‘Psychosomatic illnesses’ is a term popularly used when referring to malingering illnesses, or illnesses without an apparent physical basis, leading to the misbranding of psychosomatic disorders.1
However, the field of psychosomatic medicine delves much deeper into the underlying explanations behind illnesses, exploring the components that have the potency to affect the very biological processes that we rely on, as well as our quality of life.
The interconnection between mind and body was first discussed by the 17th-century philosopher, Descartes. Beginning with his famous proposition,
“I think, therefore I am.”
Descartes theorised that the mind is an immaterial substance distinct from the body, yet linked to it through cognitive states, such as emotion.
The introduction of psychosomatic disorders into the medical world, however, was birthed in 1977 by George Engel, in opposition to the “strict biomedical approach” of medical education, in which physicians cast a blinkered approach towards diagnoses. Engel argued that illnesses stem from beyond the body, and that biological, social and psychological factors are interlinked within humans, and much like a Domino Effect, a change in one factor could affect the others, impacting the overall health of an individual.2
Thus, the biopsychosocial model was brought forth.
The biopsychosocial model considers several elements that can affect the health of an individual, such as biological (genetic susceptibility), psychological (behaviour and beliefs) and social (cultural and childhood experiences, as well socioeconomic elements) factors.
Fig. 1  An illustration of the biopsychosocial model comprised of biological, psychological, and sociological influences3
A microscope on depression
Depression is a multifaceted disease, which psychosomatic medicine explores.
To understand the pathology of depression, knowledge of brain structures and their neurochemistry is needed.
The Nervous System and the Brain
Depression is associated with a “biologically mediated vulnerability to stress”. 4 Physiological measures like changes in heart rate characterise depressive disorders.
The central nervous system and autonomic nervous system are involved in maintaining homeostasis, through the co-ordination of physiological responses, as well as interpersonal and emotional stressors, which can in turn influence the health of an individual. The involvement of the brain in determining these responses can be influenced by social factors, for instance, early childhood experiences, which are shown to influence the nervous system when involved in responses to later stressors. 5
Research studies have shown that exposure to excessive or prolonged stress during childhood, can contribute to the loss of neurons in the hypothalamus and the amygdala, both important regions of the brain involved in emotional processing and the activation of the sympathetic nervous system (a branch of the autonomic nervous system). Such disruption to the normal functioning of these regions and, consequently emotions, are defining features of depression, showing how social factors can have a biopsychological effect on humans. 6
The role of hormones
Much like the nervous system, the function of the endocrine system can also be affected by the chronic stressors rooted in social factors.
The brain governs bodily processes, such as digestion and mood, through the sympathetic nervous system and the release of hormones -namely cortisol – from the HPA axis (hypothalamus-pituitary-adrenal axis), an endocrine system in the brain, commonly known as the body’s “stress system”.
Reflected in a research study, both patients suffering and not suffering from major depression with psychosis (which can cause hallucinations and delusions), underwent hourly blood sampling for cortisol, and it was found that patients with depression -with and without psychosis- exhibited higher levels of cortisol.7 The reason behind this is that depression disrupts the regular functioning of the HPA axis; when this section of the brain is overactive, it can lead to hypersecretion of cortisol into the blood, which can affect several biological processes.
As stated earlier, there is a Domino Effect at play, as sustained levels of cortisol can ultimately lead to atrophy of the hippocampus -a major component of the brain- impairing its ability to regulate emotions, showing how the brain and endocrine system interact with each other and can, therefore, be greatly affected in response to stressful life experiences (social factors).
In the long-term, another danger is that elevated levels of cortisol can increase the risk of hypertension (high blood pressure), as well as coronary heart disease and stroke. The onset of these physical diseases are seemingly linked to depression, and it is for this reason that depression is considered to be both a trigger, as well as a consequence of psychosomatic illnesses.8
The knowledge acquired from studies into depression has facilitated pharmaceutical advances, a key example of this being antidepressants such as SSRIs, which maintain the balance of serotonin. In doing so, it normalizes endocrine and neuronal function – helping restore biological processes to their former glory. SSRIs are also involved in the regulation of mood, appetite and sleep. 9 This reflects the holism of the biopsychosocial model, as these physiological and psychological factors can in turn influence social factors, such as interactions with friends and family, which could be negatively affected due to a bad mood and sleep deprivation.
The introduction of the biopsychosocial model emphasises to doctors the significance of considering all these factors in a diagnosis, shedding light on the importance of medical students asking about a patient’s “current state of wellbeing, health habits, stressors, moods, hopes and fears”.
This knowledge picks away at the enigma that is psychosomatic illnesses, allowing for doctors to relay how all of these components intertwine cause an illness, which might allow for patients to destigmatize their illnesses, and more readily accept psychotherapy, if required. 10
An understanding of psychosomatic medicine, allows for the medical field to move away from the reductionist view of solely considering molecular biology and genetics during diagnosis, and work towards a more holistic approach – treating the patient and not just the disease.
- Monica Grego, ‘Illness as a Work of Thought: A Foucauldian Perspective on Psychosomatics’, Routledge, (2002),p.1-2
- Novack, D.H., Cameron, O., Epel, E. et al. ‘Psychosomatic Medicine: The Scientific Foundation of the Biopsychosocial Model’, Acad Psychiatry 31, (2007), p.388–401
- ‘The biopsychosocial model and chiropractic: A commentary with recommendations for the chiropractic profession’, Scientific Figure on ResearchGate. [accessed 10 May, 2020]
- Gatt, J. M., Nemeroff, C. B., Dobson-Stone, C., Paul, R. H., Bryant, R. A., Schofield, P. R., … Williams, L. M. ‘Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety’, Molecular Psychiatry, 14(7), (2009) p.681–695.
- Singer BH, Ryff CD, ‘New horizons in health: an integrative approach’,Washington, DC, National Academies Press, (2001), as cited in Novack, D.H., Cameron, O., Epel, E. et al. ‘Psychosomatic Medicine: The Scientific Foundation of the Biopsychosocial Model’, Acad Psychiatry 31, (2007) p.388–401
- Gatt, J. M., Nemeroff, C. B., Dobson-Stone, C., Paul, R. H., Bryant, R. A., Schofield, P. R., … Williams, L. M. ‘Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety.’, Molecular Psychiatry, 14(7), (2009), p.681–695.
- Varghese, Femina P., and E Sherwood Brown. ‘The Hypothalamic-Pituitary-Adrenal Axis in Major Depressive Disorder: A Brief Primer for Primary Care Physicians.’ Primary care companion to the Journal of clinical psychiatry vol. 3,4 (2001) ,p.151-155
- Meng L, Chen D, Yang Y, Zheng Y, Hui R. ‘Depression increases the risk of hypertension incidence: A meta-analysis of prospective cohort studies’ J Hypertens. (2012);30: p.842–851
- Chilmonczyk Z, Bojarski AJ, Pilc A, Sylte I ‘Functional Selectivity and Antidepressant Activity of Serotonin 1A Receptor Ligands’. International Journal of Molecular Sciences. (2015), p.16
- Novack, D.H., Cameron, O., Epel, E. et al. ‘Psychosomatic Medicine: The Scientific Foundation of the Biopsychosocial Model.’, Acad Psychiatry 31, (2007), p.396