Over 90% of diabetes cases are related to type 1 diabetes and type 2 diabetes. From what it seems, more people suffer from type 2 diabetes (around 90%). The remaining 10% of patients suffer from type 1 diabetes.
What causes diabetes?
The cause of the disease is the destruction of β cells of the pancreatic islets responsible for the production and secretion of insulin. This leads to its absolute deficiency and, hence, the need to administer insulin in the form of injections.
Destruction of β cells usually occurs rapidly (the disease appears already at an early stage of life – in childhood or in adolescence). Although the destruction process of the pancreatic structures may be slower (the disease manifests itself after 40 years of age – LADA-type diabetes Latent Autoimmune Diabetes in Adults).
Type 1 Diabetes Mellitus
In the vast majority of cases, type 1 diabetes mellitus has an autoimmune basis, i.e. the destruction of pancreatic β-cells occurs as a result of the action of antibodies “attacking” these structures. Autoimmune process involves cells in the immune system, including T-lymphocytes, B-lymphocytes and macrophages.
It is not known why the body begins to produce antibodies directed against its own cells of the pancreas. The possible reason could be among genetic conditions or environmental factors.
The participation of the former in the development of diabetes is associated with the ability of some viruses to trigger an immune reaction in the pancreas, which can lead to beta cell damage and impaired insulin secretion. For example, infection with rubella or cytomegalovirus during fetal life may contribute to the destruction of insulin-secreting cells, especially in predisposed individuals.
An infection caused by the Coxsackie virus, Herpes or retroviruses may initiate an immune response directed not only against these pathogens, but also against their own cells.
Although diabetes is not a hereditary disease, people suffering from it have a genetic predisposition to develop other autoimmune diseases (Graves’ disease, Hashimoto, Addison, vitiligo), and this tendency may be inherited.
Signs & symptoms of diabetes
Symptoms of diabetes usually develop within a few weeks (4-12), and their appearance is the result of the destruction of about 90% of the pancreatic beta cells. The symptoms includes:
- Strong thirst (drinking even several-dozen liters of liquids daily)
- Excessive urine (polyuria)
- Weight loss
- Increased susceptibility to infection.
Drastic reduce of insulin secretion by the pancreas leads to a significant increase in blood glucose. This mechanism is responsible for the appearance of the above symptoms.
However, the most serious complications of type 1 diabetes are metabolic disorders in the form of ketoacidosis and coma — this is due to the fact that the presence of insulin is a necessary factor for glucose to be used as a source of energy at the cellular level.
In the case of insufficient insulin, other ingredients, including fats or proteins, are used as a source of energy instead of glucose.
The products of metabolism listed first are ketone bodies, i.e. acids (acetoacetic acid, β-hydroxybutyric acid), thus, an increase in their concentration leads to a decrease in blood pH, i.e. to acidosis.
The goal of diabetes treatment
The main goal of diabetes treatment is to maintain the blood glucose level in the appropriate range of values for a given group of patients. This is important due to the possibility of acute and chronic complications of diabetes (including kidney damage-nephropathy or neuropathy).
Basic diabetes therapy is based on subcutaneous injection of insulin in the form of injections.
In addition, diabetics patients must pay more attention to what they consume, because the amount of insulin administered before meals should be adjusted to the amount of carbohydrates consumed.
Cannabidiol versus type 1 diabetes in preclinical studies
Considering the fact that diabetes is a chronic and incurable disease and affects an increasing number of people around the world, there is a need for further research into this disease.
Before any studies with patients are started, an animal experiment is first performed. The same scheme also applies to studies on the possible use of cannabidiol (CBD) in reducing inflammation resulting from the destructive effects of antibodies against pancreatic beta-islet cells.
Experiment : CBD reduced leukocytes activity
In their experiment Lehman et al. hypothesized that due to inhibition of cellular response and anti-inflammatory effect of cannabidiol, it would delay the onset of type 1 diabetes.
Indeed, the researchers’ experiments show that CBD administration is able to reduce the level of proinflammatory cytokines that induce inflammation and consequently contribute to the destruction of pancreatic beta cells.
While conducting their experiments, the researchers observed one more interesting mechanism of action of cannabidiol. As a result of the administration of this compound, the activity of leukocytes, cells of the immune system was reduced. It is worth mentioning that it is these cells that are the indirect causative agent of inflammation.
Excessively activated leukocytes reach the place of already ongoing inflammation, where they carry out the phagocytosis process (they also eat inflammatory cells).
Nevertheless, as a result of this process, the release of reactive oxygen species (ROS), in which increased ROS activity occurs, is referred to as oxidative stress.
Under conditions of oxidative stress, reactive oxygen species may manifest their toxic activity not only within the “filled” leukocyte, but also outside its cell, which may contribute to the intensification of inflammation and, as a consequence, to the destruction of structures within the already ongoing inflammation.
Therefore, a reduction in the increased leukocyte activity may reduce the excessive inflammatory response.
The results of the above experiment are very promising, so the researchers hope that the CBD experiment with type 1 diabetes will be carried out with patients.
Lehmann i wsp., Cannabidiol and early pancreatic inflammation in type 1 diabetes, Clinical Hemorheology & Microcirculation, 2016
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