Type 1 diabetes (T1D)

It is also called youth-onset diabetes, because it often develops before the age of 35, accounting for less than 10% of people with diabetes. People with type 1 diabetes need to use insulin for life because the insulin-producing cells in their pancreas have been completely damaged, thus unable to produce insulin. Prior to the discovery of insulin in 1921, people had no better way to lower blood sugar in type 1 diabetic patients, and most of them soon died of various complications of diabetes. With the discovery and application of insulin, patients with type 1 diabetes can still enjoy life like normal people.

Type 2 diabetes (T2D)

It is also called adult-onset diabetes. Type 2 diabetes usually develops after the age of 35 to 40, accounting for more than 90% of patients with diabetes. The type 2 diabetes patient's ability to produce insulin is not completely lost. Some patients even produce too much insulin, but the effect of insulin is greatly reduced, which is what we often call "insulin resistance", so the insulin in patients is relatively lacking, and the therapeutic effects can be achieved by stimulating insulin secretion in the body through certain oral drugs.

High or low blood sugar is not the criterion to distinguish between T1D and T2D

Although diabetic ketoacidosis occurs more often in type 1 diabetes, it can also occur in patients with type 2 diabetes. For some patients, the differential diagnostic indicators used in the classification of diabetes mellitus still cannot meet the exact classification. For example, at the age of onset, about 5% to 15% of adults with diabetes onset is type 1 diabetes, and the incidence of type 1 and type 2 diabetes is similar in adolescents. In terms of disease course, type 2 diabetes can also cause acute onset of ketoacidosis, and some patients with type 1 diabetes can also hide the onset, especially in adult patients with islet autoantibody positive. In terms of pathophysiology, some patients with type 2 diabetes also have autoimmune disorders during the course of the disease, and pancreatic islet autoantibodies are positive. However, patients with type 1 diabetes may gradually become obese and the insulin sensitivity may decrease with it. All these have made the distinguishment of T1D and T2D more difficult.

So, is the islet autoantibody positive the gold standard to distinguish between type 1 and type 2? This criterion cannot be generalized. Testing for type 1 diabetes-associated autoantibodies is helpful in differential diagnosis but is not the only evidence for categorizing. At present, clinicians’ classification of diabetes is mainly based on the comprehensive analysis and evaluation of patients’ clinical manifestations and related auxiliary examination results. Complex and difficult cases even need follow-up observation before they are finally determined.

Blood sugar control and complication prevention are the universal goals for T1D and T2D.

T1D and T2D are classified by cause. T1D is caused by the destruction of pancreatic islet beta cells, resulting in an absolute lack of insulin, while T2D is caused by insulin resistance, accompanied by varying degrees of insufficient insulin secretion. Nevertheless, the classification of diabetes in clinical practice is still difficult. T1D is currently diagnosed mainly based on the clinical characteristics of the patient, such as abnormalities of immunological indicators, such as glutamate decarboxylase antibody, islet cell antibody, insulin antibody, and other positive antibodies.

More than 95% of the diabetes patients encountered clinically is type 2 diabetes. The onset of T2D is thought to be related to an unhealthy lifestyle. Patients with type 2 diabetes are usually accompanied by obesity, and the onset is hidden. Most patients find that their blood sugar rises through routine health examinations. Many patients also have vision loss, itchy skin, and wounds that are difficult to heal. Diabetes complications such as repeated infections of the urogenital system are discovered.

For patients with diabetes, whether it is T1D or T2D, the clinical manifestations are due to the damage to the human body caused by hyperglycemia. Therefore, in addition to the accurate diagnosis and categorization, it is more important for patients to receive standardized and individualized treatment so as to control blood sugar. Because T1D is caused by an absolute deficiency of insulin secretion due to the destruction of islet beta cells, all type 1 diabetes must be treated with insulin for a long time; Type 2 diabetes can achieve certain results through reasonable diet control and appropriate oral hypoglycemic drugs, of course, when oral hypoglycemic drugs fail, islet B cell function tends to fail or serious acute and chronic complications occur. It's also an indication for insulin.

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