Professor Merlin Thomas ( left ) Professor and program leader , department of diabetes , Monash University , Melbourne , Victoria .

Dr Tomasz Block ( right ) Advanced trainee ( endocrinology ), Monash Health , Melbourne , Victoria .

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This information was correct at the time of publication : 6 October 2023

INTRODUCTION

TYPE 1 diabetes is a common autoimmune

disorder that progressively destroys the insulin-producing beta cells ( β -cells) of the pancreas . Although the onset of type 1 diabetes is more common in adolescence , it can occur at any age .

In this How to Treat , we explore the unique challenges of type 1 diabetes when it occurs in adults . These challenges begin with making a correct diagnosis of type 1 diabetes in the adult setting , where type 2 diabetes is far more common and when a good response to diet , lifestyle and oral therapy may make type 2 diabetes initially appear to be the correct diagnosis .

However , ultimately , all patients with type 1 diabetes will need insulin to maintain good health . Whether delivered by regular injections or pump , insulin therapy needs to be individualised to each patient and their target for glycaemic control while mitigating the risks of hypoglycaemia and weight gain . Adults with type 1 diabetes are also at higher risk of complications — like heart , foot , eye and kidney disease — which require dedicated programs

for regular screening and risk reduction strategies . While the clinical outcomes of type 1 diabetes in adults are usually favourable , this can only be achieved through early education and empowerment of patients to take control of their condition and its daily management .

This How to Treat covers the management of adult-onset type 1 diabetes and aims to ensure GPs can both identify adults with type 1 diabetes and initiate an appropriate and holistic treatment plan that sets a course for the years to come .

EPIDEMIOLOGY

TYPE 1 diabetes affects more than 10 million people worldwide . Annually , there are approximately 15 new cases of diabetes per 100,000 people globally . Over the past 50 years , the incidence of type 1 diabetes has been steadily increasing by about 2 – 3 % a year . 1 The peak incidence occurs in children and adolescents ( see figure 1 ), leading to its previous , but inadequate , designation as ‘ juvenile diabetes ’. 1 However , type 1 diabetes may present at any age .

Globally , 42 % of all cases are diagnosed after the age of 30 , and

most people with type 1 diabetes are adults . 2

The incidence of adult-onset type 1 diabetes is modestly higher in men than in women . 1 Its incidence is also higher in Scandinavia and the Middle East and lowest in predominantly Asian countries . 1 These regional differences are similar for both adult-onset and childhood-onset diabetes and likely reflect the different frequencies of underlying genetic susceptibility to type 1 diabetes . 1

In Australia , more than 150,000 adults have type 1 diabetes , and at least two in five new cases occur in adults aged over 25 . 3

PATHOGENESIS

TYPE 1 diabetes is the end result of progressive autoimmune destruction of the insulin-producing β-cells ( see figures 2 and 3 ) of the endocrine pancreas . Although the first presentation of type 1 diabetes is usually acute ( as described later in this article ), in most cases , β-cell-directed autoimmunity has been asymptomatically smouldering for many years before culminating in a ‘ tipping point ’ presentation associated with acute insulin deficiency .

Autoimmunity in type 1 diabetes

is associated with the emergence of autoreactive T-cells that are primarily responsible for β-cell destruction .

In addition , type 1 diabetes is associated with the presence of circulating autoantibodies directed against β-cell antigens , including insulin autoantibodies ( IAA ), glutamic acid carboxylase ( anti-GAD ), insulinoma-associated protein ( anti-IA2 ) and zinc transporter T8 ( anti-ZnT8 ). 5 These autoantibodies in the circulation , particularly multiple different isotypes , are biomarkers of the disease process and associated with future risk of type 1 diabetes . For example , seroconversion to the presence of two or more serum autoantibodies is associated with an 84 % risk of clinical diabetes . 6

Type 1 diabetes usually occurs in genetically susceptible individuals , although most of those who carry genetic polymorphisms known to influence susceptibility to type 1 diabetes do not develop it . 6 It is not clear why self-tolerance is lost in some individuals but not in others . It is thought that an additional ‘ trigger event ’ establishes an autoreactive process in susceptible individuals . 7 The precise cause of the trigger event is unknown in most patients with type 1 diabetes , but