All you ever wanted to know about viruses but were afraid to ask

(Well not really all you ever wanted to know, but a few basic facts that will help you make sense of some of what you might hear on your TV and wireless sets during the current coronavirus crisis.)

Complex cells

Let us start with ourselves. We are made of cells. Complex cells[i]. There are a few things to be aware of: Our cells are quite large. You can just about see a human egg cell with your naked eye if you have good eyesight. To see any detail, however, you need to view our cells under a light microscope. This (and some clever preparation and staining) reveals that our cells have outer-membranes (to keep good stuff in and bad stuff out); all sorts of other bits and pieces[ii]; and a nucleus. The nucleus is where our chromosomes live, and chromosomes are basically long strings of DNA[iii].

Simple cells

Most cells in the world are not complex cells, they are simple cells[iv] - such as bacteria. Bacterial cells are generally much smaller than ours; do not have a nucleus and the (usually) single chromosomes (i.e. long strings of DNA) just live directly inside the cell rather than their own little compartment. Like our cells, their cells have outer-membranes, but they also usually have much tougher cell walls around their membranes. As we shall see, these walls are both their Achilles elbow and their Achilles heel.

Figure 1: Some Human cheek cells with accompanying bacteria.[v]

Bacterial infections (and what we can do about them)

The bacteria in the above picture are not inside the cheek cells, they are on the surface of those cells. Cells do not usually get inside other cells and live to tell the tale. It was the two or three times they managed to do this during whole of the evolution that gave rise to complex cells[vi]. Bacteria generally live in and on our bodies in complete harmony with our cells. In fact, our continued well-being depends on their presence. But when “bad” bacteria infect us, they generally do so by getting “inside” our guts or our blood stream or our hair follicles or whatever. This means that you can try to zap them without ripping apart our own cells to get at them. But you still need something that will zap bacterial cells without harming the complex cells (our cells) just next to them.

Fortunately, nature (with a little help from science) has provided a way of doing this in the form of antibiotics. As I have hinted above, there are some key differences between our cells and bacterial cells and antibiotics can exploit those differences to selectively kill bacteria without killing us in the process. One way that antibiotics often work is by attacking the cell walls of bacteria. Since our cells do not have walls, they are normally immune to such assaults.

Antibiotics

Many antibiotics (including, famously, penicillin) come from (or originally came from) other living organisms (fungi or other bacteria) that evolved these substances as chemical weapons to fight other organisms competing for the same territory. Unfortunately, evolution never stops. The target organisms of specific antibiotics tend to evolve counter measures that render them resistant to those antibiotics and we then have to try and find new antibiotics that will still work. Even more unfortunately, we have been misusing antibiotics on an industrial scale since they were first discovered. By doing things like prescribing antibiotics for viral infections (where they usually have no effect whatsoever – see below) or feeding them in bulk to farm animals in order to increase yields (now banned in Europe), we have reached the stage were many no longer work, and where some bacteria are becoming resistant to all known antibiotics. Thanks to Brexit, we may soon be “free”, again, to purchase US-reared antibiotic fed meat in our local supermarkets.

So what about viruses?

Viruses – though often described as “micro-organisms” – are not really living things. They do not, for example, feed or excrete anything or grow or respire or react to things you do to them. One key life-like thing they can do is reproduce; but they can only do that by getting inside a cell and hijacking the cell’s internal machinery.

Viruses are basically bits of chromosome. They also have a kind of coat, and often an outer envelope, but all these outer garments are discarded as (or soon after) a virus enters a cell. The viral chromosome then “tells” the cell it has invaded to make squillions of copies of the virus (complete with a new set of outer garments) and then to release those copies by letting the new viruses escape from the cell – a process that typically involves the complete destruction of the host cell.

Viral chromosomes

Imagine if you will a building site where the person in charge keeps certified copies of the architectural drawings and plans safe in his/her briefcase but hands-out photocopies of key pages to the various workers on site so they can follow them in their work. The photocopies get amended, damaged, and re-photocopied but the originals stay safe in the briefcase – taken out only for making more photocopies to hand out. This is a very rough analogy to what goes on in cells. The master copy (in this analogy) is the DNA chromosome. The slightly dodgy photocopies in the hands of the site workers are RNA copies of the DNA. While all cells have double stranded DNA chromosomes, some viruses have DNA chromosomes, and some have RNA chromosomes – which may get to work in an infected cell directly (imagine a saboteur posing as a manager and surreptitiously handing out doctored photocopies to the workers in the above analogy) or may first reverse engineer a DNA copy (and slip it in the site manager’s briefcase I suppose). Viral chromosomes may also be double or single stranded. As the two strands of double stranded D or R NA are complimentary – mirror images if you like – some viruses have to reverse-engineer a “positive” DNA or RNA chromosome strand from their own “negative” single strand before they can get going. (Imagine the site worker handed a photocopy in mirror writing in the above analogy). Viruses with RNA chromosomes are much less stable than viruses with DNA chromosomes and tend to mutate rapidly. Their general weirdness makes RNA viruses easier to try and defeat using anti-viral drugs than DNA viruses (see also discussion below) but their propensity to mutate makes them harder to defeat because they present a moving target. Both HIV and the COVID-19 viruses are single-stranded positive-sense RNA viruses but HIV is also a “retrovirus” (it makes DNA from its RNA). One of the ways in which the successful cocktail of anti-HIV drugs work is by inhibiting this reverse process - our cells don’t normally make DNA from RNA. This line of attack is not available in the case of COVID-19.

Viruses are (typically) very small. Too small to be seen under a light microscope. The average COVID-19 coronavirus is about 100nm in diameter[vii]. For comparison, a typical bacterial cell is about 1000nm across and a human cheek cell about 50 000nm.

Figure 2 Scanning electron microscope image, in false colour, showing the COVID-19 virus (coloured yellow) as it emerges from the surface of a cell (coloured blue and pink).[viii]

Viruses may attack simple (eg bacterial) cells) or complex (eg human) cells – though different types of virus specialize in different types of cell.

Because some types of virus attack bacteria, they can be used as an alternative to antibiotics to treat people (or animals) infected by bacteria[ix]. For various reasons, this use of such viruses has never really taken off as a mass treatment option.

Viruses that infect us – or, more correctly, our cells – are almost always bad news. And eliminating them from our bodies, without thereby also eliminating our bodies, is rather tricky.

As has been noted, bacterial cells that infect our bodies nevertheless live outside our cells, and they have special features that allow us to set about them with chemical weapons that are unlikely to harm our cells. These weapons are almost entirely ineffective against viruses.

One obvious strategy would be to put something inside our cells that destroys bits of chromosome. That would work very against viruses. Unfortunately, this would have the equally obvious side effect of destroying the host cell chromosomes.

In view of these facts, we have to be a bit cleverer and try to design medicines that help stop specific viruses getting into our cells, or getting  out of our cells, or getting in or out of the cell nucleus, or reproducing within our cells. In order to do the last thing, we have to try and be really clever and figure out how a virus is misusing our cellular machinery (to reproduce) in ways that are not part of the normal repertoire of activities for that machinery.

We do have a few anti-viral compounds but, with the obvious exception of treatments for infections with the human immunodeficiency virus (which are now very effective), most anti-viral drugs do not work very well. Sadly, we certainly do not have much today in the way of anti-viral drugs that we can offer to those infected with COVID-19. (See also Viral chromosomes box above.)

What should I do during the current epidemic?

[NB the information below is now out of date and some of it is incorrect]

I do not pretend to be an epidemiologist and I am loath to predict how this might all pan out. My advice is to get up-to-date information from reputable sources like the NHS[x] rather than from the media or stuff you read on the internet.

I shall, however, reiterate the advice that they give:

•  cover your mouth and nose with a tissue or your sleeve (not your hands) when      you cough or sneeze
•  put used tissues in the bin immediately
•  wash your hands with soap and water often – use hand sanitiser gel if soap and water are not available
•  try to avoid close contact with people who are unwell
•  do not touch your eyes, nose or mouth if your hands are not clean

The COVID-19 virus’s outer envelope can be defeated by alcohol gels, but thorough washing with soap and water is even better[xi]. Face masks may help you stop touching your own face and might conceivably help catch droplets of snot in the air that contain the virus (especially if worn by the sneezer) but they will not catch tiny airborne viruses and for general wear, they are almost certainly “neither use nor ornament” [but see below] - as they say in these parts.

Stay well!

PS Just to clarify some of the terminology you might hear: The virus itself has been named "SARS-CoV-2"; the illness cause by the virus has been named "COVID-19"; and SARS-CoV-2 belongs to a group of different but related viruses called the "coronaviruses".

PPS Since I wrote this, the evidence in favour of mask-wearing has become much stronger. It is still not as clear cut as many would claim and, as I suggest above, the main benefit would seem to be that mask-wearer protects others rather than him or her self, but I have now taken to wearing a mask when shopping. If I were writing today I wouldn't write that masks are “neither use nor ornament”.

---

[i] “Eukaryotic” cells in more technical language.

[ii] Such as mitochondria.

[iii] You may remember pictures of chromosomes that show them as fuzzy, roughly X-shaped beasties, but they only look like that – all scrunched up and double – when a cell is getting ready to divide; which is a good time to try an take a picture of them. Most of the time they are too thin to be visible under a light microscope. Confusingly, DNA is, itself, a double stringed molecule.

[iv] “Prokaryotic” cells in the jargon.

[v] From https://www.canadiannaturephotographer.com/guide_buying_microscope.html

[vi] Mitochondria (which help produce energy for our cells), chloroplasts (which make plants green and perform photosynthesis), and quite possibly – though we don’t know for certain - the nucleus of complex cells were all originally simple cells that took up residence inside other cells.

[vii] A Novel Coronavirus from Patients with Pneumonia in China, 2019 https://www.nejm.org/doi/full/10.1056/NEJMoa2001017

[viii] This Is What The COVID-19 Virus Looks Like https://www.sciencealert.com/this-is-what-the-covid-19-virus-looks-like-under-electron-microscopes  

[ix] Bacteriophages: potential treatment for bacterial infections. https://www.ncbi.nlm.nih.gov/pubmed/11909002

[x] Overview -Coronavirus (COVID-19) https://www.nhs.uk/conditions/coronavirus-covid-19/

[xi] How to wash your hands https://www.nhs.uk/live-well/healthy-body/best-way-to-wash-your-hands/

Nature, Nurture, and the Height of Racism

Or why biological differences between difference "races" are not necessarily anything to do with "race"

This post is not really about human height or race or nature versus nurture (though it concerns all these subjects) it is about the way in which we are so easily led astray when we think about such matters.

People from (say) the UK who go to (say) Japan (I haven’t as it happens) tend to note that the average Japanese person is shorter than the average person back home. This is certainly a recurring theme in the (sometimes borderline racist) film Lost in Translation[1] – though the visitors in that case were, of course, American.

What is the explanation for this difference? It is tempting to jump to the conclusion (as the Daily Telegraph’s questionable Short people have 'shortage' of genes - from where I stole the picture of the three women above - appears to) that it is all down to genes.

I suppose the reasoning goes something like this:

1) British people are taller (on average) than Japanese people (probably true).

2) Height is highly heritable (certainly true).

3) British people have different genes to Japanese people (sort of true).

ergo

The difference in the average height of British people and Japanese people is explained by their differing genetic make-ups (QI-style klaxon should go off).

Counter-intuitively (at least if your intuitions are the same as mine were before I knew anything about genetics) this reasoning is entirely fallacious[2]. NB: This is not to say the conclusion itself is necessarily wrong. I do not actually know how much, if any, of the average difference in height between British people and Japanese people is explained by genes and I am not sure anybody really does for certain. Moreover, I do not think this is a particularly interesting topic. The reason why the reasoning presented above is wrong is, however, rather interesting.

Let us take each of the premises in turn:

1) British people are taller (on average) than Japanese people

According to Society at a Glance 2009: OECD Social Indicators - OECD 2009, the average height of Japanese men was 1.72m (when measured in 2005) and that of UK men 1.77m (when measured in 2006). So there is an average difference, but only one of about 5cm.

2) Height is highly heritable

A few years ago there was a comedy film (which I confess I’ve never actually seen) starring Arnold Schwarzenegger and Danny DeVito masquerading as (presumably) dizygotic (non-identical) twins:

It is well established that tall parents tend to have tall children and small parents tend to have small children. Of course, we can all think of exceptions to this “rule” and if AS and DD really were twins they would constitute such an exception. In real life, we know that AS and DD are not really twins and I rather expect that AS had taller parents and DD had shorter ones. But I think we can safely assume that, even if they had been brought up in the same household and given the same diet and activities throughout life, AS would have still turned out much taller than DD. To put this into scientific terms: the variation[3] in human height across populations really is largely explained by genetics – approximately 80% of the variation according to Scientific American.

3) British people have different genes to Japanese people

What probably strikes most British people first about Japanese people is their epicanthic eye folds – though this trait is by no means exclusively found among Japanese and other East Asian people. The trait is also sometimes encountered in “white” people in places like Poland and Finland and in “black” people and in parts of Africa in places such as Namibia. The trait is nevertheless, even if not a necessary or sufficient condition of “Eastasianess”, clearly genetic. Japanese people (unlike Brits) also tend to be lactose intolerant. This is another clearly genetic trait - albeit a less visible one and one that is also found (somewhat surprisingly) in my very Teutonic looking German nephew and, as it happens, in most of the world’s population[4]. Height in humans is, to the extent it is determined by genes, determined by lots of different genes working together in complicated ways and it is entirely possible that “tallness genes” are less common among Japanese people[5]. But the fact that Japanese people have characteristic features or eschew the consumption of lactose-rich comestibles gives us no particular reason to jump to any conclusions on the presence or absence of other genes in that population[6].

But surely, the man on the Clapham Omnibus insists, consistent differences – with respect to highly heritable characteristics (like height) – between distinct populations must be largely due to nature rather than nurture?

As the song goes, “it ain’t necessarily so” …… and here’s an explanation of why:

Imagine that the aforementioned Arnold Schwarzenegger and Danny DeVito had both really been blessed with twin brothers - monozygotic (identical) twins. Let us call them Colin Schwarzenegger and Basil DeVito. Let us further imagine that the two sets of twins were cruelly separated at birth and each paired off with one of the other set of twins: Arnold and Basil banished at birth to the otherwise uninhabited “Short Island” (an Island where there were very meagre supplies of food); and the (more fortunate) Colin and Danny to “Long Island (where food was plentiful).

On Short Island, A and B both reach adulthood but their growth is stunted:

The luckier C and D on Long Island achieve their full potential (at least from a growth point of view):

(I don’t know how they came by their suits.)

So here we have a case where there is a significant average difference between the (admittedly small) populations of the two islands and where the difference relates to a highly heritable characteristic (to wit height). The variation in height (the difference between A and B on SI and the difference between C and D on LI) is (assuming they shared their rations on SI fairly) entirely due to genetics. Nonetheless, the difference between the two populations, in this thought-experiment, is entirely explained by the differences in the two environments.

This example is, of course, rather contrived. In real life, it is far more difficult to establish whether differences within and between populations have largely (or entirely) genetic or environmental bases. But what this example conclusively demonstrates is that argument presented at the start of this post is a non sequitur. Just because there are significant differences (with respect to highly heritable traits) between nations or races (or any other groups of individuals we care to demarcate) does not entitle us to conclude that those difference are explained by nature rather than nurture.

In other words, the mere fact that differences in height within the UK and within Japan are largely explained by genetics does not - in and of itself - entitle us to conclude that the difference between the UK and Japan explained by genetics. Armed only with that information, we cannot decide whether the difference between the two populations is largely (or entirely) explained by (say) diet rather than by genes. Neither conclusion is ruled out or established by the fact that height is highly heritable.

So next time you hear someone observing that “Jews are clever with money” or “Black people make good runners and have a good sense of rhythm” or “Asian people are highly intelligent” or “Hungarians are good at chess” or whatever, please bear in mind that, even if such claims are statistically true and even if being good at handling money, running, playing the drums, and playing chess are highly heritable, it doesn’t necessarily follow that Jewish, Black, Asian, or Hungarian genes have anything much to do with the observations made.

It should, perhaps, also be added that (let’s play safe here and take the most innocuous example) even if there are genes for being good at chess and these really are more common amongst Hungarians and this “fact” really does explain Hungary’s historical prowess in this field, the implications for social policy are very limited. After all, we know that men are better at running than women and that this fact is explained by biology (men are, after all, taller than women); but if you had a requirement for a fast runner and Paula Radcliffe and I applied for the job, I rather think it would be a mistake to be guided in your choice of candidate by your knowledge of general biology and gender.

In short, neither reason nor science do (or could) lend any support to racism (or sexism).

1. A film – like the even more questionable Breakfast at Tiffany’s - I confess I rather enjoyed, despite my discomfort at the casual (though unconscious and unintentional) racism.
2. Of course if the trait were 100% heritable (like blood grouping) such an inference would be valid.
3. I wrote here about the difference between explaining things like height by genetics and explaining the variation in things like height by genetics.
4. A story for another day.
5. The implication of the article I pinched my picture from.
6. I explore the theme of race and genetic essentialism here.

Why are there no unicorns …. or are there?

Charles Arthur (@charlesarthur), reacting to a question from a ten year old, posted the following tweet:

Rhinos have a single horn. Deer have two horns. Why aren’t there unicorns, ie horses (or deer) with a single horn?

— Charles Arthur (@charlesarthur) December 2, 2015

Which turns out, like many “silly questions” to be a rather profound one … and one which I certainly struggled to answer (if you have any more answers or object to any of my reasoning or claimed facts, please comment below).

The initial pedantic responses to the question from various geeks like me (and indeed – in one case - from me) pointed out that rhinos don’t have true horns (their “horns” comprise matted hairs) and that they do usually have two horns (one behind the other). But neither of these observations (relevant though they are) do anything to diminish the force of Charles’s question.

As Charles responded to one claim that rhinos don’t have horns: “let’s impale you on one and see how that goes”.

Lots of creatures have horns, antlers, tusks, swords etc, which I shall generalize to: Pointy Things Sticking Out Of Their Heads (PTSOOTHs). Swordfish, walruses, elephants, deer, narwhals, rhinoceroses, and many others spring to mind in this context.

Ptsooths may be composed of bone, cartilage, hair, skin, or tooth enamel. Ptsooths start out, in evolutionary terms, as small bumps that confer some tiny advantage, and evolve from there. They may serve (or have served in different phases of evolution) various purposes which include: protection from predation, hunting weapons, digging tools, and sexual signalling devices.

The term “sexual signalling devices” covers a multitude of sins here. Huge antlers may signal “don’t mess with me” to rival males (and may be used to actually fight rival males) and “please mess with me” to females. In this kind of situation, runaway sexual selection often occurs and – as with the peacock’s tail – we can end up with ptsooths that are far too big for the purpose for which they originally evolved and that may actually be an encumbrance for the ptsoothholder – at least in its non-sexual life.

But to get back to the real topic here, all vertebrates have basic bilateral symmetry[1]. The symmetry is not absolute. Most men have unsymmetrical testicles and while we usually have two lungs and two kidneys, humans only have one spleen, one penis/clitoris, and (timelords aside) one heart. Our single heart does not, however, offend the basic symmetry of the body as much as many imagine:

[2]

The spleen does:

[2]

But these are soft tissues. Vertebrate skeletons are far more symmetrical and (save for the backbone itself and a few other bits) contain two of everything. In particular, the skull (or at least areas of the skull from which ptsooths grow or could grow) develops (embryologically speaking) from two symmetrical sets of bones that fuse together.

[3]

You can see the join!

Jaws (mandibles), foreheads (frontal bones), crowns (parietal bones) are all made from two symmetrical halves with a join (suture) down the middle. Even “single” skull bones – like the occipital bone at the back of the skull – are formed (earlier on in embryo development) from two (or four) initial symmetrically arranged sites.

So to really come to the point (pun intended) animals with ptsooths generally have two or four or six – ie even numbers of ptsooths – because they grow ptsooths from bits of bone that come in pairs and not from the joints between them.

So this could be why there are no unicorns …… but (to go back to Charles’s initial question) what about rhinos? (Let’s just consider the long front horn or consider Asian rhinos which do only have one horn it seems[4]).

Well because the rhino “horn” is essentially a modified tuft of hair, it was free to start evolving wherever on the skull it wished to. After all, many of us have tufts of hair between our eyebrows or on our noses (which many of us pluck out in order not to further enhance our rhino resemblances). Both single or double ptsooths could be useful and the rhino went for a tandem (or single) arrangement because it could[5].

It should be noted that both rhinos and deer still have bilateral symmetry – if Damien Hirst sawed either in half down the middle he’d end up with two pieces that were essentially mirror images of each other. (By the way, I wonder what he did with the other half of his shark?)

”But what about narwhals (the ‘unicorns’ of the sea)?” I hear you all cry.

Well this is where it starts to get really interesting! (So I hope you’ve persevered this far.)

The narwhal[6] “horn” is in fact a tooth – a left canine tooth to be precise. It grows very long and in a helical fashion. The socket for the tusk has migrated very close to the line of symmetry of the narwhal and grows straight forward – providing the unicorn-like appearance:

[7]

– but narwhals are actually slightly asymmetrical:

[8]

Very occasionally, narwhals grow two tusks, but they never grow a single right tusk or reverse the handedness of the helical twist of either tusk.

Unicorns also have a twisted horns and it is often claimed that depictions of unicorn horns were based on observations of narwhal horns.

[9]

Unicorns, however, twist both ways:

[10]

There again, so does DNA – in its depictions! In real life, DNA[11] only goes one way – the opposite way to the narwhal horn.

The ancestors of modern deer also had tusks[12]. Later they evolved horns and their tusks withered away as their horns grew. I see no reason – in principle – why deer or antelope (or other ungulates) could not have evolved to grow (say) only their left horns and why that single horn could not (with a slight asymmetrical deformation in skull development) have moved over towards the centre of the head. Such a “unicorn” would not be quite symmetrical but, given that they have helical horns, unicorns aren’t really symmetrical either.

In fact, thinking about it, I don’t really see why – if the horn were composed of two fused halves (like the swordfish “bill”) – we couldn’t have had a “unicorn” with a single symmetrical untwisted horn.

Moreover, if the frontal and parietal bones of the skull withered away and the occipital bone filled in for them (stranger things have happened in skull evolution) why couldn’t a single horn develop from the middle of that bone in roughly the right place for a unicorn style horn? I know not.

In conclusion then, I have no idea why there are no unicorns …… perhaps there are!

Postscript: Since writing the stuff above, Rab Austen (‏@RabAusten) has reminded me that the triceratops also had a (front) horn on the midline of its skull. This was a "real" (bony) horn and would - as Paolo Viscardi (‏@PaoloViscardi who has forgotten more about bones than I shall ever learn about them) kindly confirmed - have been formed from the fusing of two symmetrical elements - like the swordfish bill. I'm not sure whether a horn formed like this could then grow with a helical twist (though as Paolo also points out, stranger things happen at sea) but Rab's insight certainly lends support to the claim that there is no reason - in principle - why a horse-like creature could not have evolved a bony horn in the middle of its forehead.

1. Invertebrates often have bilateral symmetry too. Even starfish - which superficially have radial symmetry - have a complicated and interesting way of forming that involves bilateral symmetry. Other invertebrates - snails and sponges spring to mind - break the "rule" in other ways.
2. http://keckmedicine.adam.com
3. http://http://fineartamerica.com
4. Thank you to Steve Jones (‏@TheEulerID) for this information
5. http://news.bbcimg.co.uk
6. Please note that evolution does not work in the way I talk about it (metaphorically) in this post. Evolution has no plan, intent, or purpose. It's all natural (or sexual) selection acting on random mutations, It is, however, often easier to describe what happens in evolution using teleological language - as long as we don't forget that it's just a metaphor! OK?
7. I'm getting all my information about narwhals from Chris McManus's excellent Right Hand, Left Hand which I urge you all to read.
8. https://cdn-images-1.medium.com
9. http://www.mermaidsrock.net
10. http://http://kristell-ink.com
11. OK I'm talking B-DNA not Z-DNA ... pedant!
12. Deer Antlers: Regeneration, Function and Evolution by By Richard J. Goss esp p72 et seq

The riddle of Ridley

This piece was inspired by Nick Cohen’s piece (which I urge you to read) in yesterday's Observer: Why do we still honour free-market intellectuals? (It's mystifying that the former chairman of Northern Rock is still garnering plaudits).

The author of our current misfortunes?

Matt Ridley (AKA The Right Hon Matthew, 5th Viscount Ridley) is famous (or perhaps infamous) for (let us put this as neutrally as possible) being “in charge” of Northern Rock when it went pear-shaped (to use a metaphor borrowed from biology) in 2007. This debacle was the first (at least the first that came to everyone’s attention) in a series of events that culminated in the virtual collapse of the UK banking system and the economic mess from which we are only just recovering (at least if the optimists are to be believed).

I, however, knew of Matt Ridley long before 2007, as the author as a series of books on evolutionary biology and genetics. While I should hesitate to recommend Dr Ridley’s financial advice to anyone (ditto his views on climate change – but that’s a story for another day), I should have no hesitation in recommending his excellent popular science books.

The only criticism I might make of those books is that Ridley is sometimes too ready to borrow metaphors from evolutionary biology and try and apply them in his thinking on how the economy works or (even more tendentiously) ought (in a moral sense) to work. You can often see this species of thinking lurking below his writing. Richard Dawkins (who writes in similar fields and has often worked alongside Ridley) is rather more keen to note (though I am paraphrasing Dawkins here) that just because nature is “red in tooth and claw” it does not follow that the best run economies are, or that (even if such economies were the most financially successful) they would be an ethical success.

But let us move on and look at some (evolutionary) science……..

First, some human psychology:

It is a puzzling fact about humans (revealed in a number of experiments) that when acting as an audience at (say) a random number guessing game, they will accord extra respect to those who guess the “correct” numbers (and less respect to those who guess the “incorrect” numbers) even though they know the game is entirely random. If popular films are an accurate portrayal of reality (I would not know as I have never entered a casino) winners at roulette accrue similarly inflated (and entirely undeserved) prestige.

Of course, winning at some gambling games – for example Black Jack – can be a sign of cleverness. If you can remember the sequence of cards and calculate the odds in your head as the game progresses you can stack the odds in your favour. But usually, gambling involves pure chance. It is often claimed that some people are “expert” poker players, but the last time I read something on this subject, the author was suggesting that the statistics on this are by no means unequivocal. It is entirely possible (he opined) that “top” poker players are simply “lucky” poker players.

So why do we admire people who happen to make the right (entirely serendipitous) guesses? One answer I have seen put forward is that we (for evolutionary reasons) prefer to ascribe what happens in the world to agency rather than to random chance: the movement in the bushes might be a random effect of the wind, but those who assumed it might be a stalking lion were more likely to live long enough to become our ancestors.

Secondly, some evolutionary theory:

It was at one time thought - even sometimes by Darwin himself (despite what we often read and despite the fact that the modern non-Lamarckian theory is styled “Darwinian”) - that a significant element in evolution is the inheritance, by offspring, of characteristics acquired in life by parents. The example usually given of this sort of phenomenon is the ancestors of the giraffe having to stretch their necks to reach the leaves of tall trees and then passing on their elongated necks to future generations who then did the same and became taller still.

Microbiologists were among the last scientists to disabuse themselves of Lamarckian notions. The example of giraffe gymnastics is clearly far-fetched but, for a long time, it really did seem as though populations of bacteria could be "trained" to survive increasing concentrations of antibiotics in their growth media – like heroin addicts learning to tolerate increasing doses of their chosen drug I suppose – and could pass this learned ability on to their daughter cells. What actually happens is that a few “lucky” mutant bacteria just happen to survive each round of antibiotic treatment and go on to produce new generations with a similar genetic make-up (plus a few new mutants).

In other words, the successful bacteria do not owe their survival to any of their own achievements in life.

Perhaps you can already see where I am going with this ………..

Bankers

Certainly until the events of the last few years, I suppose that people naturally (and as we have seen for good evolutionary reasons) tended to assume that successful bankers were successful because they were highly talented people who owed their success to their talents. Successful bankers were awarded prestige and honours and, even though some people wondered aloud whether bankers really deserved to be paid salaries and bonuses hundreds or thousands of times greater than what (say) a university researcher discovering a new antibiotic might expect, most people accepted that successful bankers deserved high salaries.

But there’s an entirely plausible alternative hypothesis for what the mechanism at work here is – made all the more plausible since the events of 2007. What if bankers make entirely random decisions? The financial environment in which they make those random decisions, selects some to survive and prosper, and some to go bust; but the bankers themselves have no more special foresight than bacteria growing on media contaminated with varying concentrations of antibiotic.

What, in short, if banking (and perhaps commerce in general in a market economy) is Darwinian rather than Larmarckian?

What if successful bankers do not deserve any more reward in life than successful bacteria?

Given Mark Ridley’s fondness for drawing parallels (at least implicitly) between evolutionary biology and the financial world, I am surprised he has never given serious consideration to this hypothesis. And, even more to the point, subscription to such a hypothesis would entirely absolve Matt Ridley of any culpability for the plight of millions who have been far less fortunate in life than the Viscount and who now find themselves at the (lack of) mercy of events which were certainly beyond their control.

(Also published at Bad Reason)

Why Michael Gove's department is confused about genes and education; and why you probably are too.

In the Guardian on Saturday October 12 it was reported that Michael Gove's special adviser Dominic Cummings had "provoked outrage" by claiming that "up to seventy percent of a child's performance is related to his or her genes".

Now it seems that Mr Cummings has been mis-quoted here. I happen know this because he told me himself in a tweet. His twitter name is @odysseanproject – which I suppose will amuse fans of Diary of a Nobody. Mr Pooter’s favourite joke about his friends Gowing and Cummings was that Gowing was always coming and Cummings was always going.

But I digress.

What the Guardian ought to have said and (it seems) Dominic Cummings did say is that "up to seventy percent of the variation in children's performances is related to their genes".

So why is that different from saying "up to seventy percent of a child's performance is related to his or her genes"? To see why, we need only consider the following simple thought experiment:

Imagine you adopted two randomly chosen children born one the same day (Mary and Jane perhaps) and gave them exactly the same upbringing, environment, life experiences, and education. (Of course that would be impossible in practice, but this is only a thought experiment.) Now imagine that we tested them both (several times perhaps to make sure one of them was not having an off day) at eighteen years old and Mary got straight Bs and Jane got straight Cs.

The variation in the results of the two individuals must, I hope you see, be entirely due to their respective genetic makeups.

Now let us repeat the thought experiment but provide much better education. This time (we could imagine) Mary gets straight As and Jane gets straight Bs. The variation in the results of the two individuals must still be one hundred percent due to their respective genetic makeups. The improvement in results is, however, entirely due to the change in environment - specifically the improvement in education.

This observation illustrates why Dominic Cummings's statement (as mis-reported) is drivel. The seventy percent figure relates to the explanation for the variation in a population not to the performance of an individual.

Asking about the relative contributions of genetics and environment to a particular child’s performance is a bit like asking what whether the height or the length of a rectangle contributes most to its area. Such a question makes no sense.

Asking about the relative contributions of genetics and environment to variation, on the other hand, makes perfect sense.

Some things in a human population may be vary a lot – like personal income. Other things in a human population may vary much less – like height – you do not find people who are two million meters tall for example.

The degree of variation in a population can actually be quantified. (This is quite complicated, and there are different ways of doing it, but let us just stick with the basic idea.) Once we have quantified the amount of variation, we can talk about what factors contribute most to that variation.

If, in the case of school children and academic performance, we took away one of the contributions to variation (which we could do in theory) by breeding a cohort of school kids who were all genetic clones (which would take away the variation due to genetics) or by giving a cohort of school kids exactly the same education (which would take away the variation due to quality of education); in either case, the amount of variation in the population would be reduced. It would obviously be reduced more if you took away whatever was making the biggest contribution.

If we pretend for the moment, and for the sake of simplicity, that education and genes are the only factors (of course there are many others such as social class, but let us keep things simple) what may seem slightly paradoxical is that if we gave all children exactly the same education, though this would reduce the variation in the population, it would increase the relative contribution of genetic factors - it must do so because all variation in a population receiving exactly the same education must be down to the genes.

Of course, as I expect almost everyone agrees (regardless of their politics) the variation in academic achievement (and many other attributes) of the population depends on a complex mixture of factors. Teasing out the relative contributions of the various factors is far more tricky than you might think. Even if we take something like height - which is far easier to measure objectively than academic ability and is undisputedly highly heritable (tall parents tend to have tall kids and vice versa) - it is still far from clear to what extent the variation in human height around the world is down to genes or environment.

I have no idea what the correct figure is for the genetic contribution to the variation in academic achievement in the population at large, but (though I am very much on the political left) it wouldn't surprise me at all to learn that the true figure is even higher than seventy percent.

But, given the fact that nobody knows the facts for sure, people at either end of the political spectrum are wont to provide ideologically-driven rather than data-driven answers to the empirical question: How much is nature and how much is nurture? Hence the irate tone of much of the discussion on this topic in the media this week.

The left's commitment to egalitarian principles lead them to conclude that it must be mostly due to nurture. Only if we believe that, they suppose, can we imagine a future where social inequities are put right through progressive social intervention.

The right's commitment to in-egalitarian principles lead them to conclude that it must be mostly due to nature. Only if we believe that, they suppose, can we justify the claim that doing anything to improve the lot of the hoi polloi is a waste of time.

So why do I claim that both sides get the whole thing rather back to front?

Let us conduct another couple of thought experiments:

First let us first suppose that we have the most extreme case possible of the frequently encountered left-wing belief about the way the world is. Everyone in our imaginary society is a genetic clone with an exactly equal genetic endowment of academic potential and any differences in ultimate achievement will be entirely due to how we nurture the individuals concerned. How would we then structure our education system? We should have to choose individuals completely arbitrarily from the pool and train some of them up to be clever enough to be surgeons or rocket scientists or whatever; and - at the other end - some of them to be just clever enough to tie their own shoe-laces so that they could perform jobs requiring very little intelligence - like the job of Education Secretary I suppose.

But isn't this more or less what right-wing education policy has always been (and what the likes of Michael Gove and Dominic Cummings seem to want to go fully back to): a system where people are picked arbitrarily from the pool on the basis of social class (rather than innate ability) and given the training they require to fulfil their allotted stations in life?

Now, instead of a society of genetic clones, let us imagine a society where everyone is born with different potentials. No matter how well I had been nurtured, I could never have become a Premiere League football player; and the likes of Michael Gove could, no matter how well he had been nurtured, never have understood averages or become a professor of thermodynamics.

...a bit like the world Dominic Cummings and other right-wingers (probably largely correctly) believe we do inhabit.

In this world, it no longer makes sense to choose people arbitrarily from the pool and nurture (only) them. The only policy that makes sense is to nurture everybody so that each person achieves the best he or she is capable of and those who come out on top represent those who started out with the best genes rather than those who were fortunate enough to be given an education.

...rather like the sort of education system left-wingers tend to argue for in fact.

Okay, I've over-simplified here and rather caricatured the various political positions, but I hope I have also successfully made a serious point: the thinking about nature and nurture, on both left and right, is often terribly confused.





A version of this post was included in the @pod_delusion podcast of 2013-10-17.