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. 2024 Apr 10;89(5):285–292. doi: 10.1111/ahg.12551

A historical perspective on Lionel Penrose: Scientist, geneticist and dedicated opponent of eugenics

Maria Kiladi 1,✉
PMCID: PMC12336927  PMID: 38597250

Abstract

The paper explores Lionel Penrose's scientific work. Penrose investigated the causes of mental disorders from clinical and genetic points of view. His investigations on phenylketonuria and Down syndrome helped to demonstrate the heterogenous character of mental disorders, whose causes can range from genetic with high penetrance, to largely environmental. He was specifically selected by JBS Haldane to become University College London's third Galton Chair as a result of his Colchester survey investigations. He became the first Galton Chair who had medical training. He never concealed his distaste for anything related to eugenics. As well as using his scientific work to reject eugenic ideas such as suggestions on sterilisation measures or the existence of a social problem group, he campaigned successfully to rename the Department of Eugenics, Biometry and Genetics to Department of Human Genetics and Biometry. With his work, he discredited prejudiced eugenic ideas on mental disorders and became an advocate for those with mental disabilities.

1. INTRODUCTION

Lionel Penrose produced ground‐breaking scientific work that paved the way for modern approaches to mental disorders at a time when there was very limited understanding of the contribution of heredity and environment to the causation of intellectual disability. His work on Down syndrome took ideas of heredity, mental disabilities and the environment from prejudiced, unsubstantiated theories, to discussions on the biological causes of mental disorders. Penrose was one of the first to investigate mental disorders using rigorous medical methods, which not only promoted better understanding of the relations between mental disorders, heredity and the environment, but also discredited long‐standing prejudices that prevailed at the time.

Penrose's work focused on understanding patients with mental disorders to help them at a time when eugenicists campaigned vigorously for their segregation and sterilisation. Anxieties over ‘national degeneration’ brought on by falling birth rates after the First World War, coupled with a perceived excessive fertility of this group, made those with mental disorders the main target group of British Eugenicists during the period 1900 to 1930 (Klaussen & Bashford, 2010, pp. 98—99; Mazumdar, 1992, pp. 45—46). Eugenicists feared that the perceived excessive fertility of those they called ‘undesirables’ and which primarily included those with mental disabilities, would inevitably lead to lowering the population's intelligence, and would be disastrous for the nation. Segregation, but mainly sterilisation, were the main solutions suggested to what was seen as a national problem. Penrose countered such arguments partially by demonstrating that those affected by severe mental disorders rarely reproduced. He also promoted the idea of their assimilation into society.

To study mental disorders, he moved away from the pedigrees of individuals deemed to be undesirable, widely used by eugenicists during that period (1900–1930), and used quantitative methods and medical information to understand their causes. Pedigrees were widely used at the time as a means of demonstrating ‘networks of relationships’ that showed Mendelian inheritance patterns (Mazumdar, 1992, p. 87). They were the main tool used by the Eugenics Education Society, particularly in showing inheritance patterns of social class characteristics such as alcoholism and pauperism. Although they were considered by Eugenicists to be useful for demonstrating ‘raw facts of heredity’ in a way that allowed them to be ‘obvious at a glance’, they did not provide any interpretation or explanation of the causes of these undesirable traits (Mazumdar, 1992). Eugenicists used them to promote the idea that certain undesirable human traits such as alcoholism, criminality, epilepsy and ‘feeble mindedness’ were inherited. The premise was that these traits were inherited in a Mendelian way. Consequently, pedigrees were drawn up using multiple and often unreliable and possibly erroneous sources to classify individuals as affected or unaffected by these traits, in an attempt to show that often unrelated conditions were inherited in a Mendelian fashion. While for many psychological or mental disabilities the diagnoses were often vague, the pedigrees were considered to mark clear phenotypes. Shifting the focus from these pedigrees to medical study, Penrose became a ‘genetically oriented psychiatrist’ (Wright, 2001) who developed a ‘detailed picture of the different kinds of mental disability’ and how this depended on the environmental factors (Rolls‐Hansen, 2010). This opened the ‘scientific dispute’ on ‘feeblemindedness’ with Penrose emerging as an ‘opponent, rather than a supporter of eugenics’ (Thomson, 2010, p. 121).

2. BIOGRAPHICAL DETAILS AND STUDIES

Lionel Sharples Penrose (Figure 1 and Figure 2) was born to a family of Quakers in 1898 (Harris, 1974; Hodgson, 1998; Laxova, 1998; Smith, 1999; Watt, 1998a). He initially studied mathematics at St John's College in Cambridge in 1919 initially on mathematics but changed to the Moral Sciences Tripos (Harris, 1974). His strong interest in psychology led him to Vienna where he studied under Sigmund Freud in 1921, sparking an interest in abnormal psychology and mental disorders (Harris, 1974). This was followed by a medical degree in Cambridge (1925) and clinical work at St Thomas's Hospital in London, out of his conviction that a medical degree was necessary for those working on mental disorders (Harris, 1974). A few years later, in 1931, he was appointed as a Research Medical Officer at the Royal Eastern Counties Institution at Colchester, a post supported by the Medical Research Council and the Pinsent‐Darwin Trust. The outcome of this post was a survey that became known as ‘the Colchester Survey’.

FIGURE 1.

FIGURE 1

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Lionel Sharples Penrose at his desk at University College London (UCL), 1946 (reprinted with permission from UCL Library Services and Special Collections).

FIGURE 2.

FIGURE 2

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Portrait of Lionel Sharples Penrose, 1969 (reprinted with permission from the National Portrait Gallery, London).

The Survey was commissioned by the Medical Research Council and the Pinsent‐Darwin Trust as a means of ‘increas[ing] existing knowledge in the causation of mental deficiency’ from a clinical and genetical point of view (Harris, 1974; Kevles, 1985; Mazumdar, 1992). To accomplish this, Penrose surveyed 1280 patients from the Royal Eastern Counties Institutions, alongside their siblings, parents and children. Overall, this amounted to about 8000 individuals. Additional sources were used such as public records and information from health authorities. All information collected was assessed to determine reliability and categorised accordingly to distinguish individuals for which little was known, or where the information collected was incomplete (Penrose Papers). One of the survey's important findings was an ‘absence of any sharp dividing line between (usually milder) causes of mental deficiency and the so‐called normal state’. The relatives of more severe cases often had much higher intelligence than the cases, suggesting that these cases had more of a genetic component. Mental disabilities thus had a ‘multiplicity of causes both genetic and environmental’ (Harris, 1973, p. 526). Penrose concluded that ‘the aetiology of mental defect is multiple and a facile classification of patients into primary or secondary, endogenous or exogenous, cases would have only led to a fictitious simplification of the real problems inherent in the data (Harris, 1973, p. 526).

A year after the completion of the Survey in 1938, Penrose moved on to become the Director of Psychiatric Research at the London Psychiatric Hospital in Ontario, Canada, and returned to the United Kingdom in 1945 to become the third Galton Chair of Eugenics at University College London (UCL), a post he held until his retirement in 1965 (Harris, 1974). He then went on to become the Director of the Harperbury Hospital Kennedy—Galton Centre, significant funding for which was provided by the Kennedy family in America, as there was a child with Down's syndrome in the family (Harris, 1974).

The Galton Professorship of Eugenics was established in 1911 after Francis Galton named in his will the University of London as his estate's residuary legatee. He also specified the founding of the Galton Chair of Eugenics, to be based at UCL. Karl Pearson was named as the first Chair. Galton's bequest enabled Pearson to also become Head of the newly formed Department of Applied Statistics and Eugenics, a post he held until his retirement in 1933 (Porter, 2004). Following Pearson's retirement, the University of London split the department into Eugenics and Statistics. Ronald Fisher was appointed as the second Galton Chair of Eugenics, while Karl's son, Egon, became head of the Department of Statistics. Fisher's departure from UCL in 1943 sparked discussions about the possibility of bringing Statistics and Eugenics together. Egon strongly opposed the idea, as he thought that his statistical investigations were ‘largely non‐biological’. As a result, the two departments remained separate (Penrose Papers, Haldane Papers, ST2/1). It was decided that the Galton Chair should be part of the Department of Biometry and Genetics, led by JBS Haldane who, having started at UCL as Professor of Biometry in 1929, was now Professor of Biometry and Genetics.

Haldane's first task was to find an appropriate candidate for the Galton Chair. He was aware of Penrose's work and his Colchester Survey and suggested him as the best possible candidate (Dromanraju, 1998; Smith, 1998). He argued that Penrose's work made important contributions to human inheritance and thought that with Penrose as Galton Chair, the ‘eugenic movement will become a good deal more concrete’ (Penrose Papers). What made Penrose's approach more concrete for Haldane was his medical training. Contrasting him with his predecessors at the Galton Chair, he noted that Pearson and Fisher came ‘from mathematics via statistics’, while Penrose came ‘from psychology via medicine’. It was the prospect of combining statistics, psychology and medicine that Haldane hoped would transform the Galton Professorship. Penrose was expected to combine them with ‘up to date clinical and psychological methods’ (Penrose Papers). As Harry Harris noted in his obituary of Penrose, this was the first time that the Galton Chair was not occupied by a statistician but by a professor with medical training (Harris, 1973). Under his leadership, the Galton Laboratory was transformed into a ‘Mecca for aspiring human geneticists from England, the Empire, the United States and the Continent’ (Fraser, 1998; Kevles, 1985; Penrose, 1949b; Povey, 1998).

Penrose never concealed his distaste for anything related to eugenics while he was at UCL. Bette Robson, Galton Chair of Human Genetics between 1975 and 1994, mentioned in her contribution on Penrose's centenary that he mainly preferred using notepaper with the ‘Galton Laboratory’ heading to avoid any connections with the ‘Department of Eugenics’ (Robson, 1998). He also changed the title of the departmental journal, the Annals of Eugenics. The journal was founded in 1925 by Karl Pearson and acquired the subtitle of ‘A journal for the Scientific Study of Racial Problems’ under Ronald Fisher, second Galton Chair (1933—1943). Penrose initially changed the subtitle to ‘A Journal of Human Genetics’, and then changed the title altogether in 1954 to Annals of Human Genetics’ (Harris, 1973; Kiladi, 2021).

In 1961, embarrassed that he was working in a department with ‘eugenics’ in its title, he suggested the renaming of the department to the Provost, Ifor Evans (Penrose Papers; UOL ST/2/1; AR 485). Writing to Evans in April 1961 discussing the possibility of renaming the department, he noted that ‘the stigma of eugenics [at the Department] has been a serious handicap in pursuing purely fact‐finding investigations. It is a continual embarrassment to have to explain that the Chair and the Laboratory are wrongly named and that there is no liaison with the Eugenics Society’ (Penrose Papers). While he still saw the Laboratory as maintaining statistical orientation on investigations, he noted that the importance of medical aspects ‘has become increasingly evident’. By ‘medical aspects’ he meant biochemistry, serology and cytology (Penrose Papers).

Archival research has demonstrated beyond doubt that Evans was very supportive to the idea and found no reason to delay the matter when it was first suggested by Penrose in June 1961, finding ‘really no difficulty before us in trying to make the change’, requesting from Penrose to put a proposal forward to the University of London (AR 485; Penrose Papers; Kiladi, 2021). Similarly, the Senate of the University of London where the original bequest was made in 1911 was supportive, but inadequate administrative understanding on the legal framework around this bequest and how to disentangle the Chair from it delayed the matter (AR 485; Penrose Papers; Kiladi, 2021). This was fully succeeded in 1963 when the department was renamed ‘Human Genetics and Biometry’ (Kevles, 1985; Penrose Papers; UoL ST/2/1; AR 485; GO 1812; AR 485; Penrose Papers; Kiladi, 2021).

3. EUGENICS AND THE ‘FEEBLE MINDED’ IN BRITAIN

By 1900 national anxieties about the quality of the British population, its ‘falling birth rate […] high infant mortality, the extent of poverty’ provided fertile ground for eugenic theories to flourish (Bland & Hall, 2010, p. 213). There was a strong sense that ‘racial quality’ was in danger, the nation was destined to ‘be swamped by the socially [and] genetically unfit’ (Soloway, 1995, p. xxi). ‘Race’ for eugenicists was genetically defined and had biological coherence (Turda, 2010, p. 63). As a result, it was believed that excessive fertility among those seen as a social group of undesirables would result in degeneration. Measures suggested were legislation, segregation and sterilisation. Inevitably, the mentally disabled became a primary target of eugenicists, particularly in the United Kingdom where eugenicists were also preoccupied with class as well as race (Kevles, 1985; Rolls‐Hansen, 2010; Searle, 1976; Thomson, 2010).

In his research on disability, psychiatry and eugenics, Mathew Thomson mentions how the physically disabled were less of a target for eugenicists, as opposed to those with mental disabilities (Thomson, 2010). Taking into account the rise of the mental asylum already from the 19th century, he claims that ideas of mental illness as hereditary developed already before eugenics emerged (Thomson, 2010, p. 117). The involvement of ‘lay magistrates, [and] lawyers’ in the decision‐making on who belongs in an asylum predates eugenic arguments for the need of legislation to allow segregation. Mental illness as a sign of degeneration preceded eugenics, and ‘played a part in providing an environment for the success of the movement when it did emerge’ (Thomson, 2010, p. 117). Psychiatry itself replicated narratives of heredity as the main cause of mental illness (Thomson, 2010, p. 118). But what really made mental illness a particularly fertile ground for eugenic narratives was the fear that those labelled as ‘feeble‐minded’ could be appearing as normal, thus remaining out in society, rather than segregated. Their perceived and unsubstantiated excessive fertility would contribute to the degeneration of the ‘race’ as a result (Thomson, 2010, pp. 118–119).

In 1904 the Royal Commission into the Care and Control of the Feeble Minded set the tone for ‘appropriate measures’ needed, providing arguments for formal legislation (Searle, 1976; Watt, 1998b, pp. 344). The Commission was organised by the government after the prison and poor law authorities who were concerned about the costs of having to maintain ‘a large number of defectives’ (Searle, 1976, p. 106). In 1908 it published the results of its investigations, concluding that ‘feeble mindedness’ was a hereditary condition that resulted in excessive fertility of its carriers, who should be segregated and controlled ‘in the interest of others as well as for their own protection’ (Searle, 1976, p. 106).

The Commission included a medical expert, Dr. Tredgold, who, in 1907, would become one of the first members of the Eugenics Education Society (Searle, 1976). The Society was founded the same year and represented the popular version of eugenics in Britain, as opposed to the ‘academic’ one which was based at UCL between 1904 (already from the founding of the Eugenics Records Office) to 1963. It aimed to promote the National importance of Eugenics, but also to ‘spread the knowledge of the Laws of Heredity’, ‘standing for active legislation’ to achieve its aims and crucially, ‘apply the laws of inheritance to the social problems of poverty and pauperism' (SA/EUG/A1; Farrall, 2019; Mazumdar, 1992, p. 7). Historians Lynsdey Farrall and Pauline Mazumdar who have worked extensively on the Society and have demonstrated that it was influential thanks to its membership, have also documented in detail the Society's operational model, which included heavy lobbying to promote its causes (Farrall, 2019; Mazumdar, 1992). Normal ‘working patterns’ for the Society included contacting legislators and parliamentary committees to influence decisions, sending deputations to the Home Office by using the help of Members of Parliament (such as the Liberal Minister of Parliament Walter Rea) who were quite often also the Society's members, forming sub‐committees to present its views to parliamentary inquiry committees, and appointing committees specifically to monitor legislation on the issues that were of interest (Farrall, 2019; Mazumdar, 1992; Searle, 1976).

The 1908 report of the Royal Commission into the Care and Control of the Feeble‐Minded provided arguments for the newly founded Society to justify the need for legislation. A lively campaign resulted in an initial draft by the Society itself of what subsequently became the 1913 Mental Deficiency Act, the ‘most substantial achievement of the British Eugenics lobby’ (Farrall, 2019; Mazumdar, 1992; Searle, 1976; Thomson, 2010, p. 188). The Act gave ‘compulsory powers to detain and segregate the feeble‐minded’ (Searle, 1976, p. 111) but did not go as far as including compulsory or coerced sterilisation. By 1929, emboldened by its success, the Society participated in the Wood Report which aimed to investigate the efficacy of the 1913 Act. It also introduced a novel term to name the problem: The ‘Social Problem Group’, also named as ‘the Submerged 10th’. The group was believed to represent 10% of the population (about 4 million people at the time). The main argument of the report was voluntary sterilisations as a mean of curbing the fertility of this group of undesirables that included ‘insane persons, epileptics, paupers, criminals, unemployables, habitual slum dwellers, prostitutes, inebriates and other social inefficient’ (Mallet, 1931).

By the time a second report was commissioned (the Brock Report, 1932–1934), it was becoming clear that British eugenicists did not have the influence they would have liked to turn ideas on sterilisation into legislation. The Report of the Vagrancy Committee which was organised by the government just before the Brock report (in 1930) without any involvement from the Society, rejected eugenic ideas on the genetical causes of the ‘social problem group’ and added environmental causes as a reason to ‘social failure’ (Mazumdar, 1992, pp. 200–201). A second report by the British Medical Association's Mental Deficiency Committee (1930–1932) also made similar arguments, stressing that ‘more research was needed before any strong claims could be made about the exact type of inheritance of mental defect’ (Mazumdar, 1992, p. 201). It also made distinctions between social behaviour and mental deficiency, concluding that the problem had been exaggerated by eugenicists. Moreover, sterilisation was mentioned only as a possible option for those with severe mental disorders and only as a means of safeguarding (Mazumdar, 1992, pp. 202–203). This report had very little involvement from the Eugenics Education Society. Out of the 21 members, only five were members of the Society. It is clear that there were eugenic opponents at the time, and that the Society's ideas on the social problem group and appropriate solutions were not endorsed further beyond the Society itself.

The Brock Report which was published in 1934 (its investigation having started in 1932) was produced with support from the Eugenics Education Society and came out in support of sterilisations, in line with the Society's campaigns of that period. When it was published in 1934 in favour of such views, the Society proceeded to form a Joint Committee on Voluntary Sterilisation in the hope that its campaign will result in the Brock Report's enactment. But it was not just the medical profession that objected to ideas on sterilisation, as was noted above with the British Medical Association's report. It was also becoming increasingly clear that the Left, as well as the Church, were opposed to such ideas. Organised Labour was against sterilisation. For example, the Mental Hospital and Institution Workers’ Union ‘proposed, and carried, an anti‐sterilisation motion at the Trades Union Congress in 1934’ (Mazumdar, 1992, p. 211). Equally, Catholics also rejected and condemned the Brock Report's sterilisation ideas as ‘absolutely unacceptable’ (Mazumdar, 1992, p. 211). While the Eugenics Education Society saw the Report's findings as a success and campaigned for the Report's enactment until 1940, it failed to gain wider support outside eugenic circles.

4. INVESTIGATIONS IN THE PATHOPHYSIOLOGY OF MENTAL DISORDERS: PHENYLKETONURIA AND DOWN SYNDROME

Inevitably Penrose's 1931 appointment in Colchester was not left unnoticed by the Society, which approached him suggesting collaboration (Penrose Papers). The early 1930s were, after all, the height of the Eugenic Education Society's sterilisation campaigns for the exact same group Penrose was studying. Penrose rejected any suggestions for collaboration, taking instead the opportunity to outright contest the existence of the so‐called social problem group. He additionally pointed out his fundamental disagreements with the society's causes as well as with its unscientific means to justify its positions (Penrose Papers). During his time in Colchester, Penrose made two significant contributions to discussions on mental disorders and heredity by investigating phenylketonuria (PKU) and Down syndrome (Penrose, 1932; Penrose, 1934). This allowed him to demonstrate the heterogenous nature of mental disorders.

In 1934 biochemist Ivar Følling (Oslo University Hospital) detected an autosomal recessive metabolic disorder characterised by the patients’ inability to metabolize the amino acid phenylalanine (Blau et al., 2010, p. 1417; Kevles, 1985, p. 159). High levels of phenylalanine led to toxicity which resulted in mental disorders. Penrose, along with biochemist Juda Quastel (Cardiff City Mental Hospital) reproduced Følling's investigations in Colchester, taking urine samples from patients to identify those that exhibited high levels of phenylpyruvic acid in urine – an indication of high phenylalanine levels. They confirmed Følling's findings in 1937 (Penrose & Quastel, 1937). Penrose was especially interested in the connection made initially by Følling between phenylalanine toxicity and mental disorders (Kevles, 1985, p. 159; Penrose, 1946a; Penrose & Quastel, 1937). He also assumed that Phenylketonuria (PKU), as Quastel named it, might be prevented by a low phenylalanine diet. It was also hoped that this could go as far as reversing the mental disorder that resulted from it. Penrose selected a patient and experimented with dietary changes, in the hope that mental disorder will be reversed. Initial results were encouraging, showing a drop in phenylpyruvic acid from urine. However, limitations such as poor preparation and expense led to abandoning the dietary treatment altogether (Kevles, 1985, p. 159). This was a pioneering idea at the time. Today, early diagnosis and dietary restrictions ‘remain the mainstay of [PKU] treatment’ (Blau et al., 2010, p. 1417; Kevles, 1985, p. 159; Penrose, 1946; Penrose & Quastel, 1937).

PKU is an autosomal recessive condition that occurs only when an individual has inherited two copies of the causative gene variant. Children of individuals with the PKU gene variant would inherit a copy from their parents and will only be affected if they inherited the PKU variant from both parents, which in most cases is unlikely. Essentially, the risk to these children of having PKU themselves is low. While PKU is hereditary, the intellectual disability in this condition is preventable by diet modification.

Penrose's investigations on PKU added to shifting discussions on mental disorders from being results of ‘arrested brain development, or brain damage, [that] could be passed down to later generations’ as eugenicists quite often claimed (Wright, 2001, p. 172). It also led to questions as to what other types of mental disorders might also have biological causes, which remained largely unknown. It provided further evidence of the complexities and heterogeneity of mental illness, putting at the same time ‘environmental influences’ at the heart of ‘mental deficiency’ (Barkan, 1992, p. 201; Mittwoch, 1998).

Penrose devoted most of his scientific work to the biological study of Down syndrome. His initial investigations started in 1931 with the Colchester Survey. He continued tirelessly beyond his retirement from UCL's Galton Chair in 1965, as the Director of the Kennedy‐Galton Centre until his death in 1972. The prevailing theory on the Syndrome in the 1930s, in place since the 1860s when it was first formulated, was that of a reversion to a Mongolian ‘race’ for the patient – hence its original name as ‘Mongolian Imbecility’. The theory stemmed from physician John Langdon Hayden Down who first identified it in 1866. (Chen, 2016, p. 238; Gould, 1981, pp. 134–135; Kevles, 1985, p. 160, Wright, 2001, p. 163). Essentially, Down categorised his patients at his Earlswood clinic into what he saw as ‘racial types’, noting that the majority of them appeared to belong to what he named the ‘Mongolian family’, some 10% of the clinic's patients (Chen, 2016, p. 238; Wright, 2001, p. 164). The theory was kept alive further in the 1920s and 1930s by popular books such as physician's Francis Crookshank The Mongol in our Midst, which replicated such theories on mental disabilities and ‘racial qualities’ (Crookshank, 1924; Kevles, 1985, p. 160; Wright, 2001, p. 173).

Penrose rejected such theories for ‘lack of evidence’ on an unscientific and ‘overtly racist taxonomy of mental disability’ that persisted (Penrose Papers; Wright, 2001, p. 155). To investigate Down syndrome, he surveyed 150 families from his Colchester patients affected by it, in an attempt to clarify the various existing theories at the time. By the 1930s, theories on the causes of Down syndrome included maternal age, paternal age or birth order, with the last child believed to have more chances of being affected (Kevles, 1985, pp. 161–162). The evidence he gathered from family histories demonstrated that the likely cause was maternal age, especially in women above the age of 35. Though it was still not clear enough what the role of genetics was in this case, Penrose demonstrated that some mental disorders did not have only one cause but could have a combination of pathological, genetic and environmental causes (Kevles, 1985 p. 162). It would not be until the late 1950s when cytogeneticists would uncover what is today recognised as ‘Trisomy 21’ – a third copy of chromosome 21 that results in Down syndrome for its carrier. He further objected to the prevailing term that described the Syndrome for being offensive, racist and highly unscientific, suggesting ‘Down's syndrome’ or ‘Down's Anomaly’ as more accurate (Kevles, 1985; Wright, 2001, p. 175). The use of outdated terms to describe Down syndrome persisted well into the 20th century (Wright 2010, p, 175). The original term was officially discredited in 1966 when the World Health Organisation finally ‘voted overwhelmingly’ for the use of ‘Down syndrome’ as the right term to describe the condition (Wright, 2001, p. 175).

5. CONCLUSIONS: ‘A DEDICATED OPPONENT OF EUGENICS’

Writing a contribution on a symposium celebrating Penrose's centenary, Bette Robson described Penrose as ‘a dedicated opponent of Eugenics which he regarded as an uninformed and dangerous policy of racial purification’ (Robson, 1998). Indeed, Penrose made a sharp distinction between eugenics and genetics, regarding eugenics as an ideology, and human genetics as science (UoL ST2/1/52; AR485). He thought eugenics was ‘open to a good deal of latitude’ and had narrow conceptions (Penrose, 1949). He rejected ideas on the excessive fertility of those with mental disabilities, noting that it had been demonstrated that those severely affected by mental disorders were ‘almost invariably sterile and at institutions’ (Penrose, 1947; Penrose, 1949; Penrose, 1950; Watt, 1998b, p. 346).

Penrose was primarily an opponent of eugenics through his scientific work which he used to demonstrate that mental and social disorders do not have a single cause as eugenicists argued. With his investigation to phenylketonuria he highlighted genetic, autosomal and environmental causes of mental disorders, demonstrating that metabolic disorders such as phenylketonuria can lead to mental effects. He used his work on phenylketonuria to make arguments against sterilisation, pointing out that in this case such measure would be ineffective: To begin with, there was no reliable method to identify carriers of the causative genetic variation at the time. But even if it were, carrying the genetic variation alone does not result in developing the trait (Penrose, 1946).

His investigation on Down syndrome placed maternal age at the heart of its causes as opposed to other theories based on ‘racial characteristics’ which were prevalent at the time, but also theories on other causes such as paternal age. He rejected connections made by eugenicists between excessive fertility and those with mental disorders and challenged ideas on the existence of a ‘Social Problem Group’ as defined by eugenicists. He has been noted by historians for his ‘humanitarian approach’, showing particular interest in his patients, especially those displaying Down syndrome, describing them as individuals with a ‘particular temperament […] a secret source of joy (Barkan, 1992; Fraser, 1998; Harris, 1973; Kevles, 1985). His campaign to rename the Department of Eugenics at UCL certainly demonstrates an individual against eugenics, but it is primarily for his scientific work that he should be celebrated as an opponent of eugenics.

SOURCES OF ARCHIVES

AR 485. Change of Title to Galton Chair of Human Genetics. UCL Special Collections/Records Office. London, UK.

GO 1812. Professor LS Penrose Appointment File. UCL Special Collections/Records Office. London, UK.

HALDANE/3/3/7. Correspondence. Department of Eugenics, Biometry and Genetics. Haldane Papers. UCL Special Collections. London, UK.

PENROSE/2/11. Administrative Papers and Correspondence Relating to Institutions where L S Penrose worked. UCL Special Collections. London, UK.

PENROSE/2/19/2/1. Papers Relating to the Colchester Survey. Draft ‘Report on 1280 Cases of Mental Defect’. UCL Special Collections. London, UK,

PENROSE/2/33/2. Papers relating to Eugenics. Penrose Papers. UCL Special Collections. London, UK.

PENROSE/3/2/41. Correspondence. Burt, Dir Cyril. Penrose Papers. UCL Special Collections. London, UK.

PENROSE/3/5/17. Correspondence. Eugenics Society, Editor of Eugenics Review. Penrose Papers. UCL Special Collections. London, UK.

PENROSE/3/5/18. Correspondence. Eugenics Society, General Secretary. Penrose Papers. UCL Special Collections. London, UK.

PENROSE/3/20/1. Correspondence. United Nations Educational, Scientific and Cultural Organisations (UNESCO). Penrose Papers. UCL Special Collections. London, UK.

PENROSE/3/20/5. Correspondence. University College London, The Provost. Penrose Papers. UCL Special Collections. London, UK.

SA/EUG/A1. Eugenics Society. Annual Reports. Wellcome Collection. London, UK.

ST2/1. Senate Meetings. University of London Archives. University of London. London, UK.

CONFLICT OF INTEREST STATEMENT

The authors declare no conflicts of interest

ACKNOWLEDGMENTS

I am extremely grateful to UCL's Presidents and Provosts, Professor Michael Arthur and Dr Michael Spence, for funding the Legacies of Eugenics Project during which this research was conducted. I am also deeply indebted to all members of staff at UCL's Department of Science and Technology studies for their support, and especially to Professor Joe Cain for his guidance during the Legacies of Eugenics Project. Thanks also to UCL Library Services and Special Collections staff for their help, and especially to Ms Katy Makin and Mr Colin Penman for all their help with archives and papers. I am extremely grateful to the Annals of Human Genetics Editor‐in‐Chief, Dr Rosemary Ekong, for suggesting this paper, and above all for her continuous support.

Kiladi, M. (2025). A historical perspective on Lionel Penrose: Scientist, geneticist and dedicated opponent of eugenics. Annals of Human Genetics, 89, 285–292. 10.1111/ahg.12551

DATA AVAILABILITY STATEMENT

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

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