The Biology of Stupidity: Genetics, Eugenics and …...eugenics movement from the early 1920s, if not earlier.4 The paper falls into four parts: the first looks at the emergence of

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The Biology of Stupidity: Genetics, Eugenics and Mental Deficiency in the Inter-War YearsAuthor(s): David BarkerSource: The British Journal for the History of Science, Vol. 22, No. 3, Genetics, Eugenicsand Evolution: A Special Issue in Commemoration of Bernard Norton (1945-1984) (Sep.,1989), pp. 347-375Published by: Cambridge University Press on behalf of The British Society for theHistory of ScienceStable URL: http://www.jstor.org/stable/4026901Accessed: 01-08-2017 18:43 UTC

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BJHS, 1989, 22, 347-375

The Biology of Stupidity: Genetics, Eugenics and Mental Deficiency in the Inter-War Years

DAVID BARKER*

INTRODUCTION

It may be thought that the title of this paper betrays a regrettable lack of sensitivity and good taste; it is as well, therefore, to explain its origin. Lewis Dexter was, I think, the first sociologist to apply a deviance perspective to the high-grade mentally retarded.1 'On the Politics and Sociology of Stupidity in Our Society' argues that our discriminatory attitudes to the retarded have deep ideological roots; our social institutions tend 'auto- matically' to penalize stupidity; and repugnance often characterizes our face-to-face interactions with the stupid. The pejorative label 'stupid' was justified precisely because identifying the stupid is a 'commonsense' rather than a scientific process, although commonsense does not have long to wait before it is bolstered by science.

In discussing the biology of stupidity, I am not suggesting that Dexter was wrong to treat the labelling of the stupid as a socio-political process, or that there is, invariably, a biological difference between 'normals' and 'defectives' which labelling theory ignores. Instead I want to examine how this socio-political process was buttressed by a theory which held that the mentally defective are genetically different from the rest of 'us'.

Although the theory was first elaborated shortly before World War One and slipped gradually from favour during the 1930s, the issues raised are not exclusively historical. Its critics, geneticists such as Haldane and Hogben in England and Morgan in America, were clear that they were confronting not just mistaken or bogus science, but a powerful socio-political doctrine, which treats social inequalities as rooted in man's biology and 'therefore' as inevitable and immutable.2 Recent work has drawn attention to the con- tinuities between successive forms of biological determinism, from nineteenth-century craniometry and Galtonian eugenics to the sociobiology of the 1970s and 1980s.3 This paper considers one phase of this movement.

It has two further aims. The first is to sketch the relationship between the genetic theory and the politics of mental deficiency. Far from being an abstract exercise, the theory was developed, elaborated and challenged during a period in which the problem

1 L. Dexter, 'On the Politics and Sociology of Stupidity in our Society', in H. Becker, The Other Side, New York, 1967, pp. 37-49.

2 See, for example,J.B.S. Haldane, Heredityand Politics, London, 1938; L.T. Hogben, Genetic Principles in Medicine and Social Science, London, 1931; T.H. Morgan, Evolution and Genetics, Princeton, 1925.

3 See, for example, S.J. Gould, The Mismeasure of Man, Harmondsworth, 1984; S. Rose, L.J. Kamin, R.C. Lewontin, Not in our Genes, Harmondsworth, 1984.

*Department of Social Policy and Social Work, University of Manchester, Manchester M13 9PL.


348 David Barker

of mental deficiency was politically contentious; it was used to justify coercive social

policies such as complusory segregative detention, often life-long; sterilization, volun-

tary, semi-voluntary and compulsory; and immigration control. Eugenic concerns were

prominent on both sides of the Atlantic. Second, I want to explore some aspects of the

relationship between geneticists and the eugenics movement during the inter-war years.

One way of addressing this question is to focus on how geneticists responded to the gen-

etic theory of mental defect; when this is done, I argue that we may reasonably question recent orthodoxy which holds that geneticists became increasingly disillusioned with the

eugenics movement from the early 1920s, if not earlier.4

The paper falls into four parts: the first looks at the emergence of high grade mental

defect as a social problem; the second expounds the genetic theory of mental defect; the third offers a critical analysis of the genetic theory, using criteria by which contemporary geneticists could, or should, have judged the theory; the final section reviews the recep-

tion of the theory from 1914 to the mid-1930s, by the scientific community, particularly

geneticists, in America and Britain, and interweaves this review with a discussion of the

politics of mental defect in inter-war America and Britain.

HIGH GRADE MENTAL DEFECT

The last decade of the nineteenth century saw the identification of a new social problem

group, the high-grade mentally defective (the 'feeble-minded' in Britain, 'morons' in

America). The main concern in the 1890s was over the education of defective children, but after 1900 it was the adolescent and young adult who came to occupy centre-stage. The class-room behaviour and performance of younger defectives was child's play beside the threat posed by their elders to the moral, social and economic order, and to the quality of the race.

In Britain the problem was referred to a Royal Commission in 1904 which, like the Interdepartmental Committee on Physical Deterioration can be seen as one of the political responses to the body-blow of the Boer War and its revelations about the sorry state

of affairs at The Heart of the Empire. The Report of the Royal Commission on the Care and Control of the Feeble-Minded was published in 1908.5 Four of its main findings will be summarized here. First, it was shown that the problem of mental deficiency was larger than was commonly thought (between four and five per thousand population and higher than this among children of school age). Furthermore there existed a class of defectives ('high grades') who had largely escaped recognition hitherto, and were not covered by existing legislation, once their school-days were over. Secondly, the overwhelming weight of evidence from expert witnesses and the Commission's medical investigators indicated that mental deficiency was strongly heritable; most concluded that over half

and up to ninety per cent of defectives owed their condition to morbid inheritance. Thirdly, the Commission accepted the evidence that defectives were abnormally prolific

(in practice, this usually meant defective women). The most commonly cited estimate

4 See, for example, K. Ludmerer, Genetics and American Society, Baltimore, 1972; D.J. Kevles, In the

Name of Eugenics, Harmondsworth, 1986.

S Royal Commission on the Care and Control of the Feeble-Minded, London, 1908, 8 vols.


The Biology of Stupidity 349

was that of Tredgold, one of its medical experts, who suggested that normal couples aver-

aged four children, while defectives produced seven.6 Finally, the Commission collected a mass of evidence to show that the mentally defective were implicated in a multitude of the social problems which afflicted Edwardian society. They were prone to delinquency and crime and were over-represented in prisons and reformatories; many were led into alcoholism or vagrancy, or both. Economically, their status was at best precarious, at worst hopelessly dependent; consequently they were found in the casual workforce, among the unemployable and recipients of intermittent outdoor relief, and in the work- house. Defectives-particularly fertile females-were believed to be over-sexed and promiscuous; they boosted the illegitimacy rate, thus burdening public funds; they operated at the rough end of the prostitution business; and they spread venereal disease, one of the insidious and virulent 'racial poisons'. Finally, if the threat they posed was serious in the here-and-now, their reproductive behaviour, interacting with the laws of inheritance, was having calamitous consequences for the future quality of the population.

This analysis was concerned crucially with high-grade defectives, who were 'actively' problematic in ways which 'low grades' were not. What was needed, it was agreed, was a specialized agency which would ascertain defectives, apply for the certification of those who met agreed criteria, and make appropriate provision usually by statutory super- vision in the community or compulsory detention in institutions. Many of the recommendations were enacted in the Mental Deficiency Act, 1913.7

The Commission also had a powerful impact in America where the 'menace of the feeble-minded' assumed even more terrifying proportions. There intelligence testing was developed earlier than in Britain and was carried out more extensively. From about 1910 the inmates of penitentiaries and reformatories, army recruits, 'fallen women' and intending immigrants were subjected to a blitzkrieg of tests which, it was claimed, revealed just how pervasive mild mental defect had become. Paradoxically, the milder the degree of mental deficiency, the greater the threat to the social fabric, and the more urgent the need for expert skills and diagnostic tools. Indeed one pioneer of mental-testing claimed in 1914 that, without careful psychological tests, the moron (the real cause of these social problems) would have remained undetected.8

It can therefore be seen that there were obvious attractions in a theory which proved that defectives were biologically abnormal and that their abnormality was transmitted in a law-governed manner. It could be plausibly maintained, for example, that serious social problems might be tackled 'scientifically' at their roots. The authorities would be able to identify sub-populations which harboured defective germ-plasm; they could estimate the effects of measures to deal with defectives; and policies which infringed civil

6 This was extensively cited: see for example the speech of R. McKenna, Home Secretary, during the Sec- ond Reading of the Mental Deficiency Bill, H.C. Debs, 4th series, vol. xxxix, col. 633, 10 June 1912; and the comments of Winston Churchill cited in W.S. Blunt, My Diaries: 1888-1914, London, 1932, pp. 813-814.

7 On the Mental Deficiency Act, see G.R. Searle, Eugenics and Politics in Britain 1900-1914, Leyden, 1976, especially chapter 9; H. Simmons, 'Explaining Social Policy: the English Mental Deficiency Act of 1913', Journal of Social History, (1977-1978), 11, pp. 387-403; D. Barker, 'How to curb the fertility of the unfit: the feeble-minded in Edwardian Britain', Oxford Review of Education (1983), 9, pp. 197-211; G. Jones, Social Hygiene in Twentieth Century Britain, London, 1986, especially chapter 2.

8 H.H. Goddard, Feeble-Mindedness: its causes and consequences, New York, 1914, chapter 1.


350 David Barker

liberties or offended natural justice, could be justified if those who were being locked up, operated on or sent back across the Atlantic were shown to be 'objectively' different and inferior. There is, in fact, good reason to believe that the quest for a genetic theory was undertaken in part to establish the legitimacy of policies already in force but vulnerable to the criticism that they had jumped the gun. Public authorities which were empowered to detain or sterilize defectives had been placed in a delicate position, as the following passage from Goddard's classic Kallikak study suggests:

Probably the most serious difficulty to be overcome before the practice of sterilization in any form could come into general use would be the determining of what persons were proper subjects to be operated upon.

This difficulty arises from the fact that we are still ignorant of the exact laws of inheritance. Just how mental characteristics are transmitted from parent to child is not yet definitely known. It therefore becomes a serious matter to decide beforehand that such and such a person who has mental defect would certainly transmit the same defect to his offspring and that consequently he ought not to be allowed to have offspring.9

Such then was the dilemma posed by the degenerate Kallikaks from which the genetic theory promised opportune deliverance. This prototype version (1912) was followed in 1914 by a study in which the theory was presented in a scientifically more convincing form and a wealth of additional supporting evidence was offered.10

No attempt is made here to discuss the reasons for the emergence of mental defect as a prominent social issue. The demands of the education systems in advanced capitalist societies; the status and treatment of economically and industrially marginal groups in these societies; intensifying economic competition and imperialist rivalry; the quest for national efficiency; concern for the quality of the population (especially in Britain after the shock of the Boer War); changing views about state intervention in, and policing of, the family; the influence of biological theories about struggle, competition and de- generation; the professional interests of doctors, psychologists and teachers; and the implications of the new biology of cytology, mendelian genetics and biometry: all would nee to be taken into account. The last of these, however, is the theme of the next section.

MENDELISM AND THE GENETIC THEORY OF MENTAL DEFECT

The genetic theory of mental deficiency originated during the surge of experimentation, theorizing and speculation which followed the birth of genetics in 1900. For both scientific and moral-political reasons these experiments were carried out on organisms other than man, but this did not mean that geneticists (or others) were reluctant to try out the new theory on humans nor were they indifferent to its implications, particularly at a time of growing concern about the quality of the race and interest in eugenic intervention. It was, in any case, not difficult to acquire knowledge about human heredity without con- ducting controlled breeding experiments; much could be discovered by meticulously observing man under 'natural' conditions. A careful review of progress in human genetics in 1909 concluded that, while there was 'but little evidence' concerning the inheritance

9 H.H. Goddard, The Kallikak Family, New York, 1912.

10 Goddard, op. cit. (8).



of 'normal' characteristics, there was much more solid evidence about 'laws of descent followed by many striking peculiarities which are of the nature of deformity or disease'.11 Of these the commonest were abnormalities of the skeletal structure and diseases of the

eye and skin, but a severe and progressive form of mental illness, Huntington's Chorea,

had also been identified as a probable Mendelian dominant.

This then was the scientific context in which the genetic theory of mental deficiency

was developed between 1910 and 1914. The theory could be seen, and was seen, to exp-

lain yet another pathological trait which appeared to follow Mendelian laws of descent. Furthermore, Goddard's major study conformed exactly to what was rapidly

becoming the classic format. Two phenotypes were identified, in this case the normal- minded and the feeble-minded; pedigree charts were compiled (over three hundred pages, covering more than 10 000 individuals); patterns of descent were observed; and

finally inferences were drawn about the genotypes of the subjects, and alternative

theories were tested to establish which, if any, best fitted the data.

The genetic theory belongs, therefore, to a scientifically respectable tradition. As we

have seen, there were other features of the climate in which it was developed which may

have disposed both experts and laymen to take it very seriously. First, it was already 'well known' that mental deficiency was strongly heritable; the Mendelian theory therefore

confirmed commonsense and intelligent observation. Secondly, mental defect was assuming the dimensions of a major social problem. Finally, it was believed that its incid-

ence was on the increase. All three points are nicely illustrated by an editorial in The Times which fulminated against the decision to drop the British Mental Defect Bill of 1912.

The majority of those defectives begin at an early age to propagate their kind with animal indif- ference to all restraint and with less than animal care for the creatures they bring into the world ... That is the cancerous sore of our civilization for which the Mental Defect Bill provided a remedy . . . the measure would have segregated from the healthy community a horde of de-

generates whose abnormal fecundity is the source of a Ierennial and growing stream of vice and crime with which ordinary legislation strives in vain.

It is not necessary to elaborate on the attractions of a theory which explained such de-

generacy and indicated how the healthy community might do something about it.

The genetic theory of mental defect was primarily the work of H. H. Goddard, Direc- tor of Research at the Vineland Training School for the Feeble-Minded in New Jersey. Professionally Goddard was a psychologist of considerable distinction; as an early con- vert to psychometrics, particularly intelligence-testing, he introduced the new Binet tests to America and played a significant role in their dissemination. In the two studies, Kallikak, (1912) and Feeble-Mindedness, (1914) where he developed the genetic theory, he used Binet tests to measure normal intelligence and feeble-mindedness and to designate a cut-

off point. There can be little doubt that the plausibility of the theory owed much to God- dard's professional reputation and to the belief, which he had done much to reinforce, that, with the advent of testing, intelligence could be accurately measured and feeble- mindedness reliably diagnosed.

11 W. Bateson, Mendel's Principles of Heredity, Cambridge, 1909, pp. 205, 210. 12 The Times, Editorial, 'A Social Misfortune', 21 November 1912.


352 David Barker

Goddard was not, however, a geneticist, which is immediately apparent in the sections of Kallikak which outlined Mendelism and introduce the genetic theory. That his Feeble- Mindedness two years later was free of the more crass errors may be due to Goddard's unaided efforts, but his awareness and handling of such methodological problems as ascertainment bias (see below p. 357) suggest collaboration with and coaching from an expert. This was perhaps Charles Davenport whose career combined the roles of respected experimental geneticist, successful research entrepreneur and dominant figure in the American eugenics movement.13

Operating with a cut-off point of Mental Age twelve years, Goddard found a close fit between his data and the theoretical expectation if feeble-mindedness was treated as the phenotypic expression of a pair of Mendelian factors, recessive to the factor for normal- mindedness.

His theory can be presented schematically as follows: There are two phenotypes:

individuals with 'normal mentality', denoted in Goddard's charts as N; individuals who lack 'normal mentality', the feeble-minded, denoted as F.

At the genotype level we use:

N to denote the unit factor for normal mentality; n to denote the unit factor for the absence of normal mentality. N is dominant; n recessive.

Corresponding to the two phenotypes, N and F, there are thus three genotypes:

individuals of normal mentality (N) are either NN (homozygous dominant); or Nn (heterozygous); the feeble-minded (F) are all nn (homozygous recessive).

Mendelian genetics is, of course, concerned with inheritance. Different types of 'mating' therefore have to be identified and the characteristics of the offspring determined. At the phenotype level there are just three types of mating (NxN, NxF, FxF), assuming that in N x F matings it is immaterial which parent is which. At the genotype level, because individuals with the N phenotype can be either NN or Nn, there are six possible types of mating:

NN x NN, NN x Nn, Nn x Nn (all phenotypically N x N) NN x nn, Nn x nn (both phenotypically N x F) nn x nn (phenotypically F x F).

13 On Davenport see, for example, C.E. Rosenberg, Charles Benedict, Davenport and the beginning of human genetics, Bulletin for the History of Medicine (1961), 35, pp. 266-276; B.A. Kimmelman, 'The Ameri- can Breeders'Association: genetics and eugenics in an agricultural context, 1903-13', Social Studies in Science (1983), 13, pp. 163-204.



The theoretically predicted outcomes of these matings are set out below:

Mating Offspring NN x NN phenotypically all of normal mentality;

all NN genotype.

NNxNn phenotypically all of normal mentality;

half NN genotype;

half Nn genotype.

Nn x Nn phenotypically three-quarters of normal mentality;

one-quarter feeble-minded;

one-quarter NN genotype,

half Nn genotype,

one-quarter nn genotype.

NN x nn phenotypically all of normal mentality;

all Nn genotype.

Nn x nn phenotypically half of normal mentality;

half feeble-minded; half Nn genotype,

half nn genotype.

nn x nn phenotypically all feeble-minded; all nn genotype.

The evidence collected by Goddard certainly appeared to bear out this interpretation.

The table below shows a close correspondence between observed and theoretically pre-

dicted frequencies. Goddard claimed that he had at first been reluctant to believe that Mendelism could

explain differences in intelligence since he was 'one of those psychologists who find it hard to accept the idea that the intelligence even acts like a unit character'. He then presented himself as overwhelmed by an avalanche of 'facts', which bore him relentlessly towards a Mendelian interpretation of the data: 'There seems to be no way to escape the conclusion from these figures'.14 (The next section examines Goddard's claim that the facts did indeed have a will of their own.)

However implausible, the theory was both long-lived and influential. The evidence marshalled below shows that eminent geneticists continued to endorse it into the late 1920s and early 30s and at times their respect for Goddard bordered on the reverential, while the sniping of critics such as Hogben, Haldane and Penrose went on well into the 30s. The British medical expert, A. F. Tredgold, observed in 1924 that there were just two worthwhile theories concerning mental deficiency, the Mendelian recessive and his own.15 In America, H. H. Laughlin's model sterilization statute was aimed at the heterozygous carriers of defect (e.g. those with the Nn genotype), and it was under such a law that Carrie Buck was deemed 'the probable potential parent of offspring as defective as herself'. Her sterilization was declared constitutional by the U.S. Supreme

14 Goddard, op. cit. (8), p. 556.

15 A.F. Tredgold, British MedicalJournal (1924), II, pp. 316-320.


354 David Barker

Table 1. Observed and theoretically predicted frequencies of defective and normal offspring from different parental genotypes

Defective offspring Normal offspring Parental Number of All

genotype matings offspring Observed Expected Observed Expected

NNXNN ignored in the final tabulation NNxNn 7 23 0 0 23 23

NNxnn 18 34 0 0 34 34

NnxNn 33 146 39 36.5 107 109.5

Nnxnn 122 371 193 185.5 178 185.5

nn x nn 144 482 476 482 6 0

Total 324 1056 708 704 348 352

Source: Goddard, Feeble-Mindedness, p. 555 (slightly modified).

Court in 1927.16 Although no comparable legislation was passed in Britain, biologists such as Fisher and Huxley played a prominent role in the campaign to secure the passage of a similar law. An important part of their case rested on the claims they made about the 'early' impact (i.e. in the first three or four generations) of selection against homozygous recessives (nn). Such selection would be even more effective, they argued, if mental deficiency were concentrated in subnormal strata of the population and if heterozygotes could be identified.17 The influential Wood Committee (1929) maintained that there did exist such concentrations of the hereditarily inferior; it went on to suggest that this subnormal or social problem group which

though not defective can in many cases be regarded as 'carriers' of the defect, will probably pro-

duce its full quota of mental defectives in the next generation.'8

In all these cases the theory was treated as the well established scientific basis from which discussion about policy, or policy itself, could proceed. The following passage from the psychologist E. A. Doll provides a striking example of the way in which the theory had by the mid-20s entered the taken-for-granted conceptual apparatus of Ameri- can mental deficiency workers.

Who of us examining a child suspected of feeble-mindedness and finding one of the parents feeble-minded, would not immediately be prejudiced toward a positive diagnosis by this fact? And yet who of us would take the pains to determine whether such parent's feeble-mindedness

16 On the Carrie Buck case, see, for example, Kevles op. cit. (4) especially pp. 110-112; Gould op. cit. (3), especially pp. 335-336 and his 'Carrie Buck's Daughter', Natural History (1984), 7, pp. 14-18; M.L. Dud- ziak, 'Oliver Wendell Holmes as an eugenic reformer: rhetoric in the writing of constitutional law', Iowa Law Review (1986), 71, pp. 833-867.

17 For example, letter from R.A. Fisher and five others, Lancet (1930), ii, pp. 161; letter from J.S. Huxley as a member of the 'Committee of the Eugenics Society for Legalising Eugenic Sterilisation', Nature (1930), 126, pp. 503.

18 Report of the Mental Deficiency Committee (Joint Committee of the Board of Education and Board of Control), London, 1929, Part 3, p. 82.



had been acquired through illness, accident, disease or whatnot, rather than being itself of hereditary type? Who of us would attempt or be able to prove that the remaining normal parent was a simplex normal rather than a duplex, since only in the former case could any of the pro- geny be feeble-minded? And again, who of us could predict that the particular child under examination was bound to be feeble-minded, since normality and deficiency result in equal ratio from such a mating? Family history interpreted on the basis of the Mendelian Law is practically useless for the purposes of diagnosis, although to be sure it may have a high presumptive value in accounting for feeble-mindedness previously diagnosed by other methods. It is only when both parents are of the hereditary feeble-minded type and lineage is certain that family history may be used with any certainty for diagnosis. If one parent is known to be of the hereditary feeble-minded type, and the other parent of the simplex normal type, both of these being rather difficult of proof, the chances are only one to one that the offspring will be feeble- minded. If both parents are simplex normal with feeble-mindedness in the family once removed, the diagnostic ratio is only one to three, and such simplicity is practically impossible of proof.'

Doll's warnings against rushing to hereditarian judgement are revealing, but even more

instructive are the language and concepts he uses. The way in which 'simplex normal'

(= Nn), 'duplex normal' (= NN) and Mendelian ratios are bandied about suggests close

familiarity with the theory among this group of professionals.

A CRITICAL ANALYSIS OF GODDARD'S THEORY

Contemporaries and more recent critics have pointed out a number of defects in God-

dard's theory. Intelligence scores, for example, show a continuous distribution which

does not lend them to Goddard's either-or categorization. It is highly unlikely that an

arbitrarily selected cut-off point would correspond with the action of a gene difference

of the kind Goddard claimed to have discovered (particularly when the cut-off point was

periodically moved). Again, while the Vineland subjects (327 in number) were formally

tested, their relatives (10000 in number) were not; many were diagnosed in absentia,

often posthumously.20 These were damaging criticisms concerning the information-

gathering process and the conceptual framework which was used to order the data. But

they do not explain how it was that the data lent such convincing support to the Mendelian recessive theory.

In what follows I concede, for the moment, that the information in Goddard's charts was accurate and consider how he manipulated and interpreted it. How do these procedures measure up when we apply standards (minimal ones at that) which contem-

porary geneticists might have been expected to use in evaluating his theory? And was

Goddard as sceptical about the Mendelian theory as he claimed? There are at least five reasons for concern.

19 E.A. Doll, 'Current Problems in Mental Diagnosis', Journal of Psycho-Asthenics, (1924), 29, reprinted in M. Rosen et al., (eds), The History of Mental Retardation, Baltimore, 1976, vol. II, pp. 27-28.

20 See, for example, Morgan, op. cit. (2), pp. 200-206; L.T. Hogben, The Nature of Living Matter, Lon- don, 1930, pp. 208-214; M. Ginsberg, Studies in Sociology, London, 1932, chapter 8 and pp. 203-205; Gould op. cit. (3), pp. 158-174.


356 David Barker

1 NN x NN matings

Table 1, which showed a close fit between the observed and theoretically predicted frequencies of normal and defective offspring from different matings, contains no information about the offspring of matings between 'normals' who were homozygous dominant (NN x NN). Goddard did not draw attention to the fact that these matings had been omitted from his analysis, and it is necessary to comb the text to discover how he did deal with this type of mating. He wrote

when both of the parents are duplex [= homozygous dominant = NN] all of the children must be normal. Of course, we have nothing to do with this type of mating in a defective family. (my emphasis)2'

This statement should have set alarm bells ringing for any competent geneticist reading Goddard in 1914. The reason is very simple: unless certain conditions were met it was impossible to be certain that a normal individual was NN (and not Nn) or that a mating was NNxNN (as opposed to NNXNn or NnxNn). These conditions were met in the geneticist's laboratory where breeding tests could establish beyond doubt (statistically) that an organism was descended from a 'pure line' and was homozygous dominant for a characteristic. This was not a condition which was satisfied by the 'defective' stocks of New Jersey, as Goddard recognized elsewhere. Consequently if NN x NN matings could not be identified, how did he know which matings he could 'have nothing to do with', and thus exclude from the analysis?

2 NNorNn?

Whether Goddard classified a 'normal' individual as NN or Nn was rarely the result of using independently verifiable data. Rather, in the words of Samuel Holmes, he decided such cases

according to whatever assumption is necessary to bring the facts into accord with the theory. It is practically impossible to determine that a person is [Nn] unless one of his immediate parents is [nn].22 (my emphasis)

The point can be illustrated from one of Goddard's charts in Figure 1.

We start with two feeble-minded sisters ?t) whose parents were both of undetermined mentality. The older sister was married twice, the second time to a 'normal' man . They had five children: a boy of undetermined mentality, a feeble-minded boy, a normal boy, a normal girl and a girl about whom nothing more was known. Although Goddard knew the husband's mentality, he had no evidence (e.g. from his parents or siblings) to enable him to determine the man's genotype (NN or Nn). Undeterred, he seems to have reasoned that since the couple had both N and F children, the man's genotype could not have been NN, since NN x nn -* Nn, heterozygotes who were phenotypically normal. He 'must' therefore have been Nn, although the only evidence supporting this inference was the presence of an F child. This was 'evidence', however, only if we accept the theory which was supposedly being tested.

21 Goddard, op. cit. (8), p. 550. 22 S.J. Holmes, The Trend of the Race, London, 1921, p. 38.



0 Female W Male N Normal-minded

F Feeble-minded

U Mentally undetermined ? Nothing more known ; Still-birth/died in infancy (Extracted from Goddard, chart 37, section 8, page 130.)

Figure 1. A Pedigree illustrating hereditary feeble-mindedness.

To summarize; the validity of Goddard's crucial data in Table 1 depends on the accurate and independent determination of the genotypes of normal individuals. In fact the genotypes were frequently determined by a process of circular reasoning in which the genotypes were 'constructed' according to the requirements of the theory.

3 Ascertainment bias

If the genotype of a normal individual can be inferred only from the phenotype of his/her offspring (a common situation in Goddard and elsewhere in human genetics), then some Nn x Nn and Nn x nn matings will not be identified as such because they have so far produced only normal children. But the high proportion of normals from these 'missing' matings means that the number of normal children in Nn x Nn or Nn x nn matings which have been identified, will fall below the theoretical expectation. An adjustment will have to be made to allow for these 'missing' matings and the 'missing' normal children.

Goddard's raw data for these matings did show the expected shortfall, and he was aware that an adjustment was necessary. Two comments however can be made about his adjustment formula. First, it was without theoretical justification. He had already identified two groups of matings which he designated NN/?Nn x Nn and NN/?Nn x nn where the oblique and query indicated uncertain genotype. (The process whereby this group of


358 David Barker

matings was distinguished from the larger group of N x N and N x F matings was itself

decided arbitrary). He then simply said of the NN/?Nn parents in the first group,

it is fair to assume that there were as many [Nn] as [NN] mates among these 27 matings and

therefore half of them properly go with our [NN x nn] group.23

This impression of impartiality and even-handedness disguises the fact that there was no reason to assume the equal probablity of an NN/?Nn being NN or Nn, and that in doing so strong assumptions were being made about the frequency of NN and Nn genotypes. Secondly, this adjustment produced broadly the result that the Mendelian recessive

theory required. The ratio of F to N children in the Nnx nn matings became 193 to 178, and in NnxNn matings 39 to 107 (close to the 1 to 1 and 1 to 3 ratios which Mendelism

predicted). We can legitimately wonder whether Goddard was the helpless prisoner of his 'facts' that he liked to make out.

4 The elevation of honorary Ns

We have just seen that Goddard 'constructed' genotypes according to the requirements of the his theory. We now find that he not infrequently 'constructed' phenotypes as well.

This point is neatly illustrated in Fig. 1. Before she married N, the older sister (i) was married to a man of undetermined mentality [U. This earlier marriage produced one normal child, one feeble-minded child and two children of undetermined mentality; there was also one miscarriage/stillbirth. That, one might have thought, was the end of the matter: if the mentality of the father was unknown, there was nothing more to be said. Goddard, however, appears to have reasoned that the man could not have been feeble- minded since his first daughter was normal and nnxnn matings never produce N offspring; he must, therefore, have been normal. But he could not have been NN; if he had been, his second surviving daughter would not have been feeble-minded (NNxnn matings never produce F offspring). So he must have been Nn, since Nn x nn can produce both N and F offspring. For the purposes of Mendelian analysis, therefore, Goddard treated this mating phenotypically as N x F and genotypically as Nn x nn. It was one of the matings from which his crucial table (Table 1) was constructed.

Two points can be made about these 'honorary' Ns. First, the example is not unique; no fewer than seventy-two matings used in Goddard's final analysis (and therefore con- tributing to the crucial table) consisted of couples in which the mentality of one partner had been decided, as Holmes might have put it, 'to bring the facts in accord with the theory'. These represent forty per cent of the matings analysed where one or both parents were 'normal minded'.

Second, in seventy-one out of seventy-two cases it was assumed that the individual who had originally been designated U (undetermined mentality) was of normal mentality. This is a remarkable sequence among these 'degenerate' stocks, where the feeble- minded slightly outnumbered normals, and it contrasts sharply with another sequence in

23 Goddard, op. cit. (8), p. 554; see also p. 555.



which Goddard tacitly assumed that 118 children of undetermined mentality from F x F matings were all F.

Honorary Ns were also recruited from among Us to swell the ranks of Nn x Nn matings. The crucial consideration here was probably the need to generate a respectable sample containing finally twenty-six matings and 185 children. But once again the selection of the honorary Ns (Nns) was carried out with scrupulous regard for the Mendelian principles which were being tested. Which were the U x N matings in which Goddard el- evated the U partner to N (Nn) status, thus creating an Nn x Nn mating? Those and only

those UxN matings (on one occasion a UxU mating!) which had produced N and F children and therefore conformed to the Mendelian law (the same point can also be made about the criteria for selecting U x F matings, above).

5 'Aberrations'

Homozygous recessives breed true and most of Goddard's hereditary feeble-minded couples duly obliged. The exceptions, six normal children out of nearly 500, were infrequent, indeed 'so few as to be hardly worth consideration';24 but they still constituted a problem which Goddard felt he had to explain. His tactic appeared to dispose satisfactorily of the exceptions: errors could have been made in measuring the child's intelligence; or in classifying the parents as F; or the husband might not be the real father,

since 'one cannot always be sure of the chastity of these feeble-minded women'.25 Goddard does not appear to have realized that these swords were decidedly double- edged. Why, after all, should such errors or improprieties have been confined to cases which infringed Mendelism?

All in all, Goddard's theory looks decidedly leaky. Since the standards are those which could and should have been used by an undergraduate geneticist in 1914, it is

difficult to see why it was not immediately pronounced unseaworthy on 'internalist' or scientific grounds.

GENETICISTS AND THE MENDELIAN RECESSIVE THEORY OF MENTAL DEFICIENCY

How was it that bad biology remained so influential? Part of the answer undoubtedly lies in the socio-political context in which the theory was elaborated; this has been briefly outlined. Another way of approaching the question is to investigate its reception by the scientific community, especially geneticists. This is not, of course, to suggest that geneticists have necessarily had a preponderant influence over the social and political applica- tions of their science. But if, as has been claimed, geneticists abandoned eugenics in the 1 920s because it rested on bad genetics, it seems reasonable to infer that they would have been sceptical, to say the least, about Goddard. What then did geneticists say about the genetic theory of mental deficiency?

Historians of genetics and eugenics have not offered a direct answer to this question, but there can be little doubt about the general direction in which recent analyses have

24 Ibid, p. 550.

25 Idem.


360 David Barker

been leading. The genetic theory was elaborated at a time (1914) when, according to

Ludmerer, American geneticists were starting to become disillusioned with eugenics for

essentially 'internalist' reasons.26 There were, moreover, specific features of the genetic

theory of mental defect (quite apart from its more glaring deficiencies) which should have

rendered it particularly vulnerable to critical scientific scrutiny. It typified the 'one gene- one trait' model demolished by East and Emerson; it made no allowance for the inter-

action of heredity and environment demonstrated by Johannsen; and even if the theory was scientifically sound, the efficacy of eugenic intervention was far less favourable than

eugenists habitually claimed, since it had been shown that selection against a recessive condition was inordinately slow.27

Kevles argues along similar lines, suggesting, for example, that we can gauge the mounting impatience of geneticists from the elementary lessons Herbert Jennings was still having to give errant eugenists in 1925:

neither eye color, nor tallness, nor feeble-mindedness, nor any other characteristic, is a unit character . . . There is, indeed, no such thing as a 'unit character' and it would be a step in advance if that expression should disappear.28

Apart from his general point, Jennings' example of feeble-mindedness suggests that

geneticists at least had consigned Goddard and tthe recessive theory to the scrap heap. By the time Jennings was writing this, eugenics represented not merely bad biology, but also reactionary, racist politics. And as eugenists threw themselves into their campaigns for the sterilization of defectives and the exclusion of undesirable aliens and 'inferior' races, it is argued, the disquiet of geneticists hardened into outright repudiation of eugenics.29

There are signs in both Ludmerer's and Kevles' accounts, however, that in some respects this thesis may need modifying. In America, for example, Jennings emerges as a courageous lone voice opposed to racist immigration legislation (1924); Ludmerer also concedes that the sterilization laws 'evoked relatively little concern among geneticists in America'. Similarly in his analysis of the scientific assault on mainline eugenics during the inter-war years, Kevles focuses on the activities of just four biologists: Jennings, Haldane, Hogben and Huxley.30 This suggests that repudiation may have been a minority rather than a mass activity. Nevertheless, these accounts all portray a profession united in at least tacit support of a front-line which, from the mid-1920s, was engaged in an unremit- ting struggle against eugenics. Their opposition rested ultimately on their perception that eugenics systematically abused and distorted their science. Ludmerer differentiates in the sharpest possible way between eugenic geneticists on the one hand, and the first genera-

tion American experimental geneticists and the new breed of statistical population

geneticists, on the other.31 The first group were biased and closed-minded; they also allowed their social views to influence their interpretation of scientific evidence. The

26 Ludmerer, op. cit. (4), chapter 4. 27 Ibid., pp. 75-77.

28 Quoted in Kevles, op. cit. (4), p. 145.

29 Ludmerer, op. cit. (4), chapter 6; Kevles, ibid., chapter 8. 30 Ludmerer, ibid., pp. 94, 123f; 94; Kevles, ibid., pp. 122-128. 31 Ludmerer, ibid., pp. 148-163.



other two groups naturally had their social biases, their political views and their beliefs

about eugenics; but

none of them permitted their feelings on social matters to compromise their scientific judgement ... They remained free enough of their personal biases so that they could properly and critically interpret scientific evidence, including that which related to man. They retained the ability to change their minds when new evidence appeared.32

Other analyses are not substantially different. Allen argues, for example, that for

'old-style' eugenics, scientific closure began around 1925, as geneticists drew attention to its theoretical shortcomings. (While scientific closure is not synonymous with repudia-

tion, the concepts do intersect.)33 Glass has similarly outlined the factors leading to the demise of American eugenics in the 1920s and 30s, focusing on the scientific criticisms of

genticists, particularly the Johns Hopkins trio of Jennings, Pearl and Weinstein, together

with Muller.34

But while there is considerable common ground between Ludmerer and Kevles, there

are significant discrepancies among these authors. Thus, for example, Ludmerer regards

East as typical of his group of first generation American experimentalists: open-minded,

scientifically principled, whose adherence to eugenics in the 1920s was no more than

nominal. Glass on the other hand argues that he is to be seen as a consistent mainline

eugenist in the Davenport mould.35 For Allen, Conklin remained throughout an unregen-

erate, old-style eugenist, whereas Glass sees him as a moderate, occupying a position bet-

ween critics of eugenics, such as Pearl and Jennings, and the scientific leaders of American eugenics, Davenport and East. Ludmerer treats him as a nominal eugenist and

emphasizes his anti-eugenic public statements.36 These examples suggest a more complex picture than is often painted, an inference which is reinforced by two further discrepan-

cies. Kevles speaks of a sustained assault on mainline eugenics during the inter-war years,

spear-headed by (among others) Haldane and Hogben; but Werskey has shown that

neither became seriously involved in public debates about eugenics until the 1930s;

indeed Haldane had been a eugenist in the 1920s, albeit an idiosyncratic and critical

one.37 Another of Kevles' public scientists who attacked eugenics was Julian Huxley; and yet Germaine Greer has argued that Huxley was consistently pro-eugenic throughout his career.38

An examination both of the reception of the Mendelian recessive theory of mental

deficiency and of the debate over its eugenic implications indicates that the process whereby geneticists became disillusioned with eugenics and abandoned the movement

32 Ibid.,p. 151.

33 G. Allen, 'The Role of experts in scientific controversy' in H.T. Englehart and A.L. Caplan (eds), Scien-

tific Controversies, London, 1987, pp. 169-202.

34 B. Glass, 'Geneticists embattled', Proceedings of the American Philosophical Society (1986), 130,

pp.130-154.

35 Ludmerer, op. cit. (4), p.124,148,151; Glass, ibid., pp.132-136; on East Allen agrees with Glass, op.

cit. (33), p. 181, 199.

36 Allen, ibid., p. 199, Glass, ibid., pp. 136-137; Ludmerer, ibid., pp. 121-122.

37 G. Werskey, The Visible College, London, 1976, chapters 3, 4 and 5; see also D. Paul, 'Eugenics and the Left', Journal of the History of Ideas (1984), 45, pp. 567-590.

38 G. Greer, Sex and Destiny, London,1984, chapters 10 and 11.


362 David Barker

was far less straightforward than has so far been suggested elsewhere. It points to the need to look much more closely at who abandoned precisely what and when; and to

establish which eugenic beliefs and policies continued to receive professional support. It

also indicates that abandonment was more erratic, less rational and less scientifically grounded than is usually claimed.

I have identified three groups of geneticists: first, those who accepted and endorsed

the Mendelian recessive theory of mental deficiency, and in most cases argued for tough

eugenic countermeasures; second, geneticists who modified and updated Goddard in the light of later developments in genetics, including population genetics; finally, those who

emerged as the major critics of the theory. Table 2 indicates who is to be found where and

when. At this stage two qualifications should be made. First, the categories were not

mutually exclusive, nor the boundaries impermeable. In some cases upholders of the theory underwent conversion: Haldane, Crew and Fisher, for example. The ambivalence

and vacillation of Samuel Holmes have placed him in all three groups. Several of those

who supported the theory also outlined and accepted the modifications introduced by East and Holmes. Second, Table 2 provides strong support for one of the main arguments

Table 2. Geneticists' responses to the Mendelian recessive theory of mental defect40

Geneticists who accepted Geneticists who modified Geneticists who criticized/ and endorsed the theory and refined the theory rejected the theory

East (1917) East (1917) Holmes (1921) Punnett (1917) Holmes (1921) Morgan (1925) East andJones (1919) Fisher (1924) Hogben (1930) Gates (1920-1921) Hogben (1931) Holmes (1921) These refinements were Hogben (1931) Newman (1921) reported in: Crew (1931-1932) paper by Downing (1920) Gates (1923 and 1929) Hogben (1933) Bateson (1921-1922) Crew (1927) Fisher (1934) Holmes (1923) Guyer (1928) (Brock Committee Report) Gates (1923) Jennings (1930) Penrose (1934) East (1926) Castle (1931) Haldane (1935) Crew (1927) Huxley (1931) Haldane (1938) Guyer (1928) For development of the Penrose (1938) Haldane (1928) Social Problem group Gates (1929) concept see also Conklin (1929) Wood Committee (1929) Jennings (1930) CaradogJones (1934) Huxley (1931) Jennings (1931)

Castle (1931) East (1931)

East (1932)

Gates (1934) Huxley (1937) Shull (1938) Huxley (1941)



of this paper: whether as upholders or as critics, leading geneticists took the theory seri-

ously and, as we shall see, had no illusions about the relationship between public policy

and this area of human genetics.

GENETICISTS WHO ACCEPTED AND ENDORSED THE MENDELIAN RECESSIVE

THEORY OF MENTAL DEFICIENCY

Most importantly, this group extends across all Ludmerer's categories (eugenists,

experimentalists and statistical geneticists) and contains three of Kevles' four anti-main-

line critics (Jennings, Haldane and Huxley). Thus the presence of Gates, a high-profile

eugenic geneticist, is not in the least surprising. But the first generation American

experimentalists are unexpectedly well represented: East, Holmes, Guyer, Conklin,

Jennings, Castle, Newman and Shull all belong in this category. Bateson, Punnett and

Crew (and indeed Gates) are British equivalents. Ironically, several of these scientists

such as Castle, Conklin, Holmes and Jennings, were singled out by Ludmerer because

they had publicly criticized eugenics on the grounds that its empirical data were

39 E.M. East, 'Hidden feeble-mindedness', Journal of Heredity (1917), 8, pp. 215-217. R.C. Punnett, 'Eliminating feeble-mindedness', Journal of Heredity (1917), 8, pp. 464-465. E.M. East and D.F. Jones, Inbreeding and Outbreeding: their genetic and sociological significance, Philadelphia, 1919. R.R. Gates, 'Heredity and Eugenics', Eugenics Review, (1920-1921), 12, pp. 1-13. S.J. Holmes, The Trend of the Race,

London, 1921. H.H. Newman, Readings in Evolution, Genetics and Eugenics, Chicago, 1921. W. Bateson, 'Commonsense in Racial Problems', Eugenics Review (1921-1922), 13, pp. 325-338. S.J. Holmes, Studies in Evolution and Eugenics, London, 1923. R.R. Gates, Heredity and Eugenics, London, 1923. E.M. East, Man- kind at the Crossroads, New York, 1926. F.A.E. Crew, Organic Inheritance in Man, London, 1927. M.F. Guyer, Being Well-Born, London, 1928. J.B.S. Haldane, 'Science and Ethics', in The Inequality of Man, Lon- don, 1932 (the essay originally appeared in 1928). R.R. Gates, Heredity in Man, London, 1929. E.G. Conklin, Heredity and Environment, Princeton, 1929. H.S. Jennings, The Biological Basis of Human Nature, London, 1930. H.S. Jennings, 'Eugenics' in E.R.A. Seligman (ed), Encyclopedia of the Social Sciences, London, 1931, vol. V, pp. 617-621. J.S. Huxley, What dare I think?, London, 1931. W.E. Castle, Genetics and Eugenics, Cambridge Mass, 1931. E.M. East, Biology in Human Affairs, New York, 1931. E.M. East, review of L.T. Hogben, Genetic Principles in Medicine and the Social Sciences, in Economica (1932), 12, pp. 235-238. R.R. Gates, letters in British Medical Journal (1934), I, pp. 120, 264, 456-457. A.F. Shull, Heredity, New York, 1938. J.S. Huxley, commentary to film Heredity in Man, G.B. Instructional, Ltd in collaboration with the Eugenics Society, 1937. (I am very grateful to the British Film Institute for providing me with a copy of their shotlist for this film, together with a review from the Monthly Film Bulletin (1939).) J.S. Huxley, 'The vital importance of eugenics', Harper's Monthly (1941), 163, pp. 324-331, cited in Ruth Hubbard 'Prenatal diagnosis and eugenic ideology', Women's Studies Int. Forum (1985), 6, pp. 568-569. R.A. Fisher, 'The elimina- tion of mental defect', Eugenics Review (1924), 16, pp. 114-116; Mental Deficiency Committee (Wood), op. cit. (18); D. Caradog Jones, The Social Survey of Merseyside, Liverpool, 1934, 3 vols. T.H. Morgan, op. cit. (2). L.T. Hogben, The Nature of Living Matter, London, 1930; also 'The foundations of social biology', Economica (1931), 11, pp.4-24. (Inaugural lecture as Research Professor of Social Biology, University of Lon- don.) Also, Genetic Principles in Medicine and Social Science, London, 1931. F.A.E. Crew, 'Mental Defi- ciency-a discussion of the genetic background', Eugenics Review (1931-1932), 23, pmp. 299-303. L.T. Hog- ben, Nature and Nurture, London, 1933. Ministry of Health, Report on the Departmental Committee on Sterilization (Brock), London, 1934. L.S. Penrose, 'A contribution to the genetic study of mental deficiency', British MedicalJournal (1934), I, pp. 10-11. J.B.S. Haldane, 'Human genetics and human ideals', inJ. Jeans, Scientific Progress, London, 1936, pp. 141-173 (Sir Halley Stewart Lecture, 1935). J.B.S. Haldane, Heredity and Politics, London, 1938. L.S. Penrose, A Clinical and Genetic Study of 1280 Cases of Mental Defect, Med- ical Research Council Report Series No. 229, London, 1938.


364 David Barker

inadequate or the science on which it rested was bogus.40 Thus Ludmerer cites Castle in 1926:

a considerable proportion of the published material [on eugenics] is probably of small

value, since it is uncontrolled by experiment and is based largely on uncritical data4'

... a verdict which fits Goddard very accurately. Yet five years later Castle scored a spec- tacular own goal. In Genetics and Eugenics he expressed no reservations about God- dard's data; 'the most complete study of the inheritance of feeble-mindedness that has ever been made'. He summarized, uncritically the main results of Goddard's crucial table (Table 1), with particular emphasis on the outcome of FxF matings; he threw in some atavistic speculation about the defective representing 'a primitive animal-like condition of the human race'; and concluded with a set of strong eugenic recommendations derived from this evidence and analysis.42 Castle's own goal was emulated by Jennings who, in 1925, had exposed the fallacy of regarding feeble-mindedness as a unit character (p. 360 above). But in 1931 he treated his lay readers to a serious discussion of the frequencies of Goddard's three genotypes (NN, Nn and nn) in the American gene pool and the prospects of effective selection against nns and Nns; at one point he spoke of the heterozygous carriers of the 'feeble-minded gene'.43

On the face of it the most surprising members of this group are Kevles' anti-mainline critics; Haldane and Huxley as well as Jennings. Haldane is interesting for three reasons. First his formulation of the recessive theory for a lay audience in 1928 suggests that he saw himself presenting a well established truth:

Feeble-mindedness is fairly strongly inherited, but unfortunately it is generally inherited in such a way that the segregation or massacre of the feeble-minded, even if continued for several generations, would not stamp it out. The feeble-minded, unless they mate with one another, do not necessarily produce feeble-minded children.44

Second, unlike most of the other geneticists cited here, he drew attention to the unfavour- able eugenic implications of this recessive mode of inheritance, as this passage shows. Third, Haldane should alert us to the need to distinguish different phases in the careers of key biologists, since he was later a prominent critic both of eugenics and of the recessive gene theory.

An examination of Huxley's output between 1926 and the early 1940s suggests three conclusions. First, he was at this time an adherent of traditional mainline eugenics, strongly committed to the equation between social class and genetic worth. Secondly, in applying this doctrine he consistently argued that priority should be given to eugenic measures against the mentally defective, mental deficiency being conceptualized as a Mendelian recessive disorder. Finally, he did more than simply expound mainline eugenics; indeed, contrary to Kelves' portrayal of him as a critic, Huxley was actively

40 Ludmerer, op. cit. (4), chapters 4 and 6. 41 Quoted in Ludmerer, ibid., p. 124. 42 Castle, Genetics and Eugenics, 1931, pp. 381-387 (op. cit. 39). 43 Jennings, The Biological Basis of Human Nature, 1930, pp. 226, 236-241, 249 (op. cit. 39). 44 Haldane, The Inequality of Man, 1932, p. 105 (op. cit. 39).



involved in the campaign to legalize the sterilization of the mentally defective.45 Endorsement of Goddard, then, covered a wide spectrum of geneticists. But, when

did they come to accept the theory and for how long; and when did they desert it? Word was obviously spreading through the scientific community as early as 1912, to judge by Punnett's comments to the International Congress on Eugenics in London.46 The works cited here range over the period 1917 to 1941, thus indicating considerable support among prominent geneticists in a period when mental deficiency was politically sensitive and eugenists were busily canvassing scientific support for policies on the defective. In America supporters of the theory seem to have been totally impervious to the work of its critics. The chronology of Table 2 shows that in many cases their endorsement survived the well-directed arguments of Holmes (1921) and Morgan (1925) and more general criticisms of much human pedigree research (for example, Muller, 1925).47 The nearest we get to a retraction are statements from Crew in 1931 and (more obliquely) Fisher in 1934, but in neither case did abandonment of the Mendelian recessive theory entail abandonment of a eugenic posture on mental deficiency.48 But these are exceptions; most supporters seem either to have been unaware of the criticisms (implausible, when the critic concerned was Morgan in Evolution and Genetics) or to have ignored them. Debates and confrontations were rare but instructive when they did occur. Thus the strength of East's commitment to Goddard can be gauged from his review of Hogben's Genetic Principles in Medicine and the Social Sciences in 1932. We are told that Hog- ben's 'most serious error' resulted from his inability to conceive how feeble-mindedness 'can possibly be the result of defectiveness in a single gene'; Goddard's data ('the most extensive collection of evidence') were then wheeled out together with the now familiar clincher that FxF invariably produced F. Then in 1934 when Penrose outlined a case in which F x F clearly did not produce F, it was Gates who rose to the bait and went to extraordinary lengths to defend the Mendelian recessive theory.49

45 J.S. Huxley, 'The case for eugenics', Sociology Review (1926), 18, pp. 279-290; What Dare I Think?, 1931, especially chapter 3; The Uniqueness of Man, London, 1941, chapter 2 (originally 1936); letter to Nature (1930) (op. cit. 17); commentary to film Heredity in Man, 1937 (op. cit. 39); 'The vital importance of eugenics', Harper's (1941), (op. cit. 39); see also Greer, op. cit, (38), and Jones, op. cit. (7), pp. 105-106.

46 R.C. Punnett, 'Genetics and eugenics', in First International Eugenic Congress, Problems in Eugenics, London, 1912, pp. 137-138.

47 H.J. Muller, 'Mental traits and heredity', Journal of Heredity, (1925), 16, pp. 433-448. 48 Crew, Eugenics Review (1931-1932), op. cit. (39). Fisher was a member of the Brock Committee on

Sterilization, in fact the only geneticist on a committee dominated by doctors. When the committee peremptor- ily dismissed Goddard's work as 'unscientific' and argued that his instructions to his field workers were 'so ten- dentious that it is not surprising that they succeeded in finding what they were told to seek', I think we can safely infer that Fisher had become more critical of Goddard than he had been at various times during the previous ten years. (Ministry of Health, Report on Sterilisation, 1934 (op. cit. 39, p. 13). In Fisher's case, acceptance of the Mendelian recessive theory had always been qualified: for example, 'there is a considerable body of pedigree evidence indicating the existence of a single Mendelian factor which, in its recessive phase, is capable alone of producing feebleness of mind. There is an even more substantial body of evidence that normal people, as well as the feeble in mind, differ very greatly in degree in just the same mental characteristics as distinguish the feeble-mindedness from the normal. Consequently, while we may speak of feeble-mindedness as due to a Mende- lian recessive, no responsible authority would claim that all feeble-minded cases are genetically alike.' Eugenics Review, 1924 (op. cit. 39), p. 115.

49 Penrose, British MedicalJournal, 1934 (op. cit. 39).


366 David Barker

Throughout the 1920s and into the 1930s, therefore, the theory received strong sup-

port from prominent geneticists on both sides of the Atlantic. And if the critics made so little impact on their professional colleagues, it is scarcely surprising if they cut no ice

with key laymen such as legislators, Congressmen, Supreme Court Judges and members of official committees. It is worth recalling that, on Ludmerer's account, the critique

should in any case have been unnecessary, since by 1930 reputable geneticists had, for fifteen years, been looking critically and suspiciously at work in human genetics and had long ago abandoned a eugenics based on shoddy genetics.

How did these geneticists use Goddard? Most were surprisingly incurious about how

feeble-mindedness was defined, how the mentality of the relatives of Vineland subjects

was assessed or how the data were manipulated. Charts were reproduced uncritically in Guyer, Crew and Newman.5" Grounds for serious disquiet were transformed into spark- ling virtues, as when Guyer solemnly declared that 'in some instances the family history has been followed back as far as five generations'.51 Similarly, the exceptions to the 'rule'

that defectives breed true were eagerly explained away by invoking illegitimacy and/or diagnostic error.52 Most were happy to award Goddard a clean bill of methodological and scientific health, speaking of 'carefully collected genealogies', 'the most extensive

collection of data', 'an abundance of material to show the heritability of this defect', 'one of our best authorities', and 'circumspection' with which the pedigree method was

used.53 Most of the geneticists who upheld the theory appear to have gone straight to

Goddard's tabulated results. We find these reproduced in more or less detail, with little or no critical comment by East, Gates, Holmes, Downing (in Newman), Conklin, Castle, Crew, Guyer and Shull. They drew especial attention to Goddard's F x F producing F, and were satisfied that the outcome of other matings was close to the theoretical expectation, all of which, as Conklin put it 'proved' the existence of the inheritance mechanism.54 Others who were similarly convinced, but did not acknowledge Goddard, included Bateson, Punnett, Huxley and Haldane (of 1928 vintage).55

One indication of the spell cast by the theory is the prominence accorded to it in some of the literature. With a wealth of available material in human genetics, Gates and, more surprisingly, Jennings started their text books by using feeble-mindedness as the clearest illustration of the Mendelian concepts of segregation and recombination, dominance and recessiveness. Gates compared brachydactyly, a Mendelian dominant abnormality, with feeble-mindedness, a recessive. Jennings used albinism and feeble-mindedness to explain

50 Guyer, Being Well Born, 1928 (op. cit. 39), chapter 19; Crew, Organic Inheritance, 1927 (op. cit. 39), 194; Newman, Readings, 1921 (op. cit. 39), p. 463.

51 Guyer, ibid., p. 346.

52 For example, ibid., p. 352; Gates, Heredity, 1923 (op. cit. 39), p. 149; Castle, Genetics, 1931 (op. cit. 39), p. 385; East and Jones, Inbreeding, 1919 (op. cit. 39), p. 240.

53 East, Economica, 1932 (op. cit. 39), p. 238; Newman, Readings, 1921 (op. cit. 39), p. 462 (Downing's paper); Guyer, Being Well Born, 1928 (op. cit. 39), p. 352; Castle, Genetics, 1931 (op. cit. 39), p. 382.

54 Conklin, Heredity, 1929 (op. cit. 39), p. 71.

55 Bateson, Eugenics Review, 1921-1922 (op. cit. 39), p. 327 ('when they interbreed ... they have no normal children but infallibly add to the asylum and institute population'); Punnett, Journal of Heredity (1917), (op. cit. 39), pp. 464-465; Huxley, What I Dare Think?, 1931 (op. cit. 39), pp. 98-100; Haldane, op. cit. (44).



the actions of pairs of genes, in both cases conveying the unmistakable message that the

genetic basis of feeble-mindedness was as securely established as that of brachydactyly and albinism.56

Haldane excepted, these writers went on to draw strong eugenic conclusions from the theory, and in doing so made it clear that they supported existing or proposed public

policies. In the early 1920s Holmes wanted something tougher than the 'feeble attempts' then in force to curtail the propagation of the defective; in the 1930s East declared that California's sterilization statutes were 'sound scientifically'.57 Guyer regarded such measures, particularly the sterilization of defective women, as indispensable in view of the

'torrent' of defectives from F x F matings.58 In America Shull, Jennings, Castle and Conk- lin expressed similar views, as did Crew, Fisher, Bateson, Huxley and Punnett in Brit-

ain.59 A more contentious question was whether action could legitimately be taken against phenotypically normal heterozygotes, assuming they could be identified. (One

way in which this problem was approached is considered in the next section.) Some American geneticists gave this argument a further sinister twist by suggesting that many heterozygous aliens were evading immigration controls and thus further contaminating

the American germ plasm. It is likewise chilling to hear Fisher speaking about the

'rate of racial purification' to be expected from eugenic measures against the mentally defective.60

56 Gates, Heredity, 1923 (op. cit. 39), pp. 17-18; Jennings, Biological Basis, 1930 (op. cit. 39), pp.

8-9, 17.

57 East, Biology, 1931 (op. cit. 39), p. 193.

58 Guyer, Being Well Born, 1928 (op. cit. 39), p. 355.

59 Shull, Heredity, 1938 (op. cit. 39), pp. 312-314; Jennings, Biological Basis, 1930 (op. cit. 39), pp.

225-226, 234-241; and in M. Seligman, 1931 (op. cit. 39), p. 619; Castle, Genetics, 1931 (op. cit. 39), pp. 386-387; Conklin, Heredity, 1929 (op. cit. 39), p. 309; Crew, Organic Inheritance, 1927 (op. cit. 39); and

Eugenics Review, 1931-1932 (op. cit. 39), p. 303; Fisher, Eugenics Review, 1924 (op. cit. 39), pp. 114-116;

Bateson, Eugenics Review, 1921-1922 (op. cit. 39), p. 327; Huxley, What Dare I Think?, 1931(op. cit. 39), pp. 98-100; and letter to Nature, 1930 (op. cit. 17); Punnett,Journal of Heredity, 1917 (op. cit. 39), p. 465.

It is worth drawing attention to Bateson here, since he is often cited as an implacable opponent of eugenics. In

this paper he described himself as cautious on eugenic/'racial' questions and urged caution on his readers; it was, he argued, the feeble-minded and only the feeble-minded against whom the state could justifiably take action to prevent their propagation. He had expressed himself colourfully on the same theme a few years earlier. 'The definitely feeble-minded we may with propriety restrain, as we are beginning to do even in England, and we may safely prevent unions in which both parties are defective, for the evidence shows that as a rule such marriages, though often prolific, commonly produce no normal children at all. The union of such social vermin

we should no more permit than we would allow parasites to breed on our bodies'. President's Address, Report of the eighty-fourth meeting of the British Association for the Advancement of Science (1914), London, 1915, p. 30.

60 For example, 'much bad germplasm comes through our gates hidden from the view of inspectors because the bearers are heterozygous, wearing a cloak of desirability over undesirable traits' in Newman, Read- ings, 1921 (op. cit. 39), p. 476 (Walter's paper). In 1938 Shull reproduced and endorsed Laughlin's data on

hereditary disorders, including mental defect, among immigrants; he went on 'one could wish that the children

of immigrants were included, since in this way one might arrive at an estimate of the various nationalities with respect to recessive inherited characters, like feeble-mindedness and epilepsy, which can to some extent or even largely be detected in those immigrants who are homozygous and can be thus excluded at the port of entry'.

The hunt for the heterozygote could then be usefully extended to the investigation of 'family histories of appli- cants in their home countries, before they set sail', Heredity, 1938 (op. cit. 39), pp. 359, 361. This may be an example of the way in which Shull set about achieving the objectives specified in the preface of his book: 'the


368 David Barker

A final point about these geneticists is that they were in most cases 'public' biologists.

Many of the works discussed here were intended to clarify recent developments in bio-

logy for the intelligent layman; others were introductory texts for freshman biologists or

for non-specialist undergraduates. Moreover, several of these geneticists, as we have

seen, were heavily involved in political campaigns in favour of eugenic policy. It is legitimate here, I think, to speak of public biologies in competition and to argue that the sci-

entific opposition to mainline eugenics had not, by the 1 920s, swept the field to the extent

that Ludmerer and Kevles have suggested. It would, at the same time, be wrong to imply that, contrary to Ludmerer and Kevles, 'underneath' these geneticists were all still unre-

generate eugenists a la Davenport, Gates or Laughlin. They did indeed, many of them, criticize eugenics. But at the same time we can observe that they did not always heed their

own methodological injunctions (mental deficiency looks like an interesting 'blind spot'), and they were quite capable of attacking eugenics in the general while continuing to sup-

port it in the particular.

GENETICISTS WHO MODIFIED AND REFINED GODDARD AND THE MENDELIAN

RECESSIVE THEORY

Until World War One it was widely believed by eugenists that once the hereditary basis of a racially harmful condition such as mental deficiency was established, then there was, ipso facto, a powerful case for eugenic intervention. It then became apparent to some, however, that if a disorder was inherited as a Mendelian recessive, selection against it would be painfully slow. Indeed, looked at from the perspective of historical, rather than biological, time, the process would be almost imperceptible. This section summarizes a series of moves and countermoves which followed when eugenists were confronted by this problem. The evidence suggests that eugenic scientists did not simply capitulate before these criticisms from population genetics. Figure 2 provides a schematic repres- entation of what went on.

In 1917 Punnett and East published estimates of the frequencies of Goddard's three genotypes in America (Fig. 2, block 2). Assuming that there were some 300 000 defectives (just under one half of one per cent), Punnett calculated that homozygous dominants (NNs) constituted ninety per cent of the population, heterozygotes (Nns) ten per cent. East's results were similar (slightly more NNs, fewer Nns).61 These results engendered disquiet for two reasons. First, the prevalence of heterozygotes was unexpectedly and alarmingly high (Fig. 2, block 3); high enough, as East put it, 'to make the stoutest heart

eager inquiry of such students [many of them non-biologists seeking a 'general education'] has seemed to the author an opportunity for missionary work seldom surpassed in college. Their interest centers largely in human affairs. To cultivate their interest in wholesome directions, to establish their social outlook on valid foundations, and to prepare them with problems, some of which they will probably live to see become acute, are tasks that challenge the wisdom and discernment of any teacher'. Thus the Professor of Zoology, University of Michigan. See also Holmes, Studies, 1923 (op. cit. 39), pp. 210-211; East, Mankind, 1926 (op. cit. 39), pp. 309-317; Fisher, Eugenics Review, 1924 (op. cit. 39), p. 155.

61 Punnett,Journal of Heredity, 1917 (op. cit. 39), p. 136; East andJones, Inbreeding, 1919, p.242 (originally in East's Journal of Heredity (1917) (op. cit. 39).



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370 David Barker

quake'. Guyer was similarly appalled at the 'enormous reserve of carriers', pointing out

that

such evils are not being confined to the original defective strains, but are continually thrusting

theftuous [sic] roots into the better blood.62

Some geneticists expressed the view that these invisible fifth columnists were dispropor-

tionately represented among recent immigrants to the USA.63

Secondly, the eugenic prospects looked decidedly bleak (Fig. 2, block 4). This had been pointed out by Dr J. MacPherson, a Commissioner in Lunacy, as early as 1912. He told the Edinburgh Eugenics Society that if mental deficiency was inherited as a Mendel- ian recessive, then the idea that its incidence could be appreciably reduced had to be dismissed as 'an extremely childish proposition'.64 His argument was apparently confirmed when geneticists began to explore the mathematics of the problem. According to Punnett, starting with three defectives per thousand and operating a policy which stopped them reproducing,

it would require something over 250 generations ... before the proportion was reduced to one in 100,000. The prospect of the success of the segregation method is not hopeful. Though it may be sure, it is very, very slow.65

Haldane made the same point, more graphically, in 1928 (p. 364 above). It was the use of Punnett's paper as 'anti-eugenic propaganda' that induced Fisher to enter the con-

troversy in 1924.

How did eugenically inclined geneticists respond to these 'difficulties'? We return to the concern of East, Guyer and others at the prevalence, dispersal and invisibility of

heterozygotes (Fig. 2, block 3). Suppose, suggested East and Holmes, we modify God- dard's model and assume that N is not completely dominant nor is n completely recessive (Figure 2, block 5). According to Holmes, this was not unreasonable since 'complete dominance is rare among those characters commonly studied by animal and plant geneticists'.66 In that case, he argued, heterozygotes (Nns) would no longer be phenotypically indistinguishable from homozygous dominants (NNs); because of 'imperfect and variable dominance' they would be of intermediate intelligence (i.e. between NNs and nns), an inference which was 'quite in accord with the large body of facts that has been accumulated on the inheritance of mental traits'.67 East dispensed with such nice

academic formulations; heterozygotes, he declared, 'are more or less dull, stupid, lacking

in real ability'.68 Now Punnett had explained that the crux of an effective eugenics policy on mental

defect was to identify the heterozygote:

the great strength of this defect . .. lies in its heterozygotic reserves; if the campaign against it is to meet with success, it is at these that it must be directed.69

62 East, ibid.; Guyer, Being Well Born, 1928 (op. cit. 39), p. 355. 63 See note 60 above.

64 J. Macpherson, 'The problem of the feeble-minded', Glasgow Medical Journal (1912), 77, p. 334. 65 Punnett, Journal of Heredity, 1917 (op. cit. 39), p. 465. 66 Holmes, Trend, 1921 (op. cit. 39), p. 35. 67 Idem.

68 East and Jones, Inbreeding, 1919 (op. cit. 39), p. 243. 69 Punnett, Journal of Heredity, 1917 (op. cit. 39), p. 465.



(Punnett was here drawing attention to the simple proposition that, while F x F always produces F, it was not the case that all Fs are produced F x F; it was in fact likely that one

or both parents of a defective were of normal intelligence.) If the heterozygote was the key to effective eugenics, the advantages of the incomplete/variable dominance

hypothesis were immediately apparent:

1 Heterozygotes could be identified using Binet or perhaps chemical tests. Huxley,

Jennings, Gates and East all speculated along these lines. Shull proposed that immigrants be rigorously tested and their ancestry probed to uncover evidence of heterozygosity.70

2 Heterozygotes, being stupid, were likely to be concentrated in the lower socio- economic strata, together with defectives; there would also tend to be assortative mating (East, Holmes and Fisher).71

3 If that were the case the total number of heterozygotes in the population would be

smaller than on the alternative assumption of complete dominance and random mating of genotypes throughout the population. Holmes took comfort from the thought that 'we need not assume that our inheritance is vitiated' to the extent that had originally been feared.72 East wondered whether it might not be possible to revise his original estimate of the prevalence of heterozygotes from one in fourteen to one in forty-two.73 His argument was that with inbreeding taking place on a larger scale, America's 300 000 defec- tices were more likely to be the result of nn x nn and Nn x nn matings rather than Nn x Nn and that some ascertained defectives were perhaps themselves Nns.

4 By the same token, this concentration of defectives and carriers meant that they did not, as East put it, 'corrupt the germ plasm of the country' as much as had been feared.74 Apart from the benefits which accrued to the country, East and his readers could rest assured that they, their neighbours and in-laws were unlikely to be heterozygotes.

5 Negative eugenics became more feasible and politically less contentious as the search for defective germ plasm could concentrate on the 'social problem group' and on the ecological blackspots which were 'known' to breed defectives (Fig. 2, block 8). These implications were forthrightly spelt out in the official Wood Report which claimed to

have identified such pockets or concentrations of defect.75 Caradog Jones also explained

70 Huxley, What I Dare Think?, 1931 (op. cit. 39), p. 99; Jennings, Biological Basis, 1930 (op. cit. 39), p. 249; Gates, Heredity, 1923 (op. cit. 39), pp. 159-160; East andJones, Inbreeding, 1919 (op. cit. 39), p. 243; for Shull, see note 60.

71 East andJones, ibid.; Holmes, Trend, 1921 (op. cit. 39), p. 36; Fisher, Eugenics Rev., 1924 (op. cit. 39), pp. 115-116.

72 Holmes, ibid., pp. 35-36. 73 East and Jones, Inbreeding, 1919 (op. cit. 39), p. 243. 74 Ibid. A neglected aspect of Goddard's Kallikak study is the implication that heterozygosity was quite

possibly rampant among the East Coast 'elite' during the inter-war years. The argument proceeds as follows. We 'know' that the girl with whom Martin Kallikak senior had a night of passion in the 1770s was feeble- minded, nn genotype (interestingly this is the one and only thing we do seem to know about her). But in that case Martin senior must have been a heterozygote. This is because Martin K junior was F (nn genotype) and we know from Goddard that where a N x F mating produces F offspring, the N partner must be Nn. But in that case there is only a chance of one in 128 that none of Martin senior's seven legitimate children inherited his n gene; and so on to the fifth and sixth generations. And this alarming discovery takes no account of the possibil- ity that the 'good' side of the family might have intermarried with yet more heterozygotes.

75 Mental Deficiency Committee, op. cit. (18), Part 3, p. 80 ff.


372 David Barker

how this reasoning led him to formulate one of the main research questions investigated

in his celebrated Social Survey of Merseyside:

of all the social and biological questions which urgently await solution, one of the most important is how to identify those persons who outwardly are normal but who inwardly carry defective 'genes', seeds which if transmitted will inevitably produce defective stock some time in the future.76

He pointed out that, according to the Wood Committee, mental deficiency was highly

concentrated, and so probably were other forms of deficiency; consequently

if a part, and possibly a large part, of mental defect is localised in certain patches and, more particularly, in certain social classes, it becomes considerably easier to identify the carriers of the defective genes. The area in which we must search for them is to that extent limited and we are saved the labour of traversing much ground where they are less frequently found.77

The survey did indeed confirm the existence of inner city black spots characterized by

extraordinarily high concentrations of defect which, Jones believed, were more convinc- ingly explained by inferior heredity than by the ravages of the environment.

'Fisher arrived at similar conclusions via a different route. It will be recalled that he was stung by the use of Punnett's paper for anti-eugenic propaganda (Fig. 2, block 4). He

made two ripostes. First, he showed that Punnett had misleadingly focused on the inter- minable succession of generations it would take to eliminate (more or less) feeble-mindedness. By contrast, Fisher maintained that negative eugenics was really in the business of significantly reducing the incidence of mental defect, and his 1924 paper set out to demonstrate that if attention was focused on the early impact of policies which prevented defectives from reproducing, it could be shown that incidence would fall by

seventeen per cent in the first generation and by forty per cent after three generations. This way of looking at the pay-off indicated that negative eugenics was well worth while

(Fig. 2, block 6).78

Second, Fisher pointed out that, from a eugenic perspective, Punnett was operating

with 'worst-case' assumptions: that the different genotypes (NN, Nn and nn) were ran- domly scattered throughout the population and mated at random; and that Nns were indistinguishable from NNs (precisely the assumptions which East and Holmes rejected

when they moved from block 3 to block 5). Suppose instead, suggested Fisher, that 'we were to regard them [defectives] as constituting one-sixteenth of an intermating group constituting five per cent of the general population'; in that case 'the effect of segregation would be to reduce the incidence of the defect by thirty-six per cent in one generation'

(Fig. 2, block 7).79 He went on to argue that these assumptions were more plausible than Punnett's or Goddard's and more consistent with the available evidence. It is, of course,

76 Caradog Jones, Social Survey, 1934 (op. cit. 39), vol. iii, p. 394; for an analysis of the concept of the 'Social Problem Group' and the part played by Caradog Jones in developing it, see J. Macnicol, 'In pursuit of the underclass',Journal of Social Policy (1987), 16, pp. 293-318.

77 Ibid., p. 395.

78 Fisher, Eugenics Rev., 1924 (op. cit. 39), pp. 114-115. He spoke here of leaving 'our children a substantial eugenic legacy'.

79 Ibid., pp. 115-116.



immediately apparent that Fisher's revised assumptions closely reflected what was believed to be social reality among the 'social problem group'.

In conclusion it should be noted that no new data had been collected by those geneticists modifying Goddard's theory: the empirical basis for the revised theory was no more secure than for the original. Furthermore, despite Fisher's subsequent claims,80 the exercise involved more than simply theoretical embellishment; in the political arena reputable geneticists such as Fisher and Huxley confidently claimed that segregation and/or sterilization would reduce the incidence of mental defect by at least seventeen per cent in the first generation. 81

GENETICISTS WHO CRITICIZED THE MENDELIAN RECESSIVE THEORY

Who were the critics? The presence of Hogben, Haldane and Penrose, all trenchant critics of eugenics, is no surprise. The most significant critic is Morgan, primarily because of his reputation for avoiding political controversy and public criticism of colleagues. We can be confident that Morgan's intervention in 1925 meant that he found something acutely disturbing going on at the intersection between science and public policy.

When were these attacks mounted? Muller and Morgan apart, there is nothing remotely resembling a concerted attack on the recessive theory until the 1930s. Since mental defect was central to mainline eugenics, this casts some doubt on Kevles' thesis

that his public biologists mounted a sustained attack on mainline eugenics during the inter-war period. This argument is reinforced when we recall the activities of prominent geneticists who endorsed Goddard and adopted a strong eugenic stance. As far as the critics are concerned, the evidence I have collected here supports Werskey who has shown that left geneticists, for different reasons, did not take on the eugenics movement until the 1930s. Moreover, the critics persisted in their attacks into the late 1930s; further evidence that the recessive theory was influential and long-lived and that mental defect was still a key issue in eugenics.

What were the critics saying? It is immediately apparent that when they did take on the eugenics movement, these geneticists saw that one priority was to develop a critique of eugenic policies on mental defect and in particular of the genetic underpinning of these policies. As Hogben explained in 1933,

of late years the discussion of preventive theory has been largely focussed upon the problem of

mental defect.82

The Mendelian recessive theory was, thus, a prominent and recurrent theme in the work

of Morgan, Haldane and Penrose. Their critiques, however, rarely involved either new evidence or recent theory. They criticized Goddard's anecdotalism; they pointed out that mental deficiency was a socio-legal concept, not a biological category, and that it com- prised a diverse range of clinical conditions. They argued that biologists often had great difficulty disentangling the effects of nature and nurture, even in carefully controlled

80 Kevles, op. cit. (4), p. 344, note 5. 81 See note 17 above.

82 Hogben, Nature and Nurture, 1933 (op. cit. 39), p. 31.


374 David Barker

experiments, but when they turned to mental differences in man where experiment was

impossible, the conceptual and methodological problems were vast and had nowhere

been recognized, let alone resolved, in the headlong rush to draw eugenic conclusions.

Holmes had shown by 1921 that Goddard constructed genotypes to meet the require-

ments of his theory. In the '30s Haldane weighed in with a devastating assault on extant

and proposed eugenic legislation, drawing attention, for example, to the involuntary character many 'voluntary' sterilizations, the dubious ethics of hazardous, non-

therapeutic surgery (especially the sterilization of women), and the dangers involved if

rights were granted or withheld on the basis of statistical probability, as in 'probable

potential parent' or 'likely to transmit their defect'.83

Apart from the coup de grace from Penrose in 1938 and Haldane's use of evidence from the Birmingham After-Care Committee which suggested that it was not always the

case that F x F produced F, there was nothing in the work of the critics which rested on

new data or new theory.84 All the material for their 'internalist' critique of the Mendelian

recessive theory had been available from the outset and had been systematically and stub- bornly ignored by geneticists. It was in precisely these terms that Morgan, Hogben and

Haldane addressed their colleagues, urging them to start behaving like scientists and to approach mental deficiency with the same rigour and impartiality which they routinely applied to other problems.

It was Hogben who finally laid it on the line for biologists in 1933. He asked them to

compare amaurotic idiocy and feeble-mindedness. It was unquestionably the case that amaurotic idiocy was inherited and was associated with a gene difference which mani- fested its presence throughout the normal environmental range. Was feeble-mindedness inherited in the same way?

Many biologists will answer in the affirmative. They will do so not because we possess precise knowledge about the gene differences which affect feeble-mindedness of the same definite and unequivocal kind as our knowledge about amaurotic idiocy. They will interpret the question in a sociological sense, and give it what is implicitly a sociological answer. The answer conceals the assumption that if we cannot control the environment we ought to take no chances with the hereditary aspect of the problem.85

It is an open question whether geneticists would have accepted this interpretation of what they had been doing; probably many would have indignantly rejected it. But it was only then that they were forced to confront what they had been saying and doing in these uncompromising terms.

CONCLUSIONS

This paper has examined a strong biological determinist theory of mental deficiency

which was espoused by many inter-war eugenists in America and Britain and was a matter of vigorous contention among geneticists. Scrutiny of its reception by geneticists suggests

83 Hogben, Nature of Living Matter, 1930 (op. cit. 39), p. 208; Morgan, Evolution, 1925 (op. cit. 39), pp. 200-205; Haldane, Heredity, 1938 (op. cit. 39), pp. 30-35 and chapter 3; Penrose, A Clinical and Genetic Study, 1938 (op. cit. 39), p. 10 and chapter 7; Holmes, note 22 above.

84 Penrose, A Clinical and Genetic Study, 1938 (op. cit. 39), Haldane Ibid., pp. 85-86. 85 Hogben, Nature and Nurture, 1933 (op. cit. 39), p. 30-3 1.



that we may need to modify some recent accounts of the relationship between geneticists

and the eugenics movement. According to these, geneticists abandoned eugenics once its

scientific shortcomings became apparent. It has been argued here that in view of both the transparent shortcomings of the Mendelian recessive theory of mental deficiency and the

salience of mental deficiency and this theory in inter-war eugenics, geneticists who were suspicious of eugenics on internalist/scientific grounds 'ought' to have given it short

shrift. They did not. Indeed, most welcomed it with open arms, impervious to the criticisms which were mounted during the 1920s; they also lent their professional weight and authority to the eugenic campaign against the defective. On this evidence abandonment and repudiation was less complete, less consistent, less rational and less scientifically

grounded than has been suggested; it also perhaps came later.

Geneticists moreover did not invariably capitulate when eugenics came under fire from population genetics. Mental deficiency was an area of eugenic policy over which

some geneticists (including a pre-eminent population geneticist, R. A. Fisher) fought a dogged rearguard action against the scientific closure which threatened mainline

eugenics.

The theory, and the eugenics policies derived from it, did, of course, come under attack, but again the evidence suggests that a concerted and effective critique did not develop until after 1930, later than is proposed in accounts which examine the more generalized opposition to eugenics. Looking at the overall performance of the scientific community on this issue, I think we can legitimately speak of public biologies in competition, certainly during the 1920s. This contrasts somewhat with the view of Ludmerer and Kevles that the authoritative statements coming from public biologists were over- whelmingly critical of eugenics.

This analysis, of course, raises as many questions as it answers. For one thing, as I have pointed out, a number of those geneticists critical of mainline eugenics nevertheless endorsed Goddard's theory during the period in question; we now need to re-examine the selective manner in which their critical skills were applied. Was there a pattern to their apparent inconsistency? Why should they have been so uncritical of Goddard? Finally we need to assess what impact, if any, this selective criticism had upon public policy.


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