How type 1 diabetes starts: signs and forms

Type 1 diabetes can begin in several ways, the main modulating factor being how quickly pancreatic beta cell function is lost. The most common forms of onset are: classic onset with typical symptoms (frequent urination, intense thirst, high water intake), onset with diabetic ketoacidosis, silent onset discovered incidentally on routine blood tests, and slow onset observed in some adults [1].

The form of onset depends greatly on age. In children and adolescents, onset is usually rapid and dramatic, compared with adults, in whom symptoms can develop gradually, over the course of months or years. Early recognition of the symptoms removes the risk of a severe onset with ketoacidosis [1].

Diabetic ketoacidosis is a serious, life-threatening acute complication. It occurs when insulin deficiency becomes so severe that the body starts to use fats as its main energy source. Ketone bodies start to accumulate in the blood, where, being acidic, they alter the body's acid-base balance. Ketoacidosis is defined by blood glucose ≥200 mg/dl (≥11.1 mmol/L), elevated ketone bodies (β-hydroxybutyrate ≥3.0 mmol/L) and metabolic acidosis with pH below 7.3 or bicarbonate below 18 mmol/L [2].

Symptoms include nausea, vomiting, abdominal pain, rapid and deep breathing, the smell of acetone on the breath, marked dehydration and sometimes altered consciousness. Ketoacidosis at onset is a medical emergency and requires immediate hospitalisation. Approximately half of children with newly diagnosed type 1 diabetes present with ketoacidosis, and children with a family history have an even higher risk of severe onset [3].

“Classic” onset refers to the appearance of the typical symptoms of uncontrolled diabetes. The hyperglycaemic triad consists of frequent urination in large amounts (polyuria), intense and persistent thirst (polydipsia) and unintentional weight loss. To these are often added fatigue, blurred vision, excessive hunger and, in children, a return of bedwetting at night (enuresis). These symptoms appear when blood glucose exceeds the renal threshold, which is 180 mg/dl (10 mmol/L). Above this threshold, glucose in the blood begins to be eliminated through the urine, dragging water from the body along with it [4].

Symptoms usually develop over a few weeks, and sometimes even within just a few days. Recognising them is essential because it allows rapid diagnosis and the initiation of life-saving insulin treatment, before the patient enters ketoacidosis. If you notice this combination of symptoms in yourself or in a family member, it is important to see a doctor as soon as possible for a blood glucose check. A simple finger-prick test can confirm or rule out the suspicion of diabetes [4].

Silent onset means discovering diabetes without dramatic symptoms, through routine blood tests or screening programmes. It occurs much more rarely than classic onset or onset with ketoacidosis and is observed especially in adults, in first-degree relatives of a person with type 1 diabetes, or in people who take part in screening studies for pancreatic autoantibodies. In these people, blood glucose may be only mildly elevated, and testing thus discovers the disease at an early stage [5].

Early detection, before severe symptoms appear, allows treatment to be started before the patient develops ketoacidosis, provides time for therapeutic education, and protects the pancreatic beta cells that are still working. This type of onset highlights the value of periodic testing for close relatives of people with type 1 diabetes, especially children and young people with a family history and genetic predisposition (HLA) [6].

Yes, type 1 diabetes can follow two patterns of clinical evolution. Acute onset appears within a few days or weeks and reflects a rapid loss of insulin production. This pattern is characteristic of children and adolescents, in whom symptoms set in suddenly and can quickly lead to ketoacidosis. Slow onset is observed especially in adults and unfolds over the course of several months or even years, with less intense symptoms and a gradual loss of pancreatic beta cell function [1].

The slow form, seen in adults, is sometimes called latent autoimmune diabetes in adults (LADA). These people may initially appear to have type 2 diabetes and may respond temporarily to oral medications, but eventually progress to insulin dependence. Correct identification of the type of onset is important because it directly influences the treatment plan and the moment when insulin is started [7].

Type 1 diabetes can occur at any age, from the first year of life to advanced old age, but there are two typical incidence peaks in children. The first peak appears between 4 and 6 years, and the second, more pronounced, between 10 and 14 years, during puberty. These stages correspond to hormonal and immunological changes that can accelerate the destruction of pancreatic beta cells [8].

Although it was traditionally considered a disease of childhood, recent data show that the majority of cases are diagnosed in adulthood. In adults, onset can appear at any time and is sometimes misdiagnosed as type 2 diabetes. Thus, age at diagnosis is no longer a sufficient criterion for establishing the type of diabetes, and assessment of the clinical picture and, where appropriate, additional tests such as pancreatic autoantibodies and C-peptide are needed [9].

In young children, under 5 years, onset is the most rapid and the most severe. Symptoms set in within a few days, and the risk of ketoacidosis at diagnosis is the highest. Young children cannot clearly express thirst or fatigue, and severe dehydration and vomiting can be confused with gastroenteritis. In adolescents, the classic symptoms are easier to recognise but can be masked by the natural changes of puberty or by weight loss attributed to growth [1].

In adults, onset is usually slower, with moderate symptoms that evolve over weeks or months. Adults can preserve a residual insulin production that temporarily protects them from ketoacidosis. For this reason many adults are misdiagnosed as having type 2 diabetes. This explains why in adults (especially younger ones) the diagnosis should not rely only on age, but also on specific tests that can bring to light the autoimmune nature of the disease [10].

In people who already have pancreatic autoantibodies and a partial loss of β-cell function, certain factors can accelerate the transition to clinically manifest disease. The best-known triggering factors are viral infections, such as enterovirus infections (especially Coxsackie B) and SARS-CoV-2 infection. Intense physical stress, major trauma, surgical interventions and puberty can also hasten onset [11].

Certain medications, such as corticosteroids, can precipitate ketoacidosis in vulnerable people who are already on their way towards type 1 diabetes onset. Intense psychological stress is also considered a possible aggravating factor. It is important to understand that these factors are not the cause of type 1 diabetes; they only accelerate the clinical manifestation of an autoimmune disease that is already present, which had been silently evolving for months or even years and was going to become clinically manifest anyway, just later [11].

When vomiting is present, hospitalisation is necessary at the onset of type 1 diabetes, especially in children and adolescents. Hospitalisation allows metabolic stabilisation, correction of dehydration and electrolyte imbalances, the safe initiation of insulin therapy and therapeutic education for you and your family. In patients who present with ketoacidosis, hospitalisation, sometimes even in the intensive care unit, is mandatory [12].

If you only have hyperglycaemia, especially in some adults with slow onset, without ketoacidosis, without severe dehydration and with moderate symptoms, treatment can be started on an outpatient basis, provided there is close supervision and rapid access to specialists. Wherever treatment begins, the initial period includes learning how to administer insulin, recognising hypoglycaemia, monitoring blood glucose and the basic principles of nutrition for type 1 diabetes. This initial education is the foundation for good long-term control [12].

Insulin therapy should be started as quickly as possible after diagnosis, ideally on the same day type 1 diabetes is confirmed. In patients who present with ketoacidosis, insulin is given intravenously, together with the measures for correcting dehydration and electrolyte imbalances, according to standard protocols. In patients without ketoacidosis, insulin is started directly subcutaneously, in doses adjusted to weight and to the blood glucose value [13].

Early initiation of insulin rapidly removes the acute symptoms, prevents progression to ketoacidosis and helps preserve the function of residual beta cells, which is associated with better long-term glycaemic control. In adults with slow onset, delaying the introduction of insulin into the treatment plan and relying for too long on oral medications alone can lead to long-term metabolic deterioration, which is why early identification of type 1 diabetes in adults is essential for a good prognosis [13].