Dr. Stamatelatou
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Diabetes Mellitus

Epidemiology, classification, risk factors and the modern, individualised management of diabetes mellitus — and why achieving control early, from the moment of diagnosis, matters.

A blood glucose meter, a lancing device and lab report sheets on a wooden desk

According to the 11th and most recent edition of the International Diabetes Federation Atlas, 589 million people aged 20 to 79 are living with diabetes mellitus — 11.1% of the world's population — and that number is set to rise to 852.5 million by 2050, an increase of some 45%. In effect 1 in 9 people is affected, and of those, 1 in 4 is over 65 years of age. A large proportion of them, 252 million, almost 1 in 2, do not know they have the disease, while 635 million people, that is 12% worldwide, have impaired glucose tolerance (a prediabetic state).

As regards Greece, according to the EMENO study the prevalence of the disease is 11.9% and the prevalence of prediabetes 12.4%, with a significant proportion of around 1.5% remaining undiagnosed. On the other hand, 9.1 million people aged 20 to 59 are living with type 1 diabetes mellitus, with 503,000 new cases appearing in 2024, of which 219,000 occur in those under 20 years of age and 56.5% in those over 20.

At this point it should not be omitted that 1 in 5 live births is affected by some form of hyperglycaemia: 79.2% by gestational diabetes, 11% by diabetes diagnosed before the pregnancy, and 9.9% by either type 1 or type 2 diabetes diagnosed during the pregnancy. At the same time it is responsible for 3.4 million deaths — one death every 9 seconds — and accounts for 1 in 10 (9.3%) deaths worldwide.

It is defined as a heterogeneous syndrome involving a disturbance of carbohydrate, fat and protein metabolism, caused by a deficiency of insulin as well as by disturbances of glucose homeostasis affecting multiple organs and systems (pancreatic beta cells, liver, kidney, brain, intestine). The insulin deficiency may be complete, partial or relative. It is characterised as relative when, despite raised blood levels, insulin is not sufficient to meet metabolic demand because its action in peripheral tissues is impeded (insulin resistance). The gold standard for diagnosis remains the glucose tolerance test, widely known as the glucose curve.

Classification is made conventionally on the basis of the causes known to date, and falls into four categories:

  1. Type 1 diabetes (T1DM): Caused by what is usually autoimmune destruction of the pancreatic beta cells, generally leading to almost complete insulin deficiency, and including latent autoimmune diabetes in adults (LADA).
  2. Type 2 diabetes (T2DM): Caused by a progressive decline in the adequate secretion of insulin by the pancreatic beta cells required to meet metabolic demand, often in combination with insulin resistance.
  3. Specific types of diabetes:
    • a) Diabetes caused by genetic defects of beta-cell function (insulin secretion). This includes the monogenic diabetes syndromes, such as neonatal diabetes and MODY (Maturity Onset Diabetes of the Young).
    • b) Diabetes caused by genetic defects affecting insulin action.
    • c) Diabetes caused by endocrinopathies, infections, diseases of the exocrine pancreas (such as pancreatitis or cystic fibrosis), or other diseases.
    • d) Diabetes caused by drugs or chemical agents (e.g. corticosteroids, statins, thiazide diuretics, second-generation antipsychotics, immune checkpoint inhibitors, and others).
    • e) Genetic syndromes associated with diabetes.
  4. Gestational diabetes (GDM): the appearance of diabetes in women in the 2nd or 3rd trimester of pregnancy, once a diagnosis of T1DM or T2DM has been excluded.

It is worth noting that the current classification is not always adequate for correctly categorising some people with diabetes, and in clinical practice many are misclassified, at least initially. The diagnoses most often confused are T1DM, T2DM, MODY and LADA. Some patients have a genetic predisposition to both main types of diabetes (for example autoimmunity as in T1DM together with obesity and insulin resistance as in T2DM), and so present a «hybrid» form of diabetes with the characteristics of «double diabetes».

Those at greater risk of developing diabetes mellitus, and in whom screening should be carried out, are people meeting some of the following conditions:

If screening results are normal, testing should be repeated every three years, with possibly more frequent testing depending on the initial findings and risk factors. Screening is recommended either by completing a dedicated questionnaire (e.g. FINDRISC) or by measuring fasting plasma glucose.

It is a systemic disease, and loss of control over time leads to both microvascular and macrovascular complications.

Turning now to the modern management of people with T2DM, in recent years a person-centred, individualised and moreover holistic approach has been followed. We take into account the particular characteristics of each person (age, glycated haemoglobin, body mass index, lifestyle, comorbidities, socioeconomic profile and so on), the effect of medicines upon them, and their adverse effects. We decide on a plan of action together with the patient, setting realistic goals; and throughout that plan we do not forget to eliminate any delay in starting treatment, with the ultimate aim of reducing the complications of diabetes and improving our patients' quality of life.

Treatment is individualised, following a holistic model of care and addressing all cardiometabolic risk factors. Beyond glycaemic control, we give particular importance to control of blood pressure and of the lipid profile, and to the management of body weight. At the same time, given their availability, the use of treatments with proven cardiovascular and renal benefit is considered imperative, while advice to stop smoking for those who smoke, and antiplatelet therapy where judged necessary, should not be omitted.

It is well known that lowering blood glucose right from the outset, from diagnosis, in a patient with T2DM appears to be important, in keeping with the phenomenon of metabolic memory, otherwise known as metabolic legacy. The long-term benefit of an earlier period of euglycaemia — even if control later deteriorates — and the long-term cost of an earlier period of hyperglycaemia — even if control later improves — have been demonstrated for years.

Studies in the international literature show that a 1% reduction in glycated haemoglobin at diagnosis leads to an 18.8% reduction in all-cause mortality over the first 10-15 years, whereas if that reduction is delayed beyond the first 10 years it produces a reduction of only around 2.7%, that is to say seven times lower. As for myocardial infarction, reducing glycated haemoglobin at diagnosis leads to a 19.7% reduction, whereas delaying by 10 years leads to a reduction of only 6.7%, three times smaller.

The conclusion we reach is that if we intervene late with good glycaemic control, the glycaemic burden that has accumulated does not translate into a reduction in the late complications of diabetes (that is, we see the emergence of adverse metabolic memory); whereas the earlier we intervene, the lower the accumulated glycaemic burden, and in this way we achieve a reduction in the late complications of diabetes as well.

References

  1. IDF Atlas, 11th edition.
  2. Clinical practice guidelines 2026 — Hellenic Diabetes Association.
  3. Standards of Medical Care in Diabetes 2026. Diabetes Care, ADA guidelines.
  4. Folz et al. Diabetologia 2021; 64:2131-2137.
  5. Lind et al. Diabetes Care 2021; 44:2231-2237.