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~ t ~ i 'fmc SCALP IN HEALTH AND DISEASE. By Howard T. Behrman.

C. V. Mosby Company, St. Louis. 566 pp . 1952.- In "The Scalpin Health and Disease" Dr. Behrman has written a thoroughly up-todate text. Admittedly expensive ($12.75), it contains 512 drawingsand photographs and a large number of references, including over500 on the embryology, anatomy, an d physiology of the hair, the skinglands, and alopecia.

'l'hongh many sections are fascinating in themselves, and DoctorBehrman's stand on detergent rinses, lotions, and hair dressings is,commendably frank, the chapters on male pattern balding an d the normal anatomy and physiology of the hair should prove of major interestto anthropologists. In discussing male pattern balding the work ofJ. B. Hamilton is followed in detail, though some space is allottedto Yonng's fat-loss theory of balding an d the multiple-factor SzaszRobinson hypothesis is reviewed. The latter, it may be recalled, invokes genes, hormones, fat, scalp muscles and muscular tensionsarising out of the cnltural context.

Chapter 1 (100 pages), devotee! to the anatomy and physiologyof hair, inclndes a comparison of the pilons systems of rodents andmen, and summarizes some of the work of Kneberg, Steggerda, Trotter,Danforth and others. Pilometric studies are discussed, and the Copleypilometer is described. 'fhe molecular structure of hair an d thealpha-beta keratin shift are also considered, as are the recent studieson the red hair pigments by Rothman and Flesch. In discussing therole of hormonal secretions on hair growth, Speert 's work on topicalapplications has no t been employed to advantage, and much basicinformation on nntritional achromotrichia has been displaced in favorof clinical studies. However, this book is directed primarily at theclinician, who in turn ma y care less for those sections that will inter,est anthropologists most.

SELECTION AND POLYMORPHISM IN TH E A-B-OBLOOD GROUPS

ALICE M. BRUESUniversity ot Ok!ahorna School ot Med'icine

T'VO F'IGURES

After many years of discussion and delmte about the racialdistribution of the A-B-O blood groups, several questions stillhave not been answered to the satisfaction of all students.Three of the questions ar e purely historical: (1) At the point'where the line of human descent diverged irrevocably fromall others, did it carry one, two, or all three of the A-B-Oallelomorphs (2) I f not all of the genes were part of thebasic human inheritance, which are the more recent mutations (3) Have these more recent mutations occurred asunique events, or ha s eaell recurred from time to time invarious populations ? The 4th question is functional, thoughclosely related to the historical questions: (4 ) Is there anyselective valne attached to the A-B-O blood group genes orto the genotypes formed by them ?

To these questions the present paper proposes to ad d a5th, which must be considered relevant to the others: (5) vVhyhas only a small part of the possible range of A-B-O bloodgroup frequencies been realized by now existing races Atfirst glance this may seem an unreasonable question, likeasking why there ar e upper and lower limits to human bodysize; but in respect to characteristics which have been frequently assumed to lack any selectlve value, the questionbecomes an interesting one. Figure la , adapted from a compilation by Wiener ('4-3) shows graphically the distributionof 215 representative human populations all checked fo r consistency by the equations of Bernste in. Our adaptation shows

559

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PER CENT OF GENE Ao 0 10 15 20 25 30 35 40 -- o

10z: IS

o.... 20z: '- ' 25....

3035

6 7 1 2 4 3 3 2 I 1I ) 4 7 10 " 7 1 1 11 2 8 13 15 16 8 1

I 4 13 10 9 22 9 6 22 7 6 2 1

I 2 2

40Fig. In QuantitatiYe distribution of 215 represeutative human populations ill

respect to f"eqllencies of the A-B-O blood gronp genes.

PER CENT OF GENE A100

z:.u""o ....z: '-'

....

100Fig;. 1b I ~ i r n i t s of the world range in A-R-O blood group frequencies, in I"elatiOll to the eomp]ete possible mnge.

560

561ELECTION IN BLOOD GROUPSonly the number of series reported in each group range, sothat it represents various races somewhat in proportion tothe number of times thcy have been studied, although duplicating and repetitious values have been largely eliminatedby the original compiler. Since the principal value of thefigure is to demonstrate the outside limits of variation sofa r recorded, a further checlc was made on the accompanyingtahular series of 351 populations, and a few at or near thelimits of variation were added,' No further data were inserted, since the sampling seemed snfiiciently broad in itscoverage to define the runge of variation for our prcscntpurposes. In order to present the distribution in properperspective, which is u:-mally not done for space-saving reasons, figure 1b has been prepared to show the outlines of the"inhabited portion" of the A-B-O gene frequency range, inproportion to the total possible range for the genes. I t willbe seen tha t about four-fifths of the possible range is vacantor nearly so. .Certain generalizations arJOut the distribution ma y he made. ITh e 0 gene is rarely reduced below 50%, and then only by asmall amount. In the absence or near-absence of the A gene, 'the B gene usually remains low. In the absence or nearahS811Ce of the B gene, the pereentages of the genes A ando are rather widely distributed, from zero to 50'10 A. Wherethe frequency of the B gene is high, on the other hand, therange in respect to 0 and A is more restricted, centeringaround 20% gene A. There 8eems no way in which the peculiarities of this distributiou can be explained in terms ofrandom independent fluctuations of the A, B, and 0 genes; tthere appeal' to be some correlative factors acting between ithem. This lllUSt be explained either 11y particnlar historicalcircnmstance or by the assumption that selective factorsoperate to mal,e certain areas of the chart" uninhabitable."The nature of the limiting faetors which have resulted in

1 1,Vc ,have COllcurred with ,ricuer in elirniu3ting one Tibetan series, with grossinc-onsistenc)' between A, B, alld AB frequencies, whicll would have showed afrequency of gene 0 lower t h ~ l l any group here included.

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562 ALICE M. BRDESthe world distribution we now have must be such as to counterac t genetic drift, which will always tend to diversify populations an d break down limits ~ m c h as appear in figure l .

The following discussion will therefore include both negative an d positive arguments. Historical reconstructions basedon the assumption that the A-B-O genes lack selective value,which include a variety of hypotheses regarding the originan d relative antiquity of the three genes, must be examinedto see wlJether they can satisfactorily account fo r the presentranges uf frequency of the three genes. To some extent thegeogra phical distrihution of the genes, especially B, so oftendiscussed before, must be reviewed again. Then it will henecessary to detenl1ine whether a hypothesis involving selective factors can explain these data more satisfactorily. Thiswill require the preparation of a mathematical model of aselective system, into which must be incorporated any directevidence now at hand for selective effects involving the A-B-Ogenes. First, however Wl, must consider genetic drift, mutation, and selection, particularly as they may apply to theblood group genes an d as they have been invoked in the pastto explain the polymorphism of the human species in respectto this gene system.

GENE'rIC DRIFT'llhe effect of genetic drift 11roducing random variations

between fragments of races, where population numbers ar esmnll, is certainly suhstantial in respect to th e blood groups,often in contrast to tIle apparent stability of a comhinationof other traits. This has been interpreted, according to theprejudice of the observer, either as indicating that othertraits are standardized by some form of selection (Boyd,'50) or that because of their multiple rather than simplegenetic determination they ar e less susceptible to the randomfluetua tions of single genes (Birdsell, '50). Genetic drift ha sbeen delicately cl(!fined in mathematical t e r m ~ by "rigllt' andothers; ("Wright, '49, '51; Dobzhansky, '41, '50) bu t since ithas somet imes heen l'a ther poorly descrihed in an thropologi-

SELECTION IN BLOOD GHOUPS 563cal literature it is well to recapitulate. The genes present in "any generation of a given group represent a statistical sampling of the genes present in the germ cells of the previousgenera tion. Within certain slight limitations (due to the fact.that there is a maximum practicable family size in the species) b.,>these genes represent a random sample of the statistical 'Iuniverse defined by the gene frequencies of the previous Igeneration. The v a ~ ' i a n c e of such a sample may be calculated Iby the formula ylNp

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564 ALICE l\ L BRUES

there is no indication that this is directly correlated with thepresent differences. Other groups which ar e reasonably homogeneous in morphological features but show a large rangein A-gene frequencies are Pre-Dravidians, with an A-generange of 34% between various subgroups; Eskimos, with arange of 32%, Polynesians, with 28%, Australians with 24%,an d Ainu with 17%. Of course the comment ma y be madethat various subgroups of the populations cited above havebeen subject to influence from different admixtures. Bu twhere the range between subgroups of a principal group ishalf or more of the total world range (a s in the first 4 casescited) it is not possible to find supposed mixing groups extreme enongh in A-B-O frequencies to produce this diversity.In marked contrast also ar e the rather mild gradients ofA-B-O frequency found within continental European nationalities or between adjacent ones. In these cases we know ofadmixtures and infiltrations from different directions as historical facts; yet, in the presence of high population densitiesin this area, the diversity of gene frequency is very low compared to the examples cited above. '1 he evidence fo r the vigorof genetic drift under more primitive conditions is so convincing as to be disturbing. I f it has acted so strongly evenafter the formation of certain races and sub races as we nowknow them, why has it no t produced, during the whole periodof the differentiation of the species, often under conditionsof isolation and smallness of numbers more marked thanhave existed subsequently, a range of variation much greaterthan we now see'? "Ve can hardly assume that A-B-O genefrequencies remained stable during the period when otherfundamental racial differences were developing, only to scattercentrifugally by genetic drift after the other racial differencesha d been clearly developed; this would virtually imply higherpopulation densities at the earlier period than at the later.Bu t if the present scatter within racial groups such as citedabove is projected over the whole period of racial differentiation, with nothing to control it, it would seem that nearlyevery possible percentage distribution of the A-B-O genes

SELECTION IN BLOOD GROUPS 565would have been realized by some now existing group. I fwe attempt to explain the control of genetic drift in the bloodgroups by assuming continual back-crossing of human strains,we cannot account for the maintenance of the other racialdifferences. "Ye might express this phenomenon in the formof a rather unorthodox equation;

2 ~ diffeI:ence in f r e q u e n ~ ~ e > J ' A gene = X o / 0 t l i f f ~ J ' e n c e _ i n f...,qlleucy of A gcnemaximum difference between Rny two difference between Australians andAustralian tribes in otl1er features any other race in other fea tllresX, which would represent the potential world rang'e for

the A gene, could clearly go up to 100% (or more) withoutviolating the terms of the equation. I t appears then that adisproportion exists between the development of local andtotal diversity in regard to blood groups, with a total worldrange of blood group frequencies somewhat restricted ascompared to what might be expected on the basis of localcondi tions.

ORIGINS 01" 'fHE A-B-O GENBSThe question of the present average range of human popu- "\lations in respect to the A-B-O blood group has always been !closely involved with hypotheses regarding the time of orig'in i

of the three allelomorphs. An early explanation assumed that Ionly one of the genes, 0, was present in the original humanstock, and that the other two" arose" and" spread" at different times from a hypothetical diffusion center for thespecies, thereby producing the general pattern of distributionnow seen. Unfortuna tely the words "arose" and "spread,"which roll so easily off the tongue or pen, ar e in the natureof genetical time-bombs. :Hany things have been calculatcdabout the future of a new-born mutation. It s situation atthe beginning is precariolls in respect even to mere survival,and even if by favorable chance it manages to arrive at alevel of frequency which preve.nts its actual loss in somegeneration, its chances of becoming abundant ar e very slight,unless it possesses some selective advantage. I t may persistas a constant minority in a large group, or achieve a fairly

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566 567LICE M. BRUEShigh percentage value in a small group, but its absolute numbers ar e likely to remain small indefinitely. Th e parallelfrequently cited of newer or mOl'e progressive t rai ts" spreading" froIl! centers, in the evolution of other genera or ordersis an entirely proper one as regards the behavior of a mutation of positive selective value; it cannot properly be appliedto a mutation which we choose to consider entirely neutralin value. One explanation which recognized this difficultyattributed the eventual f n ~ q u e n c i e s attained by genes A andB to the fact that the entil'e species, at the time the mutationsoccnrred, c o n s i ~ d of so few individuals that chance alonecould bring the new genes up to appreciable percentages.'1'he geographical distribution was accounted fo r by supposingthat A "m'ose" very shortly before the first invasion of theNew ,Vodd, so that the invading groups carried a smallamount of it, and subsequently"spread," i.e. increased itspercentage value, in the population remaining in the Old'Vorld. I f this" spread" in the Old ,Vorld occurred purelyby genetic drift, we must assume that the basic immigrationinto the New ,Vorld was accomplished while the nucleus ofthe human species in the Old ,Yorld still consisted of a fewthousand ilHlividuals. In regard to the development of B,which would appear by all evidence to have come later, thesituation is even more paradoxical. :\Tow a fairly well populated wodd is assumed, with the corners of the Old 'Worldand the New filled with the genes A and 0 in various proportions, while somewhere in Asia a small group in some wayisolated, developed a high percentage of the B gene purelyby geuetic drift from a chance mutation. Then subsequentlytllis B-bearing gronp nlllltiplied explosively, expanded outward as the result of a SllIJposed "superior culture" andeventually established the B gene in substantial amountsthroughout Asia, the Pacific Islands, Africa and EasternEurope, till it constituted about 15 of the A-B-O genes ofthe human species. I t appears to the present author that thisplot is too much contrived, adjusting population size, degreeof isolation, and even cultural advantage, to suit the case.

SELECTION IN BLOOD GlWUPS

The basic difficulty is that the word "spread" as appliedto a gene, whether the user so intends or not, implies selectiveadvantage of some kind.

Numerous variations on this general scheme have beenproposed. One attempts to explain the building up of theA an d B genes, without selective advantage, by assumingthat the mutations occurred repeatedly; this of course doesnot explain the existence of geographical difference in eli strilmtion unless a particular mutation occurred repeatedlyin one p01JUlation without occurring in another. Since thisvirtually assumes a pre-existing genetic difference predisposing to the occurrence of a particular mutation, it puslICs theprohlem hack one step without explaining it. A similar theoryspeaks of "precursors" of genes fl'Clln which the final mutations OCCUlTed to produce the gene::; as we now know them.However, for historical purpo::;es, ancl to explain the geographical distrihution of the A-B-O genes at the present time,it little matters whether at a given moment in the past a geneexisted as a predisposition to mutate, as a "l)recnrsor," ora::; the real thing; the problem of explaining the geographicaldistribution of the genes remains the same.

The notion of repeated mutations has sometimes been applied in a more logical way, by a::;::;lllning that the mutationsoccurred more or less at random in various populations,sometimes becoming extinguished, sometimes hanging on, andoccasionally multiplying with isolation and good luck. '1'hiswould serve to explain some of the erratic behavior of thegene frequencie::;, such 3S the occasional B in the New 'Wodd;undoubtedly the sporadic reCUlTence of the various lllutationsshould be taken into consideration as a possibili ty regardlessof how we propose to explain the broader aspects of A-B-Ogene distribution. However, if various mutations involvingthese genes have be-en oceuITing oceasionally throughouthuman history, it is probahle that they occurred early enoughto make all three forms, A, B, an d 0, for practical purposescoeval with the human species. Th e latter suppositiou is the

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568 ALICE llL BRDESbasis fo r tIle other principal school of thought in regard toA-B-O gene distribution.

I f it is assumed that all three allelomorphs w e l " ( ~ present! at the" birth" of the human species, th e present geographical( distributions ar e accounted fo r by relative degrees of gene: loss in the early stages of dispen:Jion when communities were

small. The probahle starting point was set by Boyd (Schiffand Boyd, '42) at 25% A gene, 15% B g(me an d 60% 0 gene

, - a present average for the species. Clearly, in the process ofdispersion and genetic drift B is the most likely to be lostby some groups, A the next. I t is assumed that a numberof groups lost B, and that the B-Iess groups were in verylarge part the ones which first populated the New ,Vorld,Australia and western Europe. (I t should be noted that thesemust have been not only small groups, but few groups, elsesome groups emiched in B hy genetic drift would have gonealong to counteract th e B-Iess groups.) The gcne n thenremained only in the la rger (pl'eSllmably) breeding group ofcontil1elltal Asia where it was protccted from cxtinetion bythe size of the group in which it occurred. Then in some wa yB, within this larger group, increased to frequencies of 20-30%in one or more subgroups, which expanded outward and spreadB by mixture over a very extensive area. Since B is supposedto have increased markedly in thl' larger central population,which would be less subject to genetic drift, it might be preferable to start out with a primeval frequency of B nearer toits maximum in present groups than near its average. Inregard to A this theory supposes that, being in the beginningcommoner than B, it rC!lched al l areas in reasonable amonnts,there to give rise by genetic drift to a variety of combinationswith O.

,Vith regard to explaining the non-random features of thetotal chart of frequencies, the two main approaches outlinedabove (addition of genes by mutation, deleLion of genes bydrift) present very much tIle same aspect. In either casethe result is best explained by assuming that at some timein the past a particular group, with a frequency of the A gene

569ELECTlON IN BLOOD GROUPSabout 2070, developed maximal values of B, and producedthe peculiar triangular distrihution of figures 1a and Ib bymixing' with a variety of B-Iess groups ranging from zeroto 50;70 in gene A. This would account fo r the tendency ofthe hig'h B groups to converge in respect to their pereentageof the A gene. Whether the high-B group was the group inwhich the B gene originated or the one in which it solelyremained after loss in other areas, does not affect the subsequent course of events. In considering the probable effects ofsuch mixture we must take into account two aspects of theproeess; the production of a basic fre(]llellcy of the B geneintermediate between the mixing groups, in proper proportionto the amount of mixture; then variations in the resultinghyhrids due to genetic drift in separate population fragments.'1'he present highest levels of the B gene (ca. 30%) includerepreselltatives of groups which ar e otherwise quite diveri:Je;Indians (including Pre-D ra vidians), Gypsies, Chinese, Indonesians, classical Mongoloids of J'vlanehuria and Siberia, andAinu. I f we assume that these groups arose by the mixtureof various gronps which lacked the B gene altogether, witha bypothetical "B-race," it is evident that even if the" Brac('" wa s 100ro saturated with the B gene, the amount ofcommon admixture in these cases would bave to be ahout31'\:'. I t seems most douhtfnl that a 100% saturation of theB-gene could have been attained hy genetic drift alone in apopulation large enough subseqnently to modify the bloodgronp picture of the world OIl a COIl tinental scale. I f the"B-race" wa s lesi:J i:Jaturated with th e gene B, the amountof mixture must have been still more. Of course, other representatives of the same groups mentioned above are muchlower in respect to B-gene frequency; Pre-Dravidians, forinstance range down to 8% B gene, Indonesians to 110/

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572 ALICE JlI. BItUESHogben, following a line of investigation first suggested byHirszreld in 1925, have shown that selection against thephenotype OA, of a very severe sort, takes place when the OAembryo develops in an 00 TllOther. The data which they haveassembled show that only 75% as many A (OA) children areborn to 0 women with A husbands as to A women with 0hushands, although the frequency of the two reciprocal typesof marriage, an d the relative pe r cents of OA and AA genotypes included under the phenotype A, would be the samefor- any population or combination of populations. The effectis shown in defici(JIlcy of recorded fertile matings, deficiencyof total number of children produced, and deficiency of Achildren produced. They estimate therefore that 25% of theOA embryos exposed to this risk are eliminated, apparentlyby an incompatibility similar to that produced by the Rhgenes. A selective effect of any such magnitude immediatelyraises a puzzling problem by rendering the A-B-O gene frequencies unstable in an y population containing both A an d 0genes, unless in absolutely equal numbers. Selection againsta heterozygote eliminates at each stroke one specimen of eachgene, and will finally eliminate whichever of the two geneswas in the heginning the less abundant. In the present casethe B gene would he affected also, since in any internecine

'Currently Bennett and Brandt ( '54) have contcsted this interpretation bybreal

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575574 ALICE 1\1. DRUEStwo reasons; til'sl, b ( ~ c u l l s e the existence of the incompatibilityphenomenon definitely demands consideration of selectivefactors in resped to these two genes; second, because th eknown approximu te magnitude of the incompa tibili ty effectgives a concrete point of departure for determining otherfactOI's quantitatively. The second step Wal,; then to examinethe possibilities of selective factors illvolving the gene B; amore speculative malter, not necessitated by known incompatibility, but "trongly sugge"ted by the apparent mannerof di ffusion of the B gene aud the lack of randomness betweenB freqnencies and A and 0 frequencies.

A HYPO'i 'lIESI8 HASED ON SELECTIONTn constructing a mathematical lllodel to account fo r thelimi ta tiOllS on exi sting A-B-O gene formulae, the basic as

sumption will be made that the present world range of distribution is in equilibrium and that no effects due to thecomparn tive recency of occu nence of anyone gene ar e evideut. 1 1 ~ v e n if B, fo r instance, is actually a "newer" gene, wewill a:,;Sllme that it has ha d sufficient time to produce all thevarious percentage combinations with A and 0 that it is likelyto form. 'V e are assllmiug, theu, that th e distribution isessentially a permanent one and that it s outlines will remainthe same though in a sllf:ficiently great length of time indi-vidual groups within it may shift. A corollary is that nodeduction can be drawn from the mathematical model as tothe greater age of any gene.

The mathematical model must satisfy several requirements.It must be such that the action of selective factors on an ygroup located outside the present world range is such as tochange that group's gene frequencies in the direction of amore normal ratio. The marginal groups will probably be(and, in fact, generally are) small and isolated groups inwhich genetic drift is snch as to defy selection to some extentin an erratic fashion. The magnitude of the selective factorsmust be such that th e "inward" trend is approximately thesame at all points along the borders of the distribution. I t

SELEC'l 'lON IN DLoon GROlTPS

was not considered sufficient to have a general illward trendtowards a central point suitably IDeated; th e selective factorsshould also account fo r the fact that the range of the A geneis less where B is high than where it is low. No attempt hasbeen made to establish the absolute magnitude of selectivepressure necessary to block genetic drift for praetical pur-poses and form a "border" fo r the world distrilmtioll. Thisis of course a relative matter, since ill bmaller populationswith greater genetic drift a group may extend further fromth e center against selective pressure than if it were morepopulous; one might picture a distrihution of blood groupgene fn'quencies of the human speeies iu Paleolithic timeshaving a fa r wider and more diffuse range than at the presenttime. Iffort was therefore concentrated on ohtainillo' correct.=,relative values of selective pressure at various points, anddemonstrating that the shape, not merely the general location,of the distribution eould he accounted fo r by some sort ofgenot ype selection.

ProcedureThe first step in deriving a mathematical model fo r selec

tion e f f ( ~ c t s \vas to se t dowll th e fre(wencies of tIw (j genotypesof the A-B-O system fo r each of Hie 50 combinations madepossible by varying the gene frequencies in 100/0 steps. Thevalue of OA in each s q u a l ' ( ~ was then adjusted downward torepresent the survivill'.\' OAs in a succeeding generation afterthe elimination of 25% of OA zygotes ill 00 mothers. Thisreduction is of course most marked in the presence of highfrequencies of the 0 gene. rrhen each square was ready forth e determination of the direction and magnitude of selectionpressure which would affect it if th e various genotypes hadsomewhat different DUrvival values. Since the survival valuesof the various genotypes would have meaning only in relationto one another, it was decided to assign a neutral value tothe abundant genotype 00, leaving only 5 variables. '1' hesurvival values of the other genotypes were designated inplus or minus per cents; minus 5% meaning of a particular

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57776 ALICE M. lJHUEStype that 57

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579578 ALICE M. BRDEShave all outstanding positive value to counteract the fetal lossdue to incompatibility. AB was at first set quite high as itwas considered to represent the principal selective advantageof the B gene; this later proved untenable.

EQuilibrium of 0 and A genesIn an arrangement of this kind there will normally be 4

points of equilibrimn (exclusive of the cases where only onegene is present at all). Three of these represent cases whereonly two of the three genes are present; th e 4th and mostcomplexly determined will be the equilibrium where all threegenes ar e present. The addition of the factor of incompati-bili ty introduces anothpr variable, however, which follows lawssomewhat different, and gives rise to the possibility of stillanother equilibrium point on the O-A axis. rrhe incompati-hiliiy loss, as previously mentioned, is not a fixed fraction ofthe n u m b c ~ r of OAs in an y population, since the number ofOAs subject to the risk clepends on the ratio of 0 0 to othergenotypes among the mothers. I f we ar e considering the O-Aaxis only, wc find that th e incompatibility effect ranges froma loss of 12.570 of all OAs where gene 0 equals 99%, to anegligible loss whel'e gene 0 equals 1ro. '11he compensationintroduced by straight selection will he a fixed fraction ofthe number of OAs llresent at an y lloint (in calculation thiswas considered a fixed fraction of th e number of OAs leftafter incompatibility loss, not of the number pre,;ent beforesuch loss). Therefore, if the effect of straight selection isplus, and between 12.5 and 0%, it will overcompensate atsome frequencies of the gene A and ulldercompensate atothers. vVhere it overcompensates, the vectors will be directedtowards 50% A gene, since the heterozygote will be at anadvantage, and where it undercompensates the vectors willbe directed away from the 50% point.

This produces a very interesting series of possibilities.Overcompensation at all levels (selective advantage morethan 12.5%) would tend to shift al l groups towards 50%

SELECTION IN BLOOD GROUPS

A gene. Undercompeusation at all levels (selective advantagezero or less) would tend to shift groups centrifugally towards100% A geml or 1001'6 0 gene. I f the selective advantage justbalances incompatibility whe1'e the A gene is 50%, the areabetween 10070 and 5070 A gene will be overcompensated, withvectors consequently directed towards 50;10 A gene, an d thearea between 5070 an d zero A gene will be undercompensated,with vectors directed down towards zero value of the A gene.In this case the A gene will progressively be eliminated, witha slight reprieve just at 5070 A gene, a precarious equilibrium.

1'ABLE 1Vectors produced by incompatibilit!l loss of 0.1 (850/,,) comb ined with selective

advantage (10%) of surviving OAs whe"e 0 and A are the onlygenes present in the popillation

~ ' Oll' A GENE IN 'l'HE I'OPULA'J'lQN10 20 20 40 50 60 7U dU 90

Vectol' (changeper generationin frequency ofA gene in %) - .16 - .10 +.01 + .07 0 - .22 - . 4 7 - . 7 9 - .63

The most complex result will ensue if the point at which selective advantage balances incompatibility loss lies between 10and 40%, or between 60 and 90% A gene. This will producea reversal in direction of vectors at the point of exact compensation (transition between over and undercompensation);moreover, it produces a reduction of vector values an d consequently an alleviation of selection pressure ncar the pointwhere the direction of vectors changes. This phenomenon canhardly be described without an example. In table 1 are givenvectors based on incompatibility loss combined with selectiveadvantage so that the two factors balance at approximately30% A gene. ( I t is assnmecl that the B gene is not present.)I t is interesting to note the slightness of the vectors, all infractions of per cents, despite the magnitude of the interactingfactors. ~ l ' h i s vector system produces a range from zero to50% A gene where selective pressure is relatively small, and

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580 ALfCE M. BRUESwould allow considerable genetic drift of populations. I t willbe noted that there ar e three points of equilibrium; one atzero A gene, with a vector slope leading towards it ; one at50% A gene, with vector slopes leading towards it from bothdirections; and one at 30% A gene, with slopes leading awayfrom it in both directions. I t will be seen that the latterpoint, though an equilibrium, is a precarious one from whicha group might fall away in one direction or another; howeverthe vectors involved ar e so small that genetic drift mightfrom time to time push groups over it s hump to the otherside. The final tendency would probably be to produce asomewhat bimodal distribution with concentrations at zeroand 5070 A gene, but always a certain numher of groups inhetween.

Table 1 presents a picture consistent in general outline withthe maintenance of the world distribution as regards populations in which the B gene is nearly or entirely absent. Thealternative vector schemes described above which would tendto produce standardization at a 50% level of both genes, orbreaking down of populations into a predominantly A divisionan d a predominantly 0 division, are quite impossil)le _ unlesswe accept the ( ~ hoc hypothesis that one or the other gene is"new" an d that a state of equilibrium has no t been reached.The vectors of ta ble 1 however could provide stabilization ona permanent basis; since the weak vectors between zero an d501'0 A gene would allow a scattering of groups throughoutthis range, ,md the much stronger vectors above 50% A genewonld keep that area unoccupied. There ar e imperfectionsin this picture, however; there is not really an optimum pointor accumulation of populations at 50% A gene; this is ratheran extreme. The real center of the distribution along the O-Aaxis is more nearly at 30% A gene; the small numher ofgroups near 50% seems to indicate that some countering ofselective pressnre is necessary to reach that point. Yet it isnot easy to shift the upper end of ou r bimodal distributiondown. I f there is an y degree of undercompensation at 50%A gene, tending to push A values down, this effect will be

SELECTION IN BLOOD GROUPS 581present all the wa y down to 100% 0 gene, and the selectiveplateau of weak vectors which served to explain the widespread of population gene frequencies from zero to 50% Ahas vanished.

This dilemma can be avoided if a negative value fo r AA ishypothecated. 'J'his possibility has already been suggestedas a deduction from the average levels of th e A an d 0 genesin the species. A negative selective value for AA will reducethe A gene differentially with the greatest effect where theAA g e n o t y p ( ~ is commonest. I t wa s found possible by increasing the positive value of OA ahove that previously set, andintroducing a negative value fo r AA, to produce a minus-A

TABLE 2Vectors produced by incompatIbility loss of 0.1 (2.5%) combined with s e l e c ~ ' i v e

advantage (15%) of surviving OAs and se1eci'ive d'isadvantage (6%) of AAs, where 0 and A are the only genes pre"ent ,in the popll.lation

% OF A G K N } ~ IN ' . r H ~ POPUL_-\.TION10 20 :JO 40 50

Vector (chn.nge per generationin frequency of A gene ill %) +,10 +.14 +.03 - ,26 - . 7 4

vedor at 50% A gene and at the same time rctain th e flatnessan d lack of strong vectors at 10-300/0 A gene. 'With the selective value of OA increased to plus 15 % (which by itself wouldresult in a piling' up of all populations by strong vectors at50% A gene) aud a selective valnc of AA set at minus 6 ; ; ~ , the vpetors of table 2 ar e produced. This was considered al'easonable vectol' system to explain the present range ofgene frequencies in populations having the A and 0 genesonly. In view of the approxirg.ateness of the iigure of 25%for incompatihility loss, w h i c l ~ is involved in all vectors, itwould he supererogatory to attempt to refine the mathematicalmodel further.

Equilibriwn of the B geneIn regard now to the B genotypes, it might be asked whether

it is necessary that they also should have a selective value.

- -- - ~ - - - - - - - - - ; : - - - - ~ " ' " ~ .

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582 ALICE M. BRUESIn a sense this question is meaningless; if 00, 011. an d A11.have different valnes nle 13 genotypes cannot he the sameas al l three; they must be placed somewhere on the scale, andt h e n ~ is certainly no necessity for them to be at that arbitraryzero point which was deilned as equal to the snrvi\Tal rateof the 00 genotype. The question then resolves itself into twoparts: are the 13 genotypes identical with one another inselective value an d where are they located on the scale formedby 00, OA, and 11.11. 1 \Ve can assume that the B gene, in somecombinations at least, mnst be better favored than 00, orelse it could not establish itself at all except where the genotype 11.11. is abundant; a picture not corresponding to theworld distribution. I t sC'ems impossible to make BB equalto 01' superior to the heterozygous B genotypes, since thenthe gene B, if estahlislled at all in the heterozygous form,would rapidly prog;rcss towards a 100% frequency, Bu t ap parently the frequency of the B gene, like that of the A gene,is self-limited. So we have little cllOice but to assign plusvalues to OR an d AB, an d a minus value to BR , On thishasis quantitative, vat'iations were tested until a pattern ofvectors for llOth A and B genes, consonant with the limitsof tile world distributiOll, was obtained,

At first the attempt was made to attrihute most of thepm,itiYe selection of the 13 gene to a high survival value ofAB, and to keep' OB "down" in survival vaIne, in order toaecollIlt for the rarity of good development of the B gene inpopulations where the A gene is rare, This proved to havethe effect, however, of encouraging B to the greatest extentwhere A was at a high ratller than at a moderate level. I twas tinally decided that the principal effort would he elevatedto obtaining a suitable vector pattern in the range in whichall three genes we,re represented, and let the separate interactions of tlw 0 awl 13 genes come out as HlPY would, Successive approximations were made by a process of enlightenedtrial and error, finally resulting in the system of which thevectors are shown in table 3 an d figure 2, This appeared tolw about as satisfactory as could be obtained without defining

. ""

SELECTION 11'1 BLOOD GROUPS 5 8 ~ ~

I t Ig 00rl

00;;' I 0 t- l0'"." I" j'+>Ga

~ l ;.-;;.. ;;..;;.. ;;..> t ?-;> >:.> ; o

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--

585584 ALICE M. BRUESsUl"vival values in fractions of pe r cenUi. One comment shouldbe made; if the survival factors of all th e g'enotypes, exclusive of the basic plus value of 1070 fo r OA which counteractsincompatibility effects, were to be changed within moderateli111i ts in proportion to one another, the vector pattel"ns wouldremain approximately the same except that th e magnitude

PER ((NT OF GUH A10 10 )0 7>- ..------- /"/.--- ".---- /,." " "0 . " " , "0 > '- .-

. " ".J ..0 '\ T /T " " so

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ALICE M. BRUESmanipulation of the quantitative value of selective factorsexcept at the cost of disrupting the successful parts of thevector system. Along the O-B axis there is found one outlying group in square 30 (the Caraja Indians of Brazil) whichon first examination was thought to be possibly an erroneousreport. Perhaps they actually represent a unique achievementof O-B equilibrium in the absence of A. (T o say this is toadmit that" newness" of genes is involved, that certain combinations have not been fully exploited, in contrast to Ourprevious statement of principle.) Bu t such an isolated development of the B gene, might very well be a comparativelynew independent mutation. The principal upward vectorsof B ar e at low A levels (squares 11, 12, 21) an d at high Alevels (squares 17, 18, 19, well outside the limits of recordedpopulations). The greatest weakness of the vector systemis in squares 21 and 31, where we would wish to see strongerplus-A vectors to account fo r the lack of populations there.'Ilhe vectors in sqnare 31, fo r instance, ar e by no means strongenough to account fo r the fact that this is an "empty" areaon fignre lb . Other marginal empty or nearly empty areassuch as squares 42, 14 an d 5, have considerably strongervectors. SOME HISTORICAL CONSIDEHATIONS

'I'he absolute magnitude of the vectors, as we have saidpreviously, cannot be determined in any a IJriori fashion; thepattern here shown could be essentially retained by a systemin which al l vectors were greater or al l less. However, it isinteresting to consider the magnitUdes suggested here, andsee whether they ar e seriously inconsistent with historicalprobabilities. Any such vector system as we have proposedwill be always interacting with genetic drift. Small or isolatedpopulations will be continually scattering as the result ofdrift, bn t in more copious populations (of the magnitudeof most European groups in the last millenium, or of thelarger sedentary groups in Asia an d Africa), genetic driftwill be quite ineffective, an d selective pressures will act withgreat constancy. (A n interesting analogy may be made with

- . - - - - : - - ~ - ~ " ; : : ; : : - = ~ ~ = - : , , ; ~ ; _ : ; : - : ~ , _ : c , , _ , : " " . _ - : : : - : : - ~ ~ ~ " " ~ ' 7 ; : : . : = : : ; = = ~ . _ __

SELECTION IN BLOOD GnOUps 587the respective effects of Brownian movement and gravity onsuspended particles of different sizes.) All such populousgroups should then tend inexorably to move towards the finalequilibrium point at about 25% gene A and 1510 gene B. Isit then possible fo r groups of this magnitude to be at thepresent time as different from one another as they now are,in view of this selective pressure ! Most of these major popula tion groups, \Yhite, Mongoloid and Negro alike, ar e locatedin squares 12, 13, 22 an d 23, with very low vectors. In square13, the typical location of most North European populations,the vectors are minus .0510 fo r the A gene and plus .10% fo rthe B gene. 'l'wentieihs and tenths of one pe r cent do notmake fo r very rapid changes, particularly in a species whichtakes a century to ru n through 4 generations. A group underthe selective pressure at square 13 would require 2,500 yearsto change it s frequency of the B gene by 10% an d its frequency of the A gene by 5% - provided the vectors remainedconstant. (The vectors actually would decrease as the groupapproached the central equilibrium point.) The magnitudeof the time factor here seems adequate to indicate that thepresent divergencies of the majOl' population groups couldbe explained as vestiges of more marked peculiarities in thepast, which ha d developed du ring the period when the ancestors of even our largest modern populations lived underconditions of low population density which favored geneticdrift. Such population densities need not be less than thoseof the Pre-Columbian New \Vorld, in which scatter due togenetic drift is very evident. I f we assume that the Old \Vorldhas overall population densities of this same magnitude up tothe beginnj.ll,g of the Neolithic at least, the primitive conditionof wide random range of blood group frequencies is not toofa r in the past to account for the diversities of the now morepopulous groups, even though constant selective factors mayhave been standardizing blood group frequencies since popula ti on levels increased. In contrast to the extreme slownesswith which selective pressures would act in the "occupied"area of figure 1, ar e the high vectors for other parts of the

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589588 ALlCE M. BRUES SELECTlON IN BLOOD GROUPSrange. A population located in square 9 (that is, an A population which had acquired lOre of the gene 0) would take only1,000 years to reach square 4, under the strong selectivepressure to which it would he subjected.

Another interesting problem in constancy of values is presented by the oft-rited case of' the similarity in hlood-groupf r e q u e n c i t ~ s of' Gypsies and Hindus, after long separation.Coon states that th e sepnration is of approximately 1,000years standing. I f the Gypsies started at square 31, withthe vectors there assigned, in the course of 1,000 years theywould, if selective pressure alone was acting (though undoubtedly genetic drift would have played a part also) havechanged to the extent of 6.8% in the A gene and 2A7c in theB g'ene; by no means enough to equatc, them with the Hungarians, with whom they ar e always compared, or otherEuropean populations. Incidentally, the group from ~ w h i c h they separated would have tended to change cOlTespondinglyin the same length of time; so that similarity of fractions ofa group 101lg separated is uo evidence against change in bloodgTOUp frequencies iu time, if the changes ar c determined byf a c ~ t o r s intrinsic to the genotypes.Another case which tests the magllitude of the vectors isthat of' the Blackfoot Indians, who, according to our vectorsystem, are presently in a position where selection alonewould tend to reduce their percentage of the A gene hy 1 rope r generation, or 10ro in 250 years. vVhether their situationis a plausible one will depend on the extent to which geneticdrift hns been able to nct on them in the past. In an y event,they would represent an extreme case. The tribe, accordingto Chown and Lewis ('53), consisted of about 10,000 membersin the 18th century; a hundred years later their numbers weregreatly reduced; how long previously they had held a highpopulation level is not known. In a group of 10,000 geneticdrift is no t very effective; each generation's sample of 20,000genes would reproduce the previous generation's percentageswith a probable error of only .240/0. This would make it diffi

cult fo r the selective vector, three or 4 times this magnitude,to be reversed or neutralized fo r even a generatioll. I f thepopulousness of the Blackfoot was not of long standing, andif the tribe had arisen by rapid breeding up of a small genetically drifting group, an u m ~ s u a l run of luck fo r the A genecould have placed them in the position they now hold. Sincein fact they are an extreme group out of many, they are e11-titled to a submarginal prolmbility. All these cases sugge"tthat the magnitude of the vectors here proposed is no t impossibly great, though perhaps somewhat too large.

IThe vector system then seems to be satisfactory according

to the requirements originally sCet up fOl' it. I t demonstrntesthat it is possihle to explain the overall range of blood g'l'ClUPgene frequencies found in the human species by the action ofselective fadm's inherent in the hlood group genotypes themselves. Some readers may I'ightly conclude that the apparentlimitations on th e range of human blood gronp gene frequencies do no t require coxplilnation, or at least do not requireexplanation so hadly that we must be forced to leap intosuch extremely hypothetical mathematics to solve the problem. However, the dulJious and fictitious chnracter of thehypothesis pre"ented here makes it all the better companyfor various other entirely unprovable theories regarding theorigin of the present A-B-O frequencies. At least an attempthas been made to make the system as fa r as possible absolutean d no t contingent; we have rejected, for instance, li'ord'ssuggestion that the maintenance of somewhat different A-B-Ofrequencies in different races is due to differences in otherfeatures of the jgenetic makeup, ,\'hieh canse the hlood groupgenes to reach\ slightly different points of equilibrium indifferent races. An d of course, 110 consideration has becngiven to the possihility that the various blood group phenotypes ar e of different sclective value in different environments.Anyone who wisl1es to introduce t h ( ~ s e possibilities can nodoubt fit a scheme to the facts fa r 1110re closely than we havco,since he will be under no limitations whatsoever.

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590 ALICE ,VI. tHIESExtralJolation toward the ongw of the genes

I t is clea ' from an examination of the vector system thatunder snch rules the range of values finally attained by th ehuman species will be the same regardless of whether allthree genes were present in the basic human population(whatever and whenever that was) and of what order theyappeared in, if they appeared at different times. rrhe sameconfiguration could be reached by starting from A or B asfrom O. There has always been an inconsistency felt betweent l l ( ~ average frequencies of the A-B-O genes in man, whichcertainly indicates 0 as the most likely original gene, and thefact that A is the only gene common to ma n and all 4 of thegreat apes. So it will be interesting, by wa y of examiningpossible ways in which selective vectors might function, tochoose as an example the case in which A was the originalgene. The historical reconstruction would run somewhatas follows: An all-A population would be extremely vulnerableto change if either the 0 or the B gene became established,hecause of th e selective advantage of OA an d AB over AA.(The term "became established" is used advisedly. Evenin the presenc.e of selective advantage, a gene may not survivethe first generations following its appearance. The likelihoodof successful establishment of a gene - a bridgehead thisside of oblivion, so to speak - will be much less than themutation rate.) I f a mutation to gene 0 occurred in th e Apopulation, it would, after becoming established an d goingthrough the slow early stages of increase to a level of 10/0,have a vector of plus .21% per generation which would continually increase as gene 0 became more abundant. Theselective advantage of OA would be very great at first sinceincompatibility effects would not appear until 00 genotypeswere encountered with some frequency. Two hundred andfifty years would then be required to bring th e 0 gene upto 5%; 100 years to carry it from 5 to 10%; an d 1,000 yearsto take it to 60%, where some population units would heginto hesitate and lag as genetic drift countered the lesseningselective pressure. There would be, that is, a sudden brealc

SELECTION IN BLOOD GROUPS 591in a stable condition, very rapid change for a period, and thensettling down in a new equililJriurn.

I f the first mutation to become established in the originalA population were B, the course would be similar, but withthe rate of reduction in the percentage of A less rapid. Aslong as the A and B genes only were present, the tendencywould he towards an equilibrium in which th e B gene wouldLe slightly in excess. At an y time, however, the introductionof 0 would cause the trend to turn towards the final equilibrium point at 15% B gene. I f the 0 gene did not appeartill B bad become commoner than this, there would be a stageof decline in hath A and B.

I f 0 was the first mutation from A, then B became established probably in some population with both the 0 and j genes. I f the establishment of B was at all delayecl, it wouldprobably no t occur until some populations were ncar 0] 'beyond 60'ii1 0 gene. 'l'he vectors in squares 14 to 17 are sostrongly downward for A an d so slightly favorable to B thatany groups in this area would be rushed through towards 0with little opportunity to stray upwards in B. '1'hen the mostlikely opportunity for 13 to develop - i.e. the strongest upwarclvectors for th e B gene - would he in gronps which had reachedSO or 90% 0 gene. Since the consensus of distributional evideuce is that tbe B gene, at least the earliest and most successful establishment of it (leaving aside local developmentsfrom scattered B mutations) is later than the 0 gene, it seemsmost likely that it got it s start in low-A fractions of a worldpopulation already well diversified in O-A frequencies in aboutthe range now found. These first O-A-B populations couldbe "proto-119ngoloids.' ,

A "polyph.{ylctic" interpretation is also possible; the 0 and13 mutations Tllay have originated in populations whicb werefo r a time isolated from one another, producing two maindivisions; an A-O division, and an A-13 devision; either orboth ma y have gone to their respective equilibrium pointsi at some time, then come in contact with one another later.j Th e A- B strain could be designated "proto-Pre-Dravidian

1\

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592 ALICE M. BRllES SELECTION IN BLOOD GHOUl'S 593and-Ainu." Th e hasic difference between the latter two possibilities is whether, of the present high-B groups, the Mongoloid or nOll-Mongoloid contrilmted the B gene.

Further detailed speculation on the basis of such a tcntative scheme would be out of place. Numerous developmentswill nndoubtedly necessitate the revision of any values fo rselective effect guessed at now. 1\[ore careful examinationma y reveal other incompatibility reactions which would replace 01' modify th e selective values now proposed. '1'he magllitude of the incompatibility between A an d 0 ma y be betterdefined in the future. The degree of complication which ma yresnlt in these matters is shown by the demonstration thatincompatibility between parents in the A-B-O system affordssome degree of protection agalust the development of hemolytic disease in response to Rll-incompatibility in the samefami ly (Levine, '43). 1 this phenomenon can he accuratelydefined it ma y contrill11te also to the selective patterll, in away correlated with the Rh-gene composition of the populationin qnestion. Another probability is that the various subtypesof the gene A, which differ in the vigor of their serologicalreactions, may well differ also in the degree to which theyar e affected hy incompatilJility or other selective phenomena.Possibly the only permanent contribution of snch a prematurellypotbesis as presented here will be to poiut ont that an ysystem of selective factors of whatever kind must eventuallybe consistent with the limitations of the world range of A-B-Ofrequencies. Once the hypothesis of absolute non-selectivityof the A-R-O blood groups has been abandoned, throughnecessi ty or choice, even if ill respect to one genotype only,we must assume that the genes ar e in a state of dynamicequilibrium, an d that the world range of frequencies in respectto the A-B-O genes is an essential piece of evidence in ascertailling' this equilibrium.

DIRECT STUDY or' A-HO SELECTIONNumerous attempts have been made to demonstrate selective effects with respect to blood groups by statistical means.

The possibility of differential slll'vival in the pre-natal periodhas already been approached by study of the precise frequencies of children produced by mating'S of various types.In th e case of the A-B-O blood groups difficulty is introducedby the fact that the genotype AA cannot be distinguishedfrom OA, or BB from OB. If selection is such as to favorheterozygotes over homozygotes, the selection effects willtend to cancel out, as fa r as phenotype is concerned. In thecase of the 1I-N blood groups, where all phenotypes ar eimmediately distinguishable, very. strong' evidence of differential survival of the heterozygous embryo (about plus 20%)has been adduced by some workers. (li'ol' an excellent accountof this and other selective effects of blood groups, see Raceand Sanger, '50; also Race, '50)." However, these results havebeen challenged by other workers as due to constant errorsin technique. The possible scope of such errors, as claimedby immunologists engaged in disputes with one anotherC\Viener, '43), is very considerable and somewhat disillusionin g to the anthropologist. Thus an y selective deviations ofth e magnitude which we have hypothecated ar e likely, evenif detected, to be challenged for a long time in the immunological field, where the anthropologist is no t properly entitledto take sides.

The question of postnatal mortality differences presentsother difficulties (aside from the confusion of homozygotesand heterozygotes). "Mortality rates and causes in civilizedpeoples ar e very different from those of primitive and prehistoric peoples, an d we cannot assume that an y differentialmortality rates which were effective through most of thehistory pf the race ar e still effective at the present time. Infact, with mortality in the age period 0-35 years reduced tolittle more than 5% as compared with a probable 5070 ormore in former times, it can hardly be said that differentiallllortality, as fa r as it affects the production of the nextgenera tion, exists at all among civilized peoples; an d selec

3 As this goes to pl'ess, Neel ( '54) has pnblished :l paper in which th e mostrecent work on this suhject is ably summarized.

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594 ALICE M. BRUEStion cannot ac t in the absence of mortality. Any study ofdifferences in blood group freqnencies at different ages ina modern population, then, can hardly show appreciablechanges with age except in the older age groups from whichsome proportion of individuals have actually been eliminated;and even here the mortality causes involved ma y be totallydifferent from those which decimated the youn g and adolescentin prehistoric times.

Still another way in which selective effects might be exercised is through differences, not in individual survival, bu till fertility. Obviously a slightly higher fertility of an yA-B-O genotype will have the same effect on the gene frequencies of' the next generation as if more individuals ofthat genotype were pnesent and reproducing at average rate.The possible complexity of this sort of selection is shown(Bryce et al., '51) in a study suggesting' that the genotype ABis produced in slightly less than expected ratios by A an d Bmothers, bu t that the surviving AR s (a t least if female)reverse the effeel by their higher fertility. Obviously theselective resultants can be very complicated, and require lUllchstudy,

I t ma y be adequately argued that the present paper ha snot clearly proved that the A-B-O blood group genes 'areselective. However, it may be pointed out that neither hasanyone ever proved that they are no t selective. Early inthe history of the stuely of blood groups, it was decided withfairly universal concurrence that the hlood group genes ha dno selective value. When analyzed, the reason for this decision appears to be the rather a pr'iori one that since theagglutinogens of the blood did not come into any very obviousor direct contact with the external environment, they did no tseem to be the sort of thing that would be selective. By continuous repetition this assumption has attained the statusof a dogma, so tha t the entire burden of proof is placed onthose who venture to contest it. In part even the dogma hasbeen cherished as a weapon in a faintly personal contestbetween those specially versed in immunology an d others

SELECTION IN BLOOD GROUPS 595specially versed in other branches of physical anthropology.Altogether too many statements about the selectivity or nonselectivi ty of varioulO traits have been preceded by the deadlyphras(, "of course." I t would be more advisaLIe to keep anopen mind on all such matters, and let the burden of prooffall equally on both pm'ties to the contest.

S1TMMAl1Y OF TI-IB; ARG1'MENTI t is pointed out that the frequencies of the A-B-O bloodgroup genes, which vary considerably among various human

races and subraces, are nevertheless suhject to certain limitations, Of the total possihle range of variation, only aboutone-fifth is found to be occupied by hl1man groups now living.rrhose areas of the range representing- less than 5070 0 gene,or an excess greater than 1 0 ~ ~ . of the B gene over the A gene,ar e ouly marginally OOCl] pied.

The traditional view is that a complete lack of selectivevalue on the part of the A-B-O genes has made possible themaintenance, from the time of inception of the species, of abasic gene formnla which ha s developed a moderate degreeof diversity but has never varied radically from its originalproportions.

.A suitable explanation for the origin of some diversity infrequency of the A-B-O genes has been seen in tIle workingsof genetic drift, by which entirely randorn factors may producealteration of gene frequencies, especially in small populations.Examples of this phenomenon ma y be seen in the diversity ofblood group gene frequencies within subgroups of a givenrace.

jA certain paradox becomes evident, llOwever, when the evi

de1"rtle fo r genetic (hift is examined carefully. '1'he moststriking case is the variation in frequency of gene A withinthe ahoriginal populations of North America. These tribesinclude examples of A gene frequencies which are absolute

1 maxima aud minima for the human species. Yet these groupsj ar e certainly racially al,in to OIle another wi thin the limitsallowed to major races, and can hardly be considered to con-

I1j = - - " : : ; ' : ; ; - ' - ~ : ; : : : ' ~ ~ ~ ~ 3 ' ' : - - . , " - " , = , " " , = ; ; ; = ; ; ; = = = = = = ~

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596 ALICE M. BUUESRtitute an "old" raee in the sense that they have had a maximum length of time in which to develop A-B-O gene di:fferencesby genetic drift. I f genetic drift ha s acted so strongly ona relatively local basis and during a limited time, why hasit not produced even more Rtriking diversity in the ~ p e c i e s as a whole during the entire period of it s evolution'? I t is, therefore suggested that positive factors of some sort actil to re:strict variation in the freqmmcies of the A-D-O hlood

. group g'enes, so that increase of time and opportunity doesnot allow genetic drift to go heyond certain limits.Since a reasonable explanation fo r such a limitation is the

If existence of selective factors discriminating against certainIi gcmotypes (in this case prohably the homozygous types AAand BE), the idea of a halanced selective system maintainingA-B-O gene frecllwncies was entertained.I C ~ n s i d c r a t i o n :vas also given . to evidence that t ~ g C ~ l O t y p e \ AO lS acted agamst by some form of maternal-fetal lllcompatibility. :FJxamination of the ultimate effects of such aplllmornenoll emphasizes the fact that the pl'('sence of a singleseleetive effect al l any olle of the A-B-O genotYIJes wouldintroduce a disturbing factor into the whole system such thatconnteracting seleetive effects Ol l the same or other genotYReswould be necessary to maintain stahility of gene frequenciesfor any length of time.

I t appears to the present anthor that t J ~ e r e is no middlegronnd between the doctrine of complete non-selectivity asan explanation fo r the persistence of a heterozygous condition

. for many millenia, and the alternativeUloctrine of a dynamiI cally balanced set of selective factors which maintains the! diversity of the gene formula within certain limits. I f nonselectivity breaks duwn at all, it hreaks down completely.On the basis of the e v i d e n c c ~ above it is concluded that thelatter doctrine must he held.

On this hasis experimental calculations were made, to showthat a system of balanced selective effects could be made toexplain in some detail the limitations on the present rangeof A-B-O gene frequencies. I t is shown that on this basis

SELECTION IN BLOOD GROUPS 597gene A, which is common to a.ll the highest primates, COUld)'very well have been the original blood group gene of man.

LITERATURE CITEDDF,KNETT', J. R. , AND JANE DRANDT 1954 Some mol'C eXRct tests of significance

for 0-,1 matenJal-fetal incompatibility. Ann. Eugen., 18 : 302-310.BIRDSELL. J. E. 1G50 Some implications of the genetical concept of race in

terms of ,patial analysis. Cold :Spring Harbor Symposia on Qnantitative TIlology, 15: 259-3]4.

BOYD, ,VILLIA1[ C. 1947 The use of gonet ieally determined cha radel'S, especiallyserologi(:al faetol's sHeh as Hh, ill physical anthropology. Southweste rn,T. A lIthrop., 3: 32-+9. Heprinted in Yearbook of Phys. Anthrop., 1947:2 1 2 - ~ 2 9 .

1950 Genetics Bnd the Races of Man. Boston. 1950.BRYCE, LllCY .M., It. ,JACOBOWICZ, )i . MACARTHUR AND L. S. P ~ N R O S E 1!Jf\1

Blood'group frequencies in a mother and infant sample of the Ans.tral1all populntinn. Ann. :Eugen" 15: 271-275.C I I O W ~ . B., AND M,'RION LE'WIS 1953 The ABO, II1NSs, P, Rh, Lntheran, Kell,

Lewis, Dnffy and Kidd blood gronps and the secretor 8ta1,s of thenJackfoot Indians of Alberta, Canada. Am: J. PhyR. Anthrop., 11:369-384.

COON, C. S. 1939 TIle Races of Europe. New York.DOBZHANSKY, THEODOSIUS 1941 Genetics anil thc Origin of Species. 2nd cd. rey.

New York.1950 HlIman Diversity allil Adaptation. Cold Spring HarllOr Sym

posia au Quantitative Biology, 15 : 385-400.FORD, E. H. 194: ] GQn