Tackling Adversity and Cardiovascular Health: It is About Time

One of the most foundational shared human experiences is adversity. Defined by MerriamWebster Dictionary as “a state or instance of serious or continued difficulty or misfortune,” adversity can catalyze personal development and shape our values. However, the potency, life-course timing, duration, and type of adversity an individual or population faces affect biological adaptation, psychosocial responses, and health behaviors. Experiences with adversity, particularly when long term, lead to untoward health and wellbeing. This effect is markedly evident within the realm of cardiovascular disease. Certainly, decades of primary research, especially in the psychosocial literature, documents associations between various types of adversity and both cardiovascular risk factors and disease. Categories of adversity include but are not limited to exposure to harsh childhood environments, life-course trauma, violence, discrimination, economic and neighborhood stressors, environmental disasters, and even sociopolitical anxiety. For example, self-reported everyday discrimination is positively associated with hypertension, poor sleep, visceral fat, elevated C-reactive protein levels, coronary artery calcification, and mortality.1 In addition, exposure to a single traumatic life event such as violence or death of someone close is related to higher odds of atrial fibrillation.2 Psychosocial stress (stress) represents a core component of adversity. However, stress is not always health damaging. For example, manageable amounts of psychosocial stress, if associated with adequate social and emotional support, along with mastery and control, may preserve healthy brain architecture. However, cumulative chronic stress (cumulative stress), defined as repeated detrimental stress exposures over time, can result in biological maladaptation, that is, allostatic load, leading to a range of conditions, including cardiovascular disease. Therefore, when we characterize adversity, it is crucial to evaluate stress from a life-course perspective to capture its full impact on physiology and well-being. Indeed, cardiologists and other clinicians often state that reports of stress are subjective and difficult to quantify, making stress problematic to adequately characterize in the context of disease. However, this assertion ignores the contextual nature of stressors and perpetuates the traditional lack of serious priority and attention given to adversity as a source of health care inequities in multiple realms. Cumulative stress is biologically embedded and results in cardiovascular disease through various mechanisms, including altered neurological activity, augmented and unchecked inflammation, and neurohormonal dysregulation through the hypothalamic-pituitary-adrenocortical axis (Figure). Life-course adversity through epigenetic processes is one potential mechanism through which intergenerational propagation of certain health conditions and disadvantage occurs from nonsurrogate pregnant individuals to their children.3 Indeed, ≈80% of cardiovascular disease is dictated by preventable factors, including behavioral, psychological, and social factors.4 Despite this, the majority of research and clinical efforts in cardiovascular medicine have focused largely on and overwhelmingly rewarded efforts outside the study of adversity and psychosocial stress. Indeed, efforts aimed at primordial, primary, and secondary cardiovascular disease prevention have limited success when their interplay with adverse life expe-