Biological Inequity
Although the prevalence and incidence of non-communicable diseases has significantly increased in the last few decades across the western world, there are parts of society that are being disproportionately affected by them. Epidemiological studies have attempted to explain these differences through genetic or epigenetic processes, which are hereditary or developed through the course of life. These imply that the individual is the sole agent that determines health outcomes. Many such studies, however, investigate health in the sterile isolated settings of laboratories, without taking into consideration the day-to-day experiences of the person nor the environment they constantly interact with.
Indeed, exposure to stressful environments and events have been shown to dysregulate the stress response, often leading to disease onset. For instance, exposure to chronic stress was shown to be linked to higher risk of dementia as well as autoimmune diseases and mental health disorders. Risk of disease also increases with higher numbers of stressors, which act in a synergistic manner to further and more powerfully disrupt the proper functioning of the stress response. As we previously discussed, stressors can derive from different sources, both psychological and environmental (eg. pollution).
Thus, in order to better understand why certain communities are being disproportionately affected by the incidence of non-communicable diseases, it is important to consider the environmental and psychosocial stressors that the community experiences daily. It is from these considerations that we propose a new term to describe the unequal distribution of stressors and their effects on health in our society: biological inequity.
We introduce a new term called biological inequity to describe the fact that different communities experience very different levels of stress - and as a result very different health outcomes - due to the systemic application of racism and classism. Chronic exposure of some communities to poverty, pollution, trauma and other stressors are drivers for biological inequity. In this framework, it is not the individual’s genetic makeup that is the indicator of health, but the environment and daily experiences they are constrained to live in. That is not to say that genetics play no role in determining health. Rather, it means that biological inequity is a more encompassing explanation for differences in health outcomes. For instance, two women carrying the same gene for breast cancer but living in different environments will have different health outcomes: it is more likely that one living in polluted areas and experiencing daily stress or trauma will experience cancer onset, while the other living in a clean environment might not.
Moreover, the mechanisms of biological inequity are more unbiased than traditional epidemiological explanations of health. In fact, epidemiological research has often proposed that genetic distinctions between ethnicities are the driver of poor health outcomes for certain minority communities. Instead, biological inequity proposes that the systemic application of racism and classism forces certain communities to live in environments with higher stressor levels than normal, thus resulting in poor health outcomes. In this framework, the epigenetic differences between ethnicities described in the literature can be explained through allostasis/allostasic overload: a permanently dysregulated stress response due to the environment can cause epigenetic changes that are transmitted from parent to offspring, becoming hereditary. The inner workings of biological inequity can be summarised in the following diagram.
Figure 3. The stress response is at the intersection between environmental (pollution), psychosocial stressors and an individual’s sensitivity (eg. based on age etc). When racism and classism are applied they increase environmental and psychosocial stressors, disproportionately affecting the stress response. The results of a constantly dysregulated stress response affect the individual’s lifespan and can be detected at different life stages: from in utero to adulthood. These changes may lead to epigenetic effects that become hereditary.
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