Obituary: Professor James H. Renwick

James Harrison Renwick, geneticist: born 4 February 1926; researcher, Atomic Bomb Casualty Commission, Hiroshima 1951-53; Professor of Human Genetics, Glasgow University 1967-68; Reader in Human Genetics and Teratology, London University 1968-79, Professor of Human Genetics and Teratology 1979-91 (Emeritus); Head of Preventive Teratology Unit, London School of Hygiene and Tropical Medicine 1977-91; married 1959 Helena Verheyden (one son, one daughter; marriage dissolved); 1981 Kathleen Salafia (two sons); died 29 September 1994.

JAMES H. RENWICK was a distinguished medical geneticist and teratologist who made important contributions to the understanding of human genetics and the causes of birth defects.

He was also one of the most principled, honest, stimulating and generous persons I have known. We met late one night, back in 1971, in the London School of Hygiene and Tropical Medicine. I had an idea, about parallels between the maintenance of genes and of infections in populations, and wanted to talk. Despite the midnight hour he listened, argued, and criticised. He liked ideas, on principle. And he always had many of them.

Foremost on his mind at that time was a method to aggregate information on the possible causes of a characteristic, and the evidence for and against alternative causes of various analogous characteristics, in order to optimise the inference of cause. He called it 'pointer analysis', and was applying it to the aetiology of anencephaly and spina bifida.

Only later did I learn something of his background: origins in Yorkshire; medicine at St Andrews; an early fascination with genetics which pushed him to the United States to meet JV Neel, who was instrumental in setting up the Atomic Bomb Casualty Commission in Hiroshima, which in turn landed Renwick an attachment there in 1951. This involvement in genetics led Renwick to a central role in the early days of human gene mapping, when he became the chief liaison between sophisticated mathematical techniques developed by Cedric Smith at the Galton Laboratory in London, and a huge computer commanded by Victor McKusick in Baltimore. His work linking the ABO blood groups and the nail-patella syndrome was seminal, and is still cited as a classic in human linkage analysis.

He might have stayed with that work, which evolved into the human genome project of today, but didn't. I have always thought he was driven towards broader questions of public health because of a fascination with the deepest implications of the Bayesian logic he used in the gene linkage analyses, and a dream to expand this to cover all causal mechanisms. (Bayesian logic takes a number of possible or expected explanations for a particular situation, and works out by means of probability which explanation fits most appropriately to it.) So he became Reader and later Professor in Human Genetics and Teratology at the London School of Hygiene, and turned his attention to birth defects, in particular anencephaly and spina bifida (ASB). It was the most common defect in those days, and his first delivery as a medical student had been an anencephalic.

His aggregation of data pointed to a novel aetiology for ASB: that it arose as a consequence of some toxin in blighted potatoes, if they were eaten early in pregnancy. He published the hypothesis in 1972, and it caused a furore. It also caused an avalanche of research, some of which provided evidence that folate supplementation can reduce the risk of ASB, but none of which supported his idea. With characteristic candour he publicly withdrew his potato hypothesis in 1974, at the Royal Society of

Medicine.

Though he accepted that his potato hypothesis had been refuted, he continued to prowl around its edges, haunted by various corroborating findings in laboratory animals, believing that the temporal correlations he had discovered must indicate some link - perhaps that blighted potatoes increased the demand for folate. The research led him in various directions, towards the role of alcohols and alkaloids in the aetiology of birth defects. He never hit on another bombshell - but continued rigorously to explore the logic of inferring causes of developmental defects until his retirement in 1991.

Jim Renwick was stimulating company. Always willing to consider any hypothesis, challenging, mischievous, stubborn for the truth, honest to a fault, and generous - once when I fell ill he came to apologise formally, on behalf of the public health profession, for not having prevented it. And he couldn't waste anything - so he wrote his memos in a neat hand on tiny scraps of paper, saved stubs of pencils, had an eye on every skip in London . . . Unable to countenance the dishonesty of politics and the increasing emphasis on administration in academia, he terrorised department heads and deans, citing chapters and verses of constitutions, and reminding them of the essential commitment of the university to learning.

His illness came suddenly, last June, as a headache. He found he could lessen the discomfort by banging his head, and figured there must be a tumour blocking the aqueduct of Sylvius. He was right. But he wanted to know more, where it came from, and insisted on a brain biopsy. Ultimately there was nothing which could be done to save him; so he called on old colleagues, told them the story with characteristic precision, enquired about their research, talked about a hundred other things, and said goodbye.

(Photograph omitted)

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