The causes of diabetes are only partially elucidated. On the one hand, it is known that the occurrence of both types of diabetes is linked to a certain extent by genetic factors. Environmental factors also play an important role.
One of the environmental factors that is believed to cause type 1 diabetes in many cases would be a virus that infects insulin-producing beta cells in the pancreas. This hypothesis is supported by clinical and experimental evidence. Viral infection can induce diabetes either by destroying insulin-producing cells or triggering an immune response.
Another factor that appears to predispose to autoimmune diabetes (type 1) would be the consumption of cow’s milk or milk products. Research suggests that cow’s milk would lead to the appearance of antibodies that affect pancreatic beta cells and thus contribute to the development of diabetes.
In type 2 diabetes, the most important modifiable factors are excessive body weight and lack of exercise.
Among the incriminated factors is also food abuse and the excessive eating of sugary products. All of these factors could explain why diabetes is more common in urban areas. Depending on the causes, diabetes is divided into primary diabetes and secondary diabetes. When there is no other associated disease, we talk about primary diabetes.
When we can identify disorders or pathological conditions that cause or favor the development of diabetic disease, we are talking about secondary diabetes. Among the causes that can lead to secondary diabetes are pancreas-related diseases ( chronic pancreatitis of alcoholics), hormonal disorders (acromegaly, pheochromocytoma, Cushing’s disease), diabetes induced by drugs and chemicals, various genetic diseases, etc.
Type 1 diabetes occurs mainly in children and young people and always requires insulin treatment because the pancreas cannot produce it anymore. For this reason, it is also called insulin-dependent diabetes. Type 2 diabetes usually occurs in middle-aged adults (40 years) or later, especially in overweight patients. In this case, the body continues to produce insulin, but it cannot perform its role normally. This second type of diabetes usually does not require insulin therapy, which is why it was called non-insulin-dependent diabetes mellitus.
It should be noted, however, that insulin dependence does not necessarily mean that the patient will follow insulin therapy; also, the term non-insulin-dependent does not always overlap with the absence of insulin therapy. Experts consider rather that the notion of “insulin dependent” draws attention to the fact that, in the absence of insulin administration, the patient is at risk of diabetic ketoacidosis. In other words, the terms “insulin dependent” and “non-insulin dependent” actually describe physiological states predisposition or resistance to ketoacidosis), while the terms “type 1” and “type 2” refer to the pathogenic, autoimmune (type 1) and non-autoimmune (type 2) mechanism.
