Whites have a more robust hypothalamic–pituitary–adrenal axis response to a psychological stressor than blacks

Summary

Objective

Differences in the hypothalamic–pituitary–adrenal (HPA) axis response to stress may confer differences in susceptibility to a variety of diseases. We hypothesized that whites would differ from blacks in HPA axis response to a psychological stressor.

Design

Healthy subjects aged 18–30 were recruited from Baltimore, Maryland. At initial assessment, they completed psychometric tests measuring anxiety, mood, and personality. Subjects then participated in the Trier Social Stress Test (TSST), which consisted of 10 min of public speaking and mental arithmetic exercises. Subjective anxiety was measured immediately pre- and post-TSST. Race effects on cortisol, adrenocorticotrophin (ACTH), and prolactin responses to the TSST were analyzed by GEE longitudinal analysis methods. The analysis controlled for gender, baseline hormone levels, socioeconomic factors, anxiety, mood, and dimensions of personality.

Results

Ninety-eight subjects participated in the TSST. Whites had 36% greater relative mean cortisol response than blacks (95% CI: 10–67%, P=0.004). Whites had significantly higher mean ACTH compared to blacks at 25 min after the start of the TSST (35%, 95% CI: 16–58% greater, P<0.001). There was no difference in prolactin response. Of note, whites and blacks did not differ in subjective anxiety response to the TSST.

Conclusions

In sum, we found that whites have a more robust HPA axis response to the TSST compared with blacks, even after controlling for several socioeconomic and psychological factors. In contrast, we observed no difference in prolactin response. There were no differences in subjective response to the TSST to explain the difference in HPA axis response. Further study is indicated to explain this finding and to test whether it can be extrapolated to other forms of stress.

Introduction

Racial disparities in the prevalence and burden of disease exist for a broad spectrum of medical conditions. For instance, there is a higher prevalence and earlier onset of hypertension among blacks than whites (Ferdinand and Saunders, 2006). Blacks are also almost twice as likely to have diabetes than non-Hispanic whites (Centers for Disease Control, 2007). As would be expected, morbidity and mortality from cardiovascular diseases is higher among blacks compared with whites (National Heart Lung and Blood Institute, 2005). In contrast, certain conditions such as osteoporosis are less common in black than white women (Department of Health and Human Services, 2007). Also, several psychoaffective conditions such as anxiety, mood, and substance use disorders are less prevalent in blacks compared to non-Hispanic whites (Kessler et al., 2005). The underlying causes of these racial disparities are likely multifactorial and may relate to socioeconomic factors, healthcare access, patient preferences, and biological differences. With respect to the latter, variations in the response to environmental stressors are likely to play a contributory role.

The hypothalamic–pituitary–adrenal (HPA) axis is a cardinal mediator of the stress response. Inappropriate and maladaptive intensification or attenuation of HPA axis-mediated responses to stress can lead to chronic diseases (McEwen, 1998; Sapolsky, 1999; Tsigos and Chrousos, 2002). Following the perception of stress, corticotrophin releasing hormone (CRH) is released from the hypothalamus. CRH stimulates the synthesis and release of adrenocorticotrophic hormone (ACTH) from the pituitary gland, which in turn stimulates cortisol synthesis and release by the adrenal cortex. HPA axis dysregulation has been shown to contribute to conditions that show a racial difference, such as several of the aforementioned diseases (Gold and Chrousos, 2002; McEwen, 1998; Tsigos and Chrousos, 2002). Thus, it is conceivable that racial differences in susceptibility to certain chronic diseases could be partially explained by physiological variations in stress hormones such as cortisol.

Several studies have suggested that cortisol patterns during the day differ between blacks and whites. For instance, cortisol levels upon waking have been shown to be higher among higher educated whites compared with blacks and lower educated whites (Bennett et al., 2004). Another study has suggested that blacks experience a less steep decline in cortisol during the course of the day, even after accounting for differences in socioeconomic status (Cohen et al., 2006).

No study has assessed for racial differences in HPA axis response to a standardized psychosocial stressor while adequately accounting for confounders. Based on the previous findings, we hypothesized that the HPA axis responses to a psychological stressor would differ between healthy whites and blacks, independent of anxiety, mood, personality, and socioeconomic factors. Thus, we administered a standardized psychosocial stress test, the Trier Social Stress Test (TSST), to healthy black and white subjects and measured their cortisol and ACTH response. This study objective was a secondary outcome of a larger study examining the relationship between genetic variation and HPA axis responses. In addition, we simultaneously measured the responses in another stress hormone, prolactin.