the Institute of Cognitive and Evolutionary Anthropology at Oxford University, a lead author on the study.

"Their brains also need to be bigger to deal with the extra visual input. Having bigger brains doesn't mean that higher-latitude humans are smarter, it just means they need bigger brains to be able to see well where they live."

This sounds quite plausible, and of course it could well be true.  But, as with most such evolutionary stories, it's easy to come up with competing explanations that may well be just as valid (or invalid).  And it's also easy to find reasons that the proposed explanation could be wrong.  Even the premise that we "had to have" bigger eyes is less than obvious.  Unfortunately, none of these propositions, including the original one, can be tested.  

So, what could be wrong with the big eyes/big brain theory?  First, let's keep in mind that the idea that there's selective pressure for larger eyes means that people with smaller eyes systematically had fewer children than people with larger eyes because they couldn't see well enough.  They were poorer hunters, or fishermen, or stumbled off the ice into the sea, or didn't see predators on time, or squinted unappealingly when they gazed at their beloved -- or whatever.  (And, the authors imply that food and predators are harder to see in the polar climes than in the dense foliage of the tropics -- also rather strange and less than obvious!)

And this in turn implies that those who couldn't see well got no help from those who could, but as far as is known, people who lived in the arctic 10,000 years ago, when, according to this theory, larger eyes were evolving, traveled in small bands of related people who hunted together and shared food.  It's not like, say, malaria as a selective pressure.  It's easy to see how malaria could reduce fitness, and resistance to the disease could raise it.  


But, for the sake of argument, let's imagine that people deprived their kinfolk of food if they couldn't see well enough to hunt it themselves, or that people with bad eyesight (related to the amount of light) couldn't find mates.  Is darkness likely to be a stronger selective force than other forces in the same environment?  There's just as much endless light as there is endless dark at the poles, not to mention the glare of the sun off the snow in winter months, so, why wasn't the need for retinal protection a strong enough selective force to keep eyes small so they would take in less light (e.g., to protect from retinal cancer or cataracts, or just to reduce glare)?  

And, at higher latitudes the landscape is rather barren most of the time, and there is a lot less to see than in the tropics: nothing but snow and sparse vegetation, and much less colorful life to discriminate.

And why waste nutritional needs to service higher energy big-eyes and the energy hungry neurons to support it?

And, if poor eyesight really did lead to lower fitness, near and farsightedness should also have been selected out of our lineage long ago, and optometrists would all be unemployed today.  We'd never even know bad eyesight once existed.  

Of course what it means to 'see well where they live' is something so open-ended that with this in mind one can probably always make up a story.  Large eyes should imply a larger visual cortex and so on  because there are more retinal cells sending messages and more integration among them needing to take place, which doesn't imply higher intelligence (as the authors do clearly say).  But other factors such as the nature of color vision or light sensitivity (fraction of rods in the retina) also would be relevant.  Bigger heads for reasons unrelated to light could lead to bigger eyes.


And so on.  

The fact, which we would have no reason to question, that some species have larger eyes towards the poles may be unexceptionable.  But what if not all species at high latitudes have large eyes?  Then do we cling to the hypothesis about light by making post hoc excuses for the exceptions, or do we give up on our "had to have" assertions?  

The problems are worth raising and the story worth critiquing because it reflects an important problem in evolutionary biology, which is assertions that far outdistance the data.  These kinds of evolutionary arguments are easy to make, crop up all the time, and often make the news. But it's bad science to propose a hypothesis that can't be tested, and then treat it as though it's true, or as though it's a deep new insight (so to speak).  Or to treat it as if it's newsworthy and a big discovery.  And it's bad journalism to report it as if it's true rather than just speculation.