ISPAD Newsletter - July 2026

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President's Message:

Tim Minchin is a singer/song writer who is known for his eye shadow, iconoclastic lyrics and ‘Matilda’, his well-known musical. He is strongly in favour of critical thinking and science based medicine. In his uplifting song “White Wine in the Sun” he makes the comment: “I don’t believe just because ideas are tenacious, it means that they’re worthy”.

 

In the immediate post-insulin discovery era, Rollin Turner Woodyatt was a leading diabetologist of the day. His lab in Chicago was one of the first to be tasked with improving and developing insulin prior to commercial production. His best known quote is: “The history of diabetes has been marked by recurrence of certain ideas which decline and disappear; only to go through a similar cycle again in an altered form in a new generation”. Originally made in 1934 but remarkably prescient and still true today. The re-branding of Michael Berger’s flexible eating approach in Germany from the 1980’s to the Dosage Adjustment for Normal Eating (DAFNE) in the UK in the early 2000’s is a good example of such therapeutic recycling.  Edwin Gale and Lynn Sawyer highlighted that many investigators have “confused circular motion with progress”. As in other areas of life, in diabetes some tenacious ideas are not worthy nor do they merit recycling. Often too long after the evidence base has disproved them, some notions do eventually become extinct. I call these ‘diabetes dodo birds’. Here are the top three from my time in diabetes care (NB Edwin Gale seems to have had a singular role in their demise):

The Somogyi Effect

In the late 1950’s Dr Michael Somogyi observed and reported an association between morning glycosuria and previous nocturnal hypoglycaemia. He surmised that early morning elevations in blood glucose levels were attributable to nocturnal hypoglycaemia and that the best strategy to avoid morning hyperglycaemia was to reduce the evening insulin dose. The cause was postulated to be an overly exuberant release of counter-regulatory hormones in response to the hypoglycaemic episode causing “rebound” hyperglycaemia. Numerous studies by Philip Cryer’s group, Edwin Gale’s group and others published in the 1980’s and 1990’s in the Lancet, New England Journal of Medicine and Diabetes Care comprehensively disproved this notion. Despite this cumulative evidence, the myth of the “Somogyi Phenomenon” persisted in many medical schools, nurse-educator training programs and medical texts well into the 2000’s. The advent of continuous glucose monitoring was required to finally lay this myth to rest.

Brittle diabetes

Gareth Williams was a well-known diabetologist most active in the 1980’s and 1990’s. Brittle diabetes was one of his research interests. He summarized the history of it masterfully in a 2012 Lancet editorial ‘What goes around, comes around’. In short, the concept was first promulgated in the 1930’s and then recycled in the 1980’s. Brittle Diabetes referred to diabetes that was so unstable that patients regularly swung between severe hypoglycaemia and diabetic ketoacidosis. Death was not uncommon. A profound clinical problem that attracted great minds with accompanying great theories. “One by one, the grand hypotheses went through the cycle of hope, hype, reality check, and oblivion. Ultimately, none of them survived the impact of evidence“. Long-term follow up studies revealed deliberate patient behavior was the root cause in most cases and that resolution occurred after life–transforming events such as employment, marriage or starting a family. Brittle diabetes proved to be a behavioural “folie à  trois, a collusion between the patient, family and doctor.”

The Accelerator Hypothesis

In the early 2000’s Terry Wilkin put forward a unifying hypothesis that type 1 and type 2 diabetes were two versions of the same disease “The Accelerator Hypothesis argues that Type 1 and type 2 diabetes are one and the same, distinguishable only by their rate of beta cell loss and the accelerators responsible”. He proposed that both forms of diabetes were disorders of beta cell apoptosis driven by the accelerators of constitution, weight and autoimmunity. This interesting hypothesis enjoyed some early notoriety with related studies and editorials variably supporting or rebutting it. In 2007, an issue of Diabetologia published an opinion piece by Terry Wilkin simultaneously with a forensic dissection of its merits by the then editor Edwin Gale. The Gale analysis was not supportive. More recent analyses of epidemiologic data have again confirmed that accelerated weight gain may drive islet autoimmunity and progression to clinical type 1 diabetes, but little is heard of Wilkin’s full “one and the same” hypothesis these days. 

Tenacious ideas that hang around longer than they should often owe their existence to a variety of human factors including cognitive dissonance and related vested interests. These confer longevity even in the face of counter-evidence. They have lived by the Dylan Thomas mantra of not going “…gentle into that good night” and have raged, raged against the evidence.

Vale.

Best to all,

Fergus