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Academic Highlights: Institutional Racism and Health Inequities

This Quarterly, we feature two summaries of articles that confront the impact of institutionally reinforced structural violence. "More than skin deep" discusses the connection between mental health, stress, and the neuro-biological mechanisms that result in mental health inequities for minoritised communities. "Racism and health service utilisation: A systematic review and meta-analysis" explores the available literature around the impact of racism on healthcare utilisation by minoritised communities. Read more by clicking the titles below.

‘‘More than skin deep’’: stress neurobiology and mental health consequences of racial discrimination

Berger M and Sarnyai Z. Stress, 2015; 18(1):1-10

Highlight by Sophia

It is widely accepted that racial discrimination leads to poor mental health through activation of stress pathways, yet the neuro-biological mechanisms by which this happens are poorly understood. Using evidence from a range of neuroimaging and endocrinology studies, this review seeks to disentangle these mechanisms.

Mechanism 1: Activation of the hypothalamic-pituitary-adrenal (HPA) axis

The first mechanism suggests that experiences of racial discrimination provoke a stress response through activation of the HPA axis and subsequent cortisol release. Cortisol is the body’s main stress hormone, causing physiological changes to mediate short and long-term responses to stress. Elevated levels can cause changes to normal metabolic, immune, and cognitive functioning.

Four studies showed that non-White adult groups (African American and Hispanic) had flatter cortisol slopes throughout the day (indicative of chronic stress), and higher evening cortisol levels, compared to their White counterparts. American-born adolescents of Mexican descent, who self-reported racial discrimination, also had higher overall cortisol levels. Conversely, one study of Native Hawaiians, who had experienced racial discrimination, had overall lower levels. The authors suggest that the direction of change in cortisol, whether heightened or attenuated, is likely dependent on methodological differences and additional mediating factors, such as social support and socioeconomic status, which warrant further exploration.

Mechanism 2: Allostatic load and impact on neural functioning

The second mechanism builds on the first: exposure to recurrent racial discrimination results in chronic activation and ‘wear and tear’ of the HPA axis – a process called allostatic load. In addition to cortisol changes, pro-inflammatory immune molecules called cytokines (such as IL-6) are released at high levels. High IL-6 was measured in one study among Black and Latina adults who self-reported low self-esteem and racial stigmatisation.

Allostatic load also increases receptor binding of glucocorticoid hormones, which if elevated for long periods of time, can cause long-term changes to brain functioning. Two areas are particularly affected: the anterior cingulate cortex (ACC) and the pre-frontal cortex (PFC), both responsible for emotional regulation. Four studies showed hyperactivity in the dorsal ACC and the PFC of individuals who reported discrimination and social exclusion, including healthy migrants in Germany and African American students in the USA, compared to controls.

Elevated glucocorticoids are also believed to alter neurotransmitters. While no studies investigated the association between racial discrimination and changing neurotransmitter release, previous evidence shows that long-term exposure to social stress causes increases in dopamine in both the ACC and PFC – a phenomenon commonly observed in individuals with schizophrenia. Reductions in 5-HT (serotonin) receptor binding in the ACC also occurs in response to daily psychosocial stress. Similarly, N-acetyl aspartate (NAA) release declined in the ACC of individuals who felt discrimination due to opioid addiction.

In light of this evidence, the authors suggest that allostatic load, with its changes to the release of cytokines, glucocorticoids and neurotransmitters, is a mechanism linking recurrent exposure to racial discrimination and poor mental health.

Mechanism 3: Imbalance of the autonomic nervous system

The third mechanism suggests that racial discrimination causes an imbalance between the two main parts of the autonomic nervous system: the parasympathetic nervous system, responsible for “rest and digest” processes, and the sympathetic nervous system, activated during “fight or flight”.

The parasympathetic system can be measured by high frequency heart rate variability (HRV) and the sympathetic system by low frequency HRV. In this review, the authors included only one study on racial discrimination and HRV: White Americans exhibited high frequency HRV at young ages, which declined with age, however their African American counterparts exhibited low HRV already at young ages. Low frequency HRV has previously been identified in individuals diagnosed with post-traumatic stress disorder, schizophrenia, depression, and anxiety. The authors believe that an imbalance of the autonomic nervous system, in favour of the sympathetic nervous system, is a potential mechanism linking racial discrimination to poor mental health.

Taken together, the authors conclude that these three mechanisms lead to heightened sensitivity and hyper vigilance of the body’s stress response, and ultimately result in emergence of psychopathologies. However, this review investigated racial discrimination in the context of individual experiences and relied on self-reported discrimination. It is likely that these results only reveal a small proportion of the actual effect of racial discrimination on mental health.

Racism and health service utilisation: A systematic review and meta-analysis


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