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There is considerable evidence to show that the prevalence of depression is increased to a moderate extent in those with prediabetes as well as undiagnosed diabetes. Moreover, this prevalence of depression is “markedly” increased in those with previously diagnosed diabetes.
The prevailing rates of depression could be up to 3 times higher in those with Type 1 diabetes and twice as high in those with Type 2 diabetes in comparison with the worldwide general population.
There seems to be a bidirectional association between diabetes and depression, a sort of complex relation that may share certain biological mechanisms, whose precise understanding could offer an enhanced treatment and successfully improve the outcomes for both these pathologies.
Pathophysiological Mechanisms
According to different reviews, there exist three possible directions for the association between diabetes and depression: both diseases share a common aetiology, diabetes increasing the risk or prevalence of future depression, and depression increasing the risk or prevalence of future diabetes.
Recent studies have shown that there are no common genetic factors to account for the positive association between depression and Type 1 or Type 2 diabetes.
That said, diverse environmental factors (or epigenetic factors) could activate common pathways that successfully promote type 2 diabetes mellitus (DM2) and depression.
One significant factor is a low socioeconomic status that increases the chances for DM2, while also appearing to be a cause for depression.
The other common causes for both DM2 and depression include inadequate or poor sleep, lack of exercise and physical activity, and an unhealthy diet.
Considering these factors, a primary candidate for a common pathway may be the activation and disturbance of the “stress system.” Chronic stress causes activation of the HPA (hypothalamus—pituitary—adrenal) axis as well as the sympathetic nervous system (SNS), thus increasing cortisol production in the adrenal cortex and production of both adrenalin and noradrenalin in the adrenal medulla.
Chronic hypercortisolaemia, as well as SNS activation, could promote insulin resistance and visceral obesity, leading to metabolic syndrome and DM2. In addition, chronic stress has behavioural consequences, too: cortisol, noradrenalin, and other hormones do activate the fear system, thus determining anxiety, anorexia, or hyperphagia. These are the same mediators that lead to tachyphylaxis of the reward system, which causes depression, food cravings, and stress. Excessive cortisol causes a disturbance of neurogenesis in the brain’s hippocampus, a region that is involved in both DM2 and depression.
In addition, chronic stress can induce immune dysfunction directly, through the HPA axis, or SNS, thus increasing the production of inflammatory cytokines. Vast amounts of inflammatory cytokines could interact with the normal functioning of the pancreatic β-cells, cause insulin resistance, and thus promote the occurrence of DM2.
These correlations suggest that both chronic stress and inflammation promote depression and DM2, offering a feasible common association between them.
The close chronological relation between Type 1 diabetes mellitus (DM1) and the onset of depression is striking: diagnosis of DM1 and its effective treatment burden occur at a time when the individual is at an increased risk for depression. Children and adolescents with DM1 have a 2-3 times greater prevalence of depression in comparison with youth without diabetes.
Similar to DM2, it appears that DM1 and depression possess common pathophysiological pathways, in a sharp contrast to traditional thought, that the burden attributed to diabetes increases the prevalence of depression.
The Risk Of Depression In Those With Diabetes
An epidemiological study conducted recently involving 90,686 participants found that depression was more prevalent in those with diabetes, regardless of whether they had diagnosed or undiagnosed diabetes.
One possible explanation could be that the psychological burden of being ill with diabetes could play a significant role in triggering depression. That said, the fact that in those individuals with previously undiagnosed diabetes, there was a higher prevalence of depression that could be the result of an unfavourable lifestyle, such as lack of physical activity, unhealthy diet, and stress.
Severe hypoglycaemia in those with DM2 and without any treatment for depression was positively associated with the severity of the symptoms of depression, which were independent of glycaemic control, lifestyle factors, insulin therapy, and diabetic complications. A meta-analysis to estimate the association between diabetic neuropathy and depression could not clarify if the relationship is bi-directional or not.
Hypothetically, the risks of depression could be increased by treatment for diabetes. A strong association between depression in individuals in their forties and orally treated diabetes was found in comparison with those in their seventies. In a sharp contrast, insulin therapy in elderly individuals with DM2 led to improvement of symptoms of depression, without affecting the health-related quality of life of these individuals.
Diabetes leads to structural changes in the brain: cerebral atrophy, lacunar infarcts, and changes in blood flow of both hypo- and hyper-perfusion. In a similar manner, depression is associated with neurodegenerative processes, especially at the level of the hippocampus and prefrontal cortex.
On A Final Note:
In those with diabetes, depression remains largely underdiagnosed, and a crucial aspect for the diabetologist would be to stay aware of this common co-morbidity. A multidisciplinary approach of the individual with diabetes would significantly help in improving the outcomes of the disease, decreasing the number of DALYs (Disability Adjusted Life Years) and mortality.
