Blood of the Isles

by Bryan Sykes

  The Herschfelds’ final legacy was less glorious. Their grand conclusions about the dual origins of humanity turned out to be completely wrong. It took the discovery of other blood group systems, unimportant in transfusion, and the amalgamation of results from several of them to get a more reasonable interpretation of human evolution. Slowly the searchlight illuminating the ‘cradle of humanity’ turned away from Europe and Asia and settled firmly on the plains of East Africa.

  After the Second World War, the task of sifting through the, by then, thousands of sets of blood-group data from transfusion centres all over the world settled on the shoulders of one man, Arthur Mourant. Born in Jersey in the Channel Islands, and emotionally attached to it throughout his life, Mourant wanted at first to become a psychoanalyst and, in order to do so, he had to enrol as a medical student. He was forced to abandon his ambition after he underwent analysis himself and was judged to be ‘emotionally unsuitable’ to continue with his training. Despite this disappointment, he did not abandon his medical training. During the Second World War his medical school, St Bartholomew’s in the City of London, was evacuated to Cambridge and he found himself working with one of the greatest geneticists of the twentieth century, R. A. Fisher.

  Fisher, among many other interests, was engaged in a bitter rivalry with the American physician Alexander Wiener on the inheritance of the Rhesus blood groups. Rhesus is another type of human blood group, discovered, as its name implies, through research on Rhesus monkeys. Unlike Landsteiner’s comparatively simple ABO system, the genetics of the Rhesus blood group are fiendishly complicated. There was a furious race to unravel the genetics by following the Rhesus group through families, and the young Mourant was assigned the task of finding and typing suitably large families. He quickly found the solution to the inheritance, thanks to his particularly fruitful research on a local East Anglian family. Fisher was understandably elated by this triumph and Mourant soon found himself an established member of Fisher’s team with a bright career ahead of him. This career he dedicated to extending William Boyd’s pre-war surveys on the geographical distribution of the ABO blood groups around the world. He also set out to enlarge on Boyd’s work by including as many of the newly discovered blood groups, like Rhesus, as possible and to build up the most complete maps of blood-group distributions in every part of the globe. Mourant, like Beddoe before him, was an extremely avid collector of information.

  In front of me as I write is his final masterpiece, The Distribution of the Human Blood Groups, published in 1976. It is an impressive tome, 6 centimetres thick and weighing 2.4 kilograms. It has 1,055 pages, 3,179 bibliographic references, 661 pages of tables and several pages of beautifully drawn maps. It has the gravitas of a life’s work. To give you a taste of the scope of Mourant’s encyclopaedic enterprise, there are tables of Rhesus blood-group data from the Bilwa, Sanpuka and Ulwas tribes of Nicaragua, the ABO blood groups of 13,000 blood donors from Benghazi in Libya, the MNS (another blood group) results from French and Spanish Basques and the Duffy (yet another) blood-group results from hundreds of New Guinea highlanders.

  But what did it all mean? Surely there was enough information here to resolve any lingering uncertainties about the whereabouts of the ‘cradle of humanity’ and how our ancestors had moved from there to populate the planet. But even a cursory inspection of the maps shows the optimism is misplaced. Working along the commonsense lines that if two peoples have similar proportions of the different blood groups, then they are more likely to be related than two with very different proportions, you soon run into trouble. For example, the highest frequencies of blood group A are found in two very different parts of the world: among native Australians on the one hand and Saami reindeer-herders of northern Norway on the other. It would be preposterous to propose that these two peoples, about as far away from each other as it is possible to be, were closely related and shared a recent common ancestry. However, when you factor in the results of the other blood groups, the relationship becomes far more reasonable. The native Australians might have the same proportions of the ABO blood groups, but the composition of the other groups, like Rhesus, MNS and Duffy, are utterly different. Bit by bit, blood groups began to draw out connections between the different peoples of the world, including western Europeans and the people of the Isles.

  The basic pattern which Mourant found across western Europe, the area of most relevance for Blood of the Isles, showed that across the whole region west of the River Elbe in Germany, group A is high and group B comparatively low. East of the Elbe the opposite is the case. There is a gradual shift from B to A, a so-called genetic cline, as we get closer to the Isles. In the Isles themselves Mourant was able to call on absolutely vast amounts of material, both from his own unit, by now incorporated as an official laboratory of the Medical Research Council, the UK’s government funding agency for medical research, and from other published works. Among these were detailed records of blood-group frequencies from Ireland, Wales and the Scottish Highlands.

  Mourant gave the task of collecting all the records from the ‘missing’ bits – that is to say England, lowland Scotland and Northern Ireland – to his long-term assistant Ada Kopec, who, with a librarian and a secretary, made up the entire staff of the Blood Group Centre. It is plain from reading the account of this mammoth piece of assimilation and statistical comparison of a grand total of 477,806 results that Ada Kopec was far more concerned with mathematical manipulation of the figures than with explanation. Indeed it is left to Mourant himself, writing in the Foreword, almost to excuse his assistant from any genetic or anthropological interpretation, which, he writes, ‘will have to be made by others’. Fortunately, there were ‘others’ prepared to stick their necks out.

  The conclusions of Mourant and Kopec’s gigantic enterprise can be summarized very concisely. In Ireland there are very high levels of blood group O, the highest in Europe. The further west you go, the higher the group O proportions. And, as elsewhere in Europe, where O is high, A is low and vice versa, so in the eastern counties of Ireland, where O is lower than in the west, A is higher. The differences in different parts of Ireland are not dramatic, but because the number of individuals taking part is so high, the figures can be relied upon to be statistically reliable. So whereas in County Clare, in the far west of Ireland, 80 per cent of people are in group O, this drops to 73 per cent in County Wexford in the south-east, with a mirror-image result for blood group A. Turning to blood group B, there is a slight reversal of the trend across the rest of north-west Europe. Instead of following the rule of the further west, the lower the proportion of B, there is a distinct and statistically significant rise in the far west of Ireland compared to the east. It goes from 6.6 per cent in Wexford to 8 per cent in Kerry.

  Now comes the explanation. According to Professor Geoffrey Dawson from Trinity College Dublin, the high levels of A in south-east Ireland are a direct result of successive waves of immigration into Ireland from England. In the first of many papers on the blood groups of Ireland, written in the 1950s, Dawson kicks off with a summary history of Ireland. He explains the blood-group changes from east to west by the Anglo-Norman invasion in the twelfth century, which we will revisit in a later chapter, and by attempts to settle English immigrants under Queens Mary and Elizabeth in the late 1500s.

  I much prefer it when authors do advance a theory to explain their results, rather than leave it to others. But how can Dawson possibly know this is the reason for the blood-group differences? Why could they not be equally well explained by other movements of people in prehistoric times? Or by a mixture of both? The whole thrust of the explanation is based on historical events that we already know about. If we had not had a reasonable explanation to hand, would the blood-group evidence be strong enough to come up with one on its own? I really doubt that. Instead of proposing something completely original, the genetic data is rationalized and fitted in to what we already suspect from other sources.

  The rationalizations reach their peak
in relation to Iceland. Iceland was unoccupied until the late 800s when the systematic settlement from Scandinavia began. The language, the culture, even the written histories recorded in the Icelandic sagas, including the Histories of Settlement, leave no one in any doubt that the great majority of settlers were Norse. And yet, the blood-group proportions in Iceland are very different from those of modern-day Norway and almost identical to those of Ireland, as the table shows.

  A B O

  Iceland 19 7 74

  Norway 31 6 62

  Ireland 18 7 75

  By any token, the only conclusion from the blood-group composition is that Iceland was not settled from Norway at all. Far more likely, from the blood-group results, is a wholesale settlement from Ireland or somewhere else with similar blood-group proportions, like parts of Scotland. As we will see in a later chapter, there is at least a partial explanation for this discrepancy, but that is not the main message I want to get across here.

  Faced with this disagreement in the blood results, instead of having the confidence to overturn the theory of Norse settlement, Mourant tries to rationalize by finding Scandinavian ‘homelands’ that might heal the discrepancy. He cites parts of western Norway around Trondelag that have a blood-group composition a little more like Iceland than the rest of the country, then reports an isolated population in northern Sweden in the province of Vasterbotten with an even more Icelandic composition. Northern Sweden isn’t even close to the Atlantic and no traditions link it to the settlement of Iceland. Mourant then highlights an old settlement at Settesdal in southern Norway with ‘Icelandic’ blood-group compositions. Finally, to resolve this awkward disagreement, he suggests that the modern-day Scandinavians are the descendants of people moving in from the south and east who displaced the Vikings and drove them to settle in Iceland.

  All of these attempts to resolve the disparity between, on the one hand, mountains of cultural and historical evidence on the Scandinavian origin of the Icelanders, and the blood-group results on the other, highlight a fundamental weakness in the value of using blood groups to infer origins. If the results from the labs agree with what you already believe about the origins or make-up of people, then there is a cosy feeling that the genetics, archaeology and history are all in agreement with each other. But when they do not there is a temptation to fabricate an agreement with increasingly unlikely scenarios, as with Iceland.

  I suspect the same has been done in the south-west corner of Wales. The southern part of Pembrokeshire surrounding the deep-water inlet of Milford Haven delights in the sobriquet of ‘Little England beyond Wales’, a reference to the anglicized place-names and the long use of the English as opposed to the Welsh language. The levels of group A in this small region of Wales are 5–10 per cent higher than in the surrounding areas. It is known that Henry I forcibly transferred a colony of Flemish refugees fleeing political repression in Holland and Belgium to the area in the early twelfth century. The high levels of blood group A have been attributed to this historical influx and are often quoted in popular accounts as a classic success of blood grouping confirming history. This is despite the levels of blood group A in the Low Countries not being particularly high. However, a very different explanation was favoured by the Welsh scientist Morgan Watkin, the man who originally noticed the high proportion of group A in parts of Pembrokeshire. He put it down to a substantial Viking settlement in the region, despite the fact that there is very little in the way of archaeology or place-names to support it. But the fact remains that, even after thousands of blood samples from Wales and hundreds of thousands from all over Britain and Ireland, it is still impossible to decide whether the unusual blood-group composition of this part of Wales was caused by rampaging Vikings or by a few cartloads of Belgians.

  The root of the problem is that, despite there being vast amounts of very reliable data, blood groups just do not have the power to distinguish these two theories, nor the power to propose new ones that might fly in the face of historical or archaeological evidence. Blood groups, despite the advantage of objectivity, are a very blunt instrument indeed with which to dissect the genetic history of a relatively small region like the Isles. Fortunately, we can sharpen our genetic scalpel. Now we can do something that William Boyd, Arthur Mourant and the others could not. We can move to the next stage and take the last step towards the final arbiter of inheritance. We can move to the DNA itself.

  6

  THE SILENT MESSENGERS

  Whatever their shortcomings as a guide to the past, the fact that blood groups are 100 per cent genetic makes it self-evident that they are inherited from ancestors. They are not DNA, but they are the expression of DNA. You may like to compare the relationship between DNA and blood groups like this. When you listen to a piece of music you are not hearing the written notes themselves, but the expression of the notes as interpreted by the musicians. Our inherited features, both those we notice, like hair and eye colour, and those, like blood groups, that we need tests to reveal, are the music we hear. The DNA is the equivalent of the notes on the sheet, which the musicians are reading to produce the music.

  Arthur Mourant and his fellow blood-groupers were too early to see the sheet music on which the blood-group notes were written, but they knew from the way it was inherited in families that it must be very simple. The four different blood groups A, B, AB and O are the expression of three versions of a single gene, a single piece of DNA. Once it became possible to read the notes behind the music, the true cause of the blood groups was revealed to be very slight changes in the DNA of the blood-group gene itself. DNA is a coded message in the form of a sequence of four slightly different chemicals attached to each other. If you think of it as a very long string of beads, where each bead is one of these DNA chemicals, then that will give you an idea of what a strand of DNA looks like. Now imagine that there are four different colours of bead on the string, each one representing one of the four DNA chemical bases, as they are called. You can see how the string of beads might become a code purely by virtue of the sequence in which the different coloured beads are arranged. The DNA of the blood-group gene is about 1,000 beads, or bases, long.

  Though it calls the shots, DNA doesn’t actually do the work in the body, just as the notes on a sheet of music need musicians to be heard. DNA is the code that tells cells, all of which contain DNA, what to do. Just as notes on a musical score tell the orchestra what to play, DNA tells cells which proteins to make. And it is proteins that build and run the body. Proteins are made up of amino-acids arranged in a specific linear sequence and it is this sequence of amino-acids that gives the protein its particular properties. No two proteins are the same. The protein collagen, for example, has a very strong and rigid structure which it needs to do its job in strengthening bones and teeth. That strength is a direct result of the way the amino-acids are arranged, just as the oxygen-carrying capacity of haemoglobin comes about by the particular sequence of its own amino-acids. The same goes for the blood-group protein that sits in the membrane of red blood cells. It is all down to the sequence of amino-acids.

  The DNA instructs the cell how to make proteins through the coded instructions held in the sequence of the coloured beads on the string. Cells know how to interpret this code and how to translate the DNA sequence into the amino-acid sequence of a protein. The differences between alternative versions of the same gene, which are what produce the three different blood groups, are caused by mutations. This is when, very rarely, there is an error in copying the DNA. A bead suddenly changes colour and the DNA sequence changes slightly. Cells read the new sequence like the mindless automata they are. They don’t realize that they are now producing a slightly different version of the protein, which may have different properties. They just do as they are told.

  Most mutations happen when DNA is being copied. Since every cell contains a full set of DNA, it has to be copied every time a cell divides. We all start off as a single cell, a fertilized egg, and grow from that by cell division to an adu
lt with 10 million billion cells, so there is an enormous amount of DNA copying going on and plenty of opportunity for DNA mutation. However, the fidelity of copying DNA is absolutely fantastic, and of course it needs to be. If it were as poor as the average photocopier, by the time the fertilized egg had divided and divided to produce at first an embryo, then a foetus, then a baby, the DNA instructions would become so fuzzy that every child would be born with every genetic disease under the sun – if he or she ever got born at all. To prevent this happening, there are proofreading and editing mechanisms which scan the newly copied DNA to make sure it matches the original sequence. All of this is to reduce the chance of mutation. And in this we are very successful. On average, a DNA base mutates only once in every thousand million times it is copied. Even so, this minuscule error rate is enough to produce all the genetic variation in our own species and in every other living creature that we see in the world around us. Mutation is the life-blood of evolution.