 |
| Credit: Pixabay |
Depression is common in individuals with endocrine-metabolic disorders and vice versa. In a study of 2.2 million individuals in the Swedish population, researchers at Karolinska Institutet saw that those with endocrine-metabolic diseases also have an increased incidence of depression. The researchers also found higher frequencies of depression in the group's siblings. The study is published in the American Journal of Psychiatry.
Further analyzes described the relative contribution of genetic and environmental factors underlying the concomitant occurrence of depression for a variety of endocrine-metabolic diseases. It is already known that there is an increased simultaneous occurrence of endocrine-metabolic diseases and depression, but the relationships are still unclear.
Whether the overlap between these conditions is mainly genetic or environmental has consequences for whether the development of pharmacological or behavioral interventions would be more effective for treatment or prevention, says Sarah Bergen, senior researcher at the Department of Medical Epidemiology and Biostatistics at Karolinska Institutet, who led the study.
Co-occurrence in families
 |
| Sarah Bergen, senior researcher at the Department of Medical Epidemiology and Biostatistics Photo credit: Gunilla Sonnebring |
In the study, the researchers identified 2.2 million individuals born in Sweden between 1973 and 1996, as well as their full and half siblings, and followed them up to the age of 40. A number of medical conditions were studied; depression and various endocrine-metabolic diseases, including three autoimmune diseases (autoimmune hypothyroidism, Graves' disease and type 1 diabetes) and three non-autoimmune diseases (type 2 diabetes, obesity and polycystic ovarian syndrome).
People with endocrine-metabolic disorders had 1.4 to 3.5 times the risk of depression compared to those without these diagnoses. Their full- and half-siblings also had a certain increased risk of depression, suggesting that genetic and / or environmental risk factors shared between family members play a role in the simultaneous occurrence of these mental and physical disorders.
Genetic and environmental impact
 |
| Marica Leone, PhD. Photo Credit: Emiliano Abballe |
By comparing whole-siblings (which share about half of their genes) with half-siblings (which share about a quarter of their genes), it was possible to calculate the relative contribution of genetic and environmental factors to the simultaneous occurrence of depression and.
Results varied between non-autoimmune and autoimmune diseases; The overlap between depression and non-autoimmune conditions was mainly explained by shared genetic influences diabetes, especially type.
This indicates that the association between depression and various endocrine-metabolic disorders can be driven by different mechanisms. For example, shared biological mechanisms, such as immunoinflammatory and metabolic dysregulations, may be the basis for consistent occurrence of depression and type 2 diabetes, obesity and polycystic ovarian syndrome. However, the absence of shared genetics in the relationship between type 1 diabetes and depression may reflect the presence of environmental factors affecting the risk of both conditions and / or a direct link between these conditions through mediating factors - e.g. biological and psychosocial mechanisms linked to type 1 diabetes, including inflammation, brain damage, as well as stress from this lifelong condition that is often diagnosed early in life and that requires a complex treatment regimen for both patients and their families.
Our results emphasize that physicists should be aware of increased risks of depression in individuals with endocrine-metabolic disorders, and vice versa, and be vigilant for common symptoms. Our study also provides a useful basis for future research aimed at identifying and targeting the biological mechanisms and modifiable risk factors underlying consistent morbidity in endocrine-metabolic diseases and depression, says Marica Leone, the study's first author.
The study was funded by the European Union Horizon 2020 Research and Innovation Program under Marie Sklodowska-Curie grant agreement no. 721,567th.
psyt092922_01
.jpg)
.jpg)
