Blunted neuroendocrine responses linking depressive symptoms and ECG-left ventricular hypertrophy in black Africans

Abstract

Objective Chronic psychosocial stress as experienced in an urban environment plays an important role in the aetiology of depression-related cardiovascular risk. It is uncertain whether acute mental stress responses aggravate this risk. Therefore, we aimed to explore the associations between depressive symptoms, neuroendocrine acute mental stress responses and cardiovascular risk, that is ECG-left ventricular hypertrophy (ECG-LVH), in a black South African cohort. Materials and methodsThe substudy sample consisted of 179 black African men and women from the Sympathetic Activity and Ambulatory Blood Pressure in Africans study. Depressive symptoms were evaluated using the nine-item Patient Health Questionnaire and the participants were stratified into black Africans with depressive symptoms and without. Cortisol and 3-methoxy-phenylglycol (MHPG) responses were analysed during rest and exposure to the Stroop mental stressor. Cortisol median split responses were determined and stratified sex groups accordingly into above (> 1.5 ng/ml) and below (r 1.5 ng/ml) responders. Blood pressure and ECG-LVH data were obtained from 24-h ambulatory monitoring and 12-lead ECG. ResultsThe Africans with depressive symptoms demonstrated mean hypertensive status, blunted cortisol and MHPG acute mental stress responses (P r 0.05).In Africans with depressive symptoms and low cortisol stress responses, blunted MHPG acute mental stress responses were associated with ECG-LVH in Africans [adjusted R 2 = 0.20; b = 0.92 (95% confidence interval 0.74, 1.10); P r 0.02].Conclusion Blunted neuroendocrine responses were linked to depressive symptoms and ECG-LVH in black Africans. When coupled to their hypertensive status, these vasoconstrictive agent responses may underpin the increased long-term depression and vascular disease risk in urban Africans.

Defensive coping and renovascular disease risk — Adrenal fatigue in a cohort of Africans and Caucasians: The SABPA study

“…Considering sex differences; African men in the low cortisol category have a ten times higher risk of increased ACR, than those in the high cortisol category. This confirms results from previous studies, where African men revealed attenuated cortisol responses associated with structural wall remodelling [32] and poorer health than their female and Caucasian counterparts [2,13,32,42]. From these results, it is evident that African men with low or possible down-regulated cortisol levels reveal more vulnerability for renovascular disease than their high cortisol as well as Caucasian counterparts.…”

“…The HPAA thus seems to have become non-responsive or hypoactive to stress in these participants. Possible down-regulation occurred, decreasing sensitivity of the HPAA and adrenal fatigue may have set in, with subsequent lower levels of cortisol [24,32,[38][39][40]. Thus, with further exposure to stress, the desensitised or habituated HPAA defensive coping response may not be able to increase cortisol for effective coping, and becomes dysfunctional.…”

“…Nonetheless, the Africans also revealed probable alcohol abuse and this might further enhance dysregulation of the HPAA [29][30]. Subsequently, the damaging effects of increased cortisol, in prolonged unmanageable stress (when defensive coping "fails" or dissociate) [11], as well as the probable cortisol sensitivity of the Africans, may affect end-organ function [2,24,[31][32]. Indeed, we were able to demonstrate more prominent increased renovascular disease risk in the defensive coping Africans within the low and high cortisol categories.…”

Cortisol:brain-derived neurotrophic factor ratio associated with silent ischaemia in a black male cohort: the SA BPA study

“…During chronic stress, a maladaptive cortisol response is elicited due to structural changes in the HPA axis 21-23. A state of psychological distress in Africans may therefore be present 12,19,20…”

“…If this state is further supported by high levels of alcohol abuse, the central depressant effect of alcohol may disturb central cardiometabolic homeostasis 21. Chronic psychological stress induces sympathetic hyperactivity,17 higher circulating levels of catecholamine and cortisol, and ultimately down-regulation will occur 12,22-24. Therefore, the lower cortisol level may act as the driving force behind a possible down-regulated BDNF.…”