Cancer and Stress: Does It Make a Difference to the Patient When These Two Challenges Collide?

Abstract

A single head and neck Cancer (HNC) is a globally growing challenge associated with significant morbidity and mortality. The diagnosis itself can affect the patients profoundly let alone the complex and disfiguring treatment. The highly important functions of structures of the head and neck such as mastication, speech, aesthetics, identity and social interactions make a cancer diagnosis in this region even more psychologically traumatic. The emotional distress engendered as a result of functional and social disruption is certain to negatively affect health-related quality of life (HRQoL). The key biological responses to stressful events are moderated through the combined action of two systems, the hypothalamus–pituitary–adrenal axis (HPA) which releases glucocorticoids and the sympathetic nervous system (SNS) which releases catecholamines. In acute stress, these hormones help the body to regain homeostasis; however, in chronic stress their increased levels and activation of their receptors may aid in the progression of cancer. Despite ample evidence on the existence of stress in patients diagnosed with HNC, studies looking at the effect of stress on the progression of disease are scarce, compared to other cancers. This review summarises the challenges associated with HNC that make it stressful and describes how stress signalling aids in the progression of cancer. Growing evidence on the relationship between stress and HNC makes it paramount to focus future research towards a better understanding of stress and its effect on head and neck cancer.

The Influence of Psychological Stress on HPV Infection Manifestations and Carcinogenesis

“…As crucial components of the stress response, the HPA axis and the autonomic nervous system (ANS) interact with other vital centers in the central nervous system (CNS) and peripheral tissues/organs to mobilize an adequate/appropriate adaptive response against stressors. Thus, different stressful events are recognised by the hypothalamic paraventricular nucleus, which participates in a biological circuit that integrates personal experiences, physiological signalling and the release of corticotropin-releasing hormone (CRH) [31]. CRH acts on the pituitary gland, which then releases adrenocorticotropic hormone (ACTH), followed by ACTH signals to the adrenal cortex to release glucocorticoids [31].…”

“…Thus, different stressful events are recognised by the hypothalamic paraventricular nucleus, which participates in a biological circuit that integrates personal experiences, physiological signalling and the release of corticotropin-releasing hormone (CRH) [31]. CRH acts on the pituitary gland, which then releases adrenocorticotropic hormone (ACTH), followed by ACTH signals to the adrenal cortex to release glucocorticoids [31]. Thus, the body's adaptive stress response depends on many interconnected neuroendocrine, immune, cellular, and molecular mechanisms.…”

“…In addition, the sympathetic nervous system (SNS) is activated and stimulates the adrenal medulla to release catecholamines, adrenaline and noradrenaline, allowing the body's systems to transport energy to the organs more quickly. Consequently, homeostasis is re-established, provided the stressor falls into the adaptive capacity [31]. However, during severe and/ or chronic stress, dysregulation of the stress system (hyperactivation or hypoactivation) can disrupt homeostasis and lead to cacostasis or allostasis with possible various clinical manifestations [30].…”

“…Prolonged activation of stress mechanisms with increased glucocorticoid and catecholamine levels causes a condition where the demand on the individual exceeds their personal adaptive capacity (allostatic load). Therefore, according to research results, chronic stress and increased glucocorticoid/catecholamine levels may participate in cancer progression in different diseases, including HPV-related carcinogenesis [31].…”

Association of psychological status with first diagnosed pulmonary tuberculosis in men

“…It is also assumed that the chances of developing tuberculosis are significantly increased in patients with depression at the background of a decrease of immune defences [6]. It is known that with the background of depression there is a suppression of cellular immunity factors activity and an increase of catecholamines, histamine, opioids and some pro-inflammatory cytokines expression, which negatively affect the susceptibility to tuberculosis infection [7]. In turn, the chronicity of the tuberculous process causes the progression of tissue hypoxia, contributing to the development of anxiety and depression [8].…”