The purpose of the present study was to evaluate inflammatory and metabolic impairments among patients with depression. This study was conducted by categorizing depression patients into four-dimensional profilers which are (1) atypical energy-related symptom dimension, (2) melancholic dimension, (3) childhood trauma dimension, and (4) anxious distress dimension.
Laboratory assessment was done for evaluation of inflammatory and metabolic impairments among the four-dimensional depression profilers and the control group.
Results of the current study revealed that all patients with metabolic impairments (including hypertension, impaired glycemic control, low/high-density lipoprotein, elevated triglycerides, and central obesity) had reported significantly higher scores in the atypical, energy-related symptom dimension.
These results are indicating more metabolic dysregulation in patients with higher scores in the atypical, energy-related symptom dimension.
According to , the atypical, energy-related symptom dimension included the following items: increased appetite, increased weight, hypersomnia, leaden paralysis, and low energy.
A possible explanation for these significant findings in this dimension of depression may be that increased appetite, hypersomnia, leaden paralysis, and low energy present in the atypical depression may lead to higher fat and carbohydrate intake as well as decreased daily physical activity and weight gain leading to significant impairment in blood glucose and lipid levels.
In the same area of research, Alshehri et al.  reported the association between abdominal obesity and depression, Simmons et al.  revealed that appetite changes are related to metabolic impairments in the depression subgroups.
The results of the current study are agreeing with prior similar studies showing that metabolic dysregulation is strongly related to atypical energy-related symptom dimension [32, 33].
Also, the results of [34, 35] confirmed our results that depression with atypical features is associated with an increase in waist circumference and fasting glucose and a higher incidence of metabolic impairment.
On the other hand, according to the results of this study, the melancholic symptom dimension is less likely to be linked to inflammatory and metabolic impairments.
This may be due to the lower appetite present in melancholic depression which will lead to lower fat and carbohydrate intake, resulting in lowering blood glucose and lipid levels and less be linked to inflammatory and metabolic impairments.
Recent studies [36, 37] had the same findings, reporting that melancholic forms of depression are associated with a lower prevalence of metabolic syndrome.
Also, the results of the current research highlighted that patients with impaired glycemic control had reported significantly high scores in the anxious distress symptom dimension.
This important finding can be explained as anxiety is frequently associated with poor metabolic functions and serious medical problems. Anxiety is associated with increased levels of the stress hormone cortisol which block the effect of insulin from taking glucose from blood into cells all over the body causing high blood sugar and finally impaired glycemic control.
A recent study  reported the association between anxiety and metabolic syndrome emphasizing the role that cortisol plays in this relation.
Another important finding in this study is that patients with inflammatory impairment (serum CRP > 3 mg/L) had reported significantly higher scores in the childhood trauma symptom dimension.
This can be explained as childhood trauma (emotional neglect, psychological abuse, physical abuse, and sexual abuse) usually leads to heightened stress response in the childhood period leading to impaired emotional regulation, sleep problems, and autoimmune diseases. Also, childhood exposure to trauma can trigger a systematic inflammatory response.
These data are consistent with some recent studies [38,39,40] who had reported that childhood trauma was found to be significantly associated with higher inflammatory markers among patients with depression.
The last finding is the presence of statistically significant metabolic impairments (including hypertension, impaired glycemic control, low/high-density lipoprotein, elevated triglycerides, and central obesity) and inflammatory impairment (serum CRP > 3 mg/L) among the cases group in comparison with the control group.
Patients with depressive disorder are prone to metabolic and inflammatory impairment due to their poor health-related behaviors. In addition to the genetic, biological, and psychosocial models involved in the pathogenesis of depression, recent studies revealed that the metabolic and immune-inflammatory impairments as higher levels of inflammatory markers, dyslipidemia, and metabolic syndrome are also reported. Such findings represent serious risk factors for diabetes and cardiovascular diseases . Also, the role of antidepressants cannot be ignored as certain antidepressants may predispose to cardio-metabolic dysfunction .
Finally, this study highlights that all patients with metabolic impairments (including hypertension, impaired glycemic control, low/high-density lipoprotein, elevated triglycerides, and central obesity) had reported significantly higher scores in the atypical, energy-related symptom dimension.
Also, patients with impaired glycemic control had reported significantly high scores in the anxious distress symptom dimension while patients with inflammatory impairment (serum CRP > 3 mg/L) had reported significantly higher scores in the childhood trauma symptom dimension.
Based on these results, these results can be applied clinically to improve treatment and prognosis in patients with depression. For example, depressed patients with atypical, energy-related symptoms should increase their daily physical activities and exercise, and they should follow a special diet. Also, anti-inflammatory medications could be added to depressed patients of the childhood trauma symptom dimension.
Before we conclude, we would like to discuss the limitations of this study. A limited number of studies on the dimensions of depression are available. Depression subtypes are often overlapping which acquires further assessment of the correlations between profilers.
Research on larger samples is needed to confirm our findings.
In addition, the previous medical history of those patients and drug treatment they receive for these conditions should have been taken into consideration.
Also, in the coming research in this area, the role of pharmacotherapy for depression should be more adjusted as it may predispose to cardio-metabolic dysfunction.
Finally, lifestyle-related behavior is a risk factor, which needs further assessment.