Sir Harold Himsworth
Article first published online: 17 NOV 2011
© 2011 The Authors. Diabetic Medicine © 2011 Diabetes UK
Volume 28, Issue 12, pages 1438–1439, December 2011
How to Cite
Himsworth, R. (2011), Sir Harold Himsworth. Diabetic Medicine, 28: 1438–1439. doi: 10.1111/j.1464-5491.2011.03399.x
- Issue published online: 17 NOV 2011
- Article first published online: 17 NOV 2011
- Accepted manuscript online: 3 AUG 2011 04:33PM EST
Diabet. Med. 28, 1438–1439 (2011)
My father enrolled as a medical student at University College, London in 1924 and proceeded to the adjacent University College Hospital and Medical School the following year. To his own surprise he had a brilliant student career, qualifying as MB in 1928 and proceeding to MD in 1930, and winning the University Gold Medals on each occasion. During his last student year, he carried out research for a short time under the supervision of the biochemist C. R. Harington, who was then working on the structure and synthesis of thyroxine. My father, to the dismay of his family, thereafter decided on a career in medical research and, in January 1931, joined the Professorial Medical Unit.
At that time, University College Hospital and Medical School had just been transformed by a huge investment by the Rockefeller Foundation to provide extensive laboratory and clinical research facilities. This investment was attracted by the scientific distinction of its academic staff, notably the cardiologist Sir Thomas Lewis, who was promoting rigorous ‘clinical science’ as a novel and valid discipline, and T. R. Elliott, the Professor of Medicine, who was a close friend of Sir Henry Dale, the great pharmacologist, then Director of the nearby Medical Research Council National Institute for Medical Research. All three men greatly influenced my father’s research and career. Importantly, Dale had purified and then standardized insulin for therapeutic use in 1925.
Why did my father choose carbohydrate metabolism and diabetes as his fields of research when no one else in the Medical School and Hospital was working in these areas? Probably because diabetes was a common disease and had become a ‘hot topic’ following the dramatic isolation of insulin and its introduction into clinical practice. Nevertheless, little was known about the biochemical disorder underlying the disease. Although acute and chronic forms of diabetes were recognized in the 10th edition of Osler’s textbook of medicine used by my father, it was stated that there was ‘no essential difference between them’. He had been intrigued, however, by a patient with diabetes whose fasting blood glucose did not vary despite the excretion of large quantities of glucose in the urine; this suggested to him some form of continuing biochemical regulation of carbohydrate metabolism.
Over the next 4 years, working mostly without assistance in the laboratory and on the ward, my father demonstrated in normal volunteers and patients with diabetes the differential effects of high-carbohydrate and high-fat diets on the glucose tolerance test curve and on sensitivity to insulin. He used as indicators of insulin sensitivity the response to the injection of small doses of insulin in fasting subjects, the difference in the configuration of the glucose tolerance curves with and without concurrent administration of insulin, and the difference between the capillary and venous blood glucose concentrations during tolerance tests in normal subjects and patients with diabetes. These clinical studies were complemented by experiments in animals. In January 1936 he published The Lancet paper  which this issue commemorates and which concludes:
‘It is shown that two different types of disease can be distinguished as causing the symptom-complex of diabetes mellitus. One, the insulin-sensitive type, appears to be caused by deficiency of insulin; the other, the insulin-insensitive type, is apparently due not to lack of insulin, but to lack of an unknown factor which sensitises the body to insulin. A test for distinguishing these two types of diabetes mellitus is described. The appropriate dietetic treatment of the two diseases may differ.’
My father continued to develop his clinical and physiological research in the broad area of diabetes and carbohydrate metabolism, and attracted to his unit a number of clinical research fellows from the UK and the Commonwealth. He summarized their work in three lectures to the Royal College of Physicians in 1939, in which he characterized the two broad types of diabetes :
‘On the whole the sensitive diabetics tend to be younger and thin and to have a normal blood pressure and normal arteries, and as a rule their disease is of sudden and severe onset. The insensitive diabetics, on the other hand, tend to be elderly and obese and to have hypertension and arteriosclerosis, and in these patients the onset is insidious.’
Shortly after delivering these lectures, my father was appointed Professor of Medicine in succession to Professor Elliott. And then came the war. The hospital and medical school were evacuated out of London. Despite the chaos, shortage of staff, poor facilities and heavy burdens of clinical service and of administration, he began research in a new field—liver disease. After the war ended, he maintained his interest in diabetes, but did not resume research in the field. His clinical and scientific career came to an end with his appointment as Secretary (Chief Executive) of the Medical Research Council in 1949.
A complete list of my father’s publications is appended to his extended obituary in the Biographical Memoirs of the Royal Society (Volume 41, pp 201–218). His meticulous laboratory notebooks covering his research in the broad field of diabetes are in the Wellcome Library, London.