Insulin Therapy, 1921–23

By the early twentieth century physicians increasingly distinguished an abrupt wasting illness in younger patients from slower forms often seen in older or heavier adults, although the modern categories “type 1” and “type 2” were not yet in use. The most dramatic early responses to insulin came from the first group—then described with terms such as “juvenile,” “severe,” “thin,” or “early-onset” diabetes. Those period labels were clinical descriptions, not exact equivalents of current diagnoses (Moore 2020).

Treatment was not simply an absence of care. Physicians debated fasting, carbohydrate restriction, fat-rich diets, and how closely to use sugar and ketones in urine as guides. Frederick Allen's undernutrition regimens and Elliott Joslin's closely supervised diets could reduce glycosuria and ketoacidosis and sometimes extend life. For a severely insulin-deficient child, however, success could mean remaining profoundly underweight while death was deferred rather than prevented. The phrase “starvation treatment” captures the extremity of some regimens but should not be mistaken for a single universally applied protocol (Tattersall 1995; Bliss 2007).

Clinicians already thought in terms of balancing food intake against measurable sugar loss. Insulin expanded what could be eaten and reversed dangerous metabolic deterioration, but it also made that balance more technically complex. The new therapy carried an immediate danger of hypoglycaemia—period writers often called severe episodes “insulin reactions”—if dose, meals, or exertion were mismatched.

Even the name was not a Toronto invention. Belgian physiologist Jean De Meyer proposed insuline in 1909, and Edward Schäfer independently used it in 1916. Banting and Best called some preparations “isletin” before the Toronto group adopted “insulin” in 1922. At that point the word referred to active material in an extract, not the chemically isolated and structurally characterized molecule understood later (Rostène and De Meyts 2021).

The first paper by Banting and Best, published in February 1922 but reporting the 1921 dog experiments, was confident that the extract contained the pancreas's internal secretion. It also stated that the results did not yet justify clinical administration. That contemporary limit is important: lower glucose in a surgically diabetic dog was evidence of activity, not proof that a stable, safe medicine existed (Banting and Best 1922).

Calling Thompson simply the “first person given insulin” hides earlier attempts with pancreatic preparations, including Zülzer's injections and Joseph Gilchrist's ineffective oral dose of Toronto extract in December 1921. The defensible narrower claim is that Thompson's response on 23 January supplied the Toronto group with its first convincing evidence of effective injected treatment in a person. The separate Leonard Thompson timeline entry examines the two January administrations in more detail.

Patent history is often reduced to a claim that insulin was “given away for one dollar.” Banting, Best, and Collip did assign their patent rights to the University of Toronto for one dollar each on 1 January 1923. The purpose was to prevent a private monopoly and let the university control quality and licensing; the university nevertheless received royalties, and licensed firms sold insulin commercially. The gesture expressed a public-interest policy, not a patent-free or cost-free supply system (University of Toronto Libraries; Lewis and Brubaker 2021).

Banting originated the Toronto project and supplied persistence and surgical skill; Best performed measurements, prepared extracts, and sustained the 1921 experiments; Macleod supplied the laboratory, experimental design, supervision, institutional authority, and scientific presentation; Collip made the preparation tolerable enough for convincing clinical use. Campbell, Fletcher, Jeffrey, production workers, and patients were indispensable to treatment, although they rarely appear in the four-man discovery formula (Bliss 2007).

The historical record is unusually contentious because Banting, Best, and Macleod later defended incompatible versions of events. Banting and Best minimized Macleod's early guidance; notebooks and correspondence document his instructions, demands for controls, resources, and later coordination. Collip left few laboratory notes and generally avoided the public quarrel. Later memoirs are evidence of how participants remembered and claimed the discovery, but they are not neutral substitutes for the contemporary record (University of Toronto Libraries; Bliss 2007).

The 1923 Nobel Prize went to Banting and Macleod “for the discovery of insulin.” Banting shared his prize money with Best and Macleod shared his with Collip. The award confirmed a compact public story while intensifying arguments about omitted contributors and earlier work. It did not adjudicate every experimental priority; it recognized the Toronto programme whose extract had become an effective therapy (Nobel Prize Outreach 1923).

Photographs of emaciated children before treatment and better-nourished children afterward became powerful evidence and publicity. They documented real changes but encouraged a resurrection narrative centred on physicians. Patients supplied the bodies on which potency, dose, diet, and adverse effects were learned. Their accounts also show that improvement depended on continuing injections and food, not on a completed cure (Banting et al. 1922; Gardner 2019).

Early preparations were short-acting and variable. Treatment required one or more injections each day, scheduled meals, attention to exertion, and recognition of hypoglycaemia. Home urine testing involved chemical reagents, heat, test tubes, and colour comparison; reusable glass syringes had to be sterilized and needles maintained. Manuals and specialist clinics taught these practices, often presenting discipline and compliance as moral traits rather than acknowledging differences in income, housing, literacy, work, family support, and access to care (Gardner 2019; Moore 2020).

Insulin's arrival was also geographically uneven. Toronto's public-ward patients, privately connected patients who reached Banting, selected U.S. clinics, and British trial centres did not represent all people with diabetes. Scarcity, price, distribution rules, and clinical capacity decided who received early supplies. “Available by 1923” therefore describes expanding production networks, not universal access.

Insulin changed the prognosis of severe insulin-deficient diabetes and became a model for laboratory-based replacement therapy. Its early history also helped formalize biological standardization, university patent policy, public-laboratory and pharmaceutical cooperation, specialist clinics, and patient education. Those consequences arose from the whole 1921–23 system, not from the first dog experiment alone.

The stronger historical claim is narrower than the familiar miracle story. Toronto's achievement was not the first suggestion of a pancreatic internal secretion, the first glucose-lowering animal extract, or the first attempt to inject pancreatic material into a patient. It was the first programme to turn such evidence into an effective, repeatable human treatment and then organize expanding production. That achievement was collective, depended on animal and human subjects, and remained constrained by the burden and distribution of lifelong care.

Explore the longer history of diabetes and insulin, read about Frederick Banting, or compare how another unstable biological substance became a manufactured medicine in the penicillin timeline entry.