Critical Times

Psychosocial interventions for cancer. by P Henry 3May26

Cancers are multifactorial illnesses. Genetic predispositions, human activities, endogenous & exogenous phenomena can all trigger or increase cancer. They cause the most life-years’ disability[1], requiring a multidisciplinary approach.

Considering these complexities, more investigation is required: hopefully these notes can help further research.

Psychosocial

Exploring psychosocial interventions require both qualitative and quantitative indicators. Cancers’ prognosis and unknown factors stimulate stresses and anxieties. The many dimensions of what a patient understands, and what professionals imply, create a confusing liminal area.

Stresses and anxieties arise with this ambiguity about what is understood and unknown. There are multilayers of what is stated or suggested, increasing the threat of unpredictability. These experiences of isolation, rejection, impairment, suffering, confusion, and death threat are all common as unmitigated existential realities.

Lifestyle changes need to be quantified, or many will not make changes. Sexuality and gender influences are under-addressed. Sex and intimacy have a direct effect on emotional, psychological and physical stability. Their dysfunction is common and silently suffered. [2] How and why gender is part of disease pathology and immune functioning[3] needs to be delineated.

To increase treatment efficiency and dispel cursory rejection of Psychooncology practices require clarifications.  These include: 1) Detailing techniques and application efficiency for specific cancers, describing under what circumstances. 2) Address how distress and foreboding accompany cancer’s onset and its symptoms. 3) Confirm the role of emotions in cancers’ maintenance and outcome.  4) Indicate how significant the impacts of suffering, impairment, rejection, confusion and the death-threat of cancer are. 5) Clarify how stressors and individual defences are related to environment and developmental issues. 6) Examine the impact of all alternative interventions. 7) Detail PNI applications. 8) Directly connect psychosocial therapies to biochemical treatments.

Which psychological techniques would be the most helpful in addressing these complex, often repressed experiences? Would cathartic[4] activities, that might release tension, build a more solid base for change, or using simpler psychological techniques, such as palliative rather than remedial, are more helpful for cancer. This should consider the fragile balance of health, how survival allostasis is limited, and return to healthy homeostasis is maintained and enriched[5].

Biochemistry

Detailing the functions of the HPA axis (hypothalamic-pituitary-adrenocortical) influences on cancer[6] is necessary. The HPA releases hormones, secretes glucocorticoids and acts on many organs. It interacts with them, having diverse biofeedback biochemical systems. This variation increases or reduces stressors. This HPA dysregulation affects diurnal variation and cancer progression[7]. HPA interacts (along with the autonomic, central & peripheral nervous systems) to stressor perceptions. Responses fight, flight or freeze alter human bio-systems from homeostasis to an allostasis, increasing risk[8].

Repeated stressors, over time, change healthy homeostasis to allostatic, attempting to cope[9]. This often leads to overload affecting the endocrine, HPA, and immune systems, influencing oncogenesis[10]. Understanding this reciprocity may help understand the immune system’s difficulties in dealing with cancer.

Genetics’ connection with cancer has only been initially described. Oncogenes and tumour suppressor genes vary through life. Cancer promotion, progression, tumorigenesis and reoccurrences are connected to epigenetic changes[11]. Epigenetics shows that inherited but repairable genetic DNA modifications affect gene expression[12]. 

The cancer gene, or proteins responsible for it, can allow changes of cancerous gene mutation.[13]

Abnormal epigenetic changes can incorrectly activate oncogenes, creating cancer abnormalities. Epigenetics influences “regulatory pathways, signalling, DNA methylation, microRNAs modulation of serotonin and dopamine….”[14].  It can be modified through psychological, developmental and environmental activities[15].

Telomeres (chromosome caps) are psychologically[16] and developmentally modifiable[17]. Their status regulates cancer cell growth by participating directly in cellular metabolism, signal transduction, and the regulation of gene expression in ways that are critical for tumorigenesis. With telomerase they help chromosome stability, homeostasis and maintenance.[18] A connection between telomeres’ length and risk of cancer is identified. Telomere length has been shown to be affected by stress, modified by therapy, and an indicator of vulnerability to cancer. The length of the telomeres is significant to cancer outcome[19]. It can affect pathways, genome instability and induce cancer changes[20]. 

This summary indicates cancers’ complexity. It requires interdisciplinary cooperative collaboration, to understand the complex interplay of factors.

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[1] Evaluating intrinsic and non-intrinsic cancer risk factors. (298Aug18) Song Wu et al. Nature Commun. 9.

Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life Years …. (30Dec21) J McCormack et al. Jama Oncology 8(3). Cancer Global cancer burden: progress, projections, and challenges. (11Oct25) Qingwei Luo et al. The Lancet 105 (10512). All cancers combined mortality statistics | Cancer Research UK.

[2] Gender and sex interactions are intrinsic components of cancer phenotypes. (19May25)J B. Rubin. Nat Rev Can 25.  Sexuality After Cancer as an Unmet Need …. (3Jun22) A Katz et al. Am Soc Clin Oncol 42.  Sexual health toxicity in cancer survivors…. (1Nov20) J Taylor et al. Int J Radiology QPO supplement 108(3)

[3] The impact of sex on the immune system …. (7May26) S Yazar et al. AJHD 113 (5).  Structural Sexism and Cancer Care…. (8May23) B P. Keenan et al. Am Soc Clin Oncol 43.  Low testosterone linked to cancer risk in men. (23Jun26) L Locke et al. Univ West Aus. Testicular Cancer Treatments and Sexuality… (31Mar24) M Raffo et al. Medicina 60(4).

[4] Acceptance and commitment therapy for psychosomatic outcomes and quality of life in adults with cancer. (Apr26) Z Kang e al. Euro J Oncol Nurs. 81. … Lifestyle medicine for people with cancer. (15Mar22) N B Ferrara. Mayo Clinic.  Living through …. cathartic methodologies, cancerous spaces …. (16De14)  C Madge. Soc Cul Geog.17(2). Influence of catharsis and cognitive therapy …lung cancer. (Jul05) P. He et al. Chin J Clinl Rehabi 9(28). 

[5] Cancer Benefits and Risks…. (10Mar26). B Piersol et al. Mem Sloan Kettering. Global and regional cancer burden attributable to modifiable risk factors …. (3Feb26) H Fink et al. Nat Med 32.  Reactive oxygen species in cancer. (25) N Ma et al. Cell Stress & Cha. Oxidative Stress: the Delicate Balance Between Health and Cancer – Williams Cancer Institute. Health inequalities in cancer care…. (Oct24) E C S Scott et al. The Lancet, Discovery 76.  Immune health is all about balance …. (20Nov23) A P Bernard) The Conversation.  Complementary Psychological and/or Physical Approaches for Cancer …. (Nov23) NCCIH Clin Dig. Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia. (6Jan21) V Rausch et al. Oncogenesis 10. A Fragile Balance… Intestinal Microbiota in the Prevention …Cancer. (jun20) D Toumazi et al. Oncology 98(9). Cancer cachexia, mechanism and treatment. (15Apr15) T Aoyagi et al. World J Gastrointest Oncol 7(4).

[6] Hypothalamic–Pituitary–Adrenal Axis Dysfunction in People With Cancer:… (2023) N G Kanter et al. Cancer Medicine 13(22).

[7] Hypothalamic–Pituitary–Adrenal Axis Dysfunction …. (21Nov24) N G Kante et al. Cancer Medicine 13(2). The neuroscience of cancer. (Jun23) R Mancusi et al.  Nature 618(7965). Pathophysiological implications of neuroinflammation mediated HPA axis …. (15Jan21) Mir Hilal et al. Molecular and Cellular Endocrinology (520). Regulation of circadian rhythms and H P A axis…. (17Sept10) P F Innominato et al. The Lancet Oncology- Reflections 11.

[8] Allostatic load and cancer risk, progression, and mortality …. (28Feb25) N Ishibe et al. Am J Epidemiology 194(6). Allostatic load and risk of all-cause, cancer-specific…. (11May23) D Yang et al. Aging Cancer 4(2). Association of Allostatic Load with All-Cause and Cancer Mortality …. (26Jun20) T Akinyemiju et al.  Cancers (Basel)12(6).

[9] Allostatic load and cancer risk, progression…. ibid. Cell competition in development, homeostasis and cancer. (29Sept22) S M van Neerven et al. Mol Cell Bio 24.  Cell competition in development, homeostasis and cancer. (29Sept22) S M van Neerven et al. Mol Cell Bio 24.  Cancer as a Homeostatic Challenge: The Role of the Hypothalamus. (21Set21). N Francis et al. Trends Neurosci. 2021 Sep 21;44(11). …Integrating homeostasis, allostasis and stress. (26Sept09) B S McEwen et al. Horm Behav. 57(2).

[10] Retrospective operationalization of allostatic load in patients with cancer…. (Sep24) E N McQuitty et al. Psychoneuroendocrinology 167.  How cancer hijacks the body’s homeostasis through the neuroendocrine system. (Apr23) M.Radomir et al. Trends in Neurosciences 46(4).  Allostatic Load in Cancer:… (3Nov23) A Mathew et al. Biol Res Nurs. 23(3). …Integrating homeostasis, allostasis and stress. (26Sept09) B S McEwen et al. Horm Behav. 57(2).

[11] Unravelling the genetics and epigenetics …cancer (8Sep25) H Easwaran et al. Nat Rev Can 25.   Mechanisms and technologies in cancer epigenetics. (1Jan25) Zaki A Sherif et al. Front Oncol.14.  Cancer …. (2024) Xinyang Yu, et al. Cell Death Discovery 10(28).

[12] Allostatic load and cancer risk, progression, and mortality in epidemiologic studies. (2025) N Ishibe et al.  m J of Epidemiology, 194(6).  Cancer as a Homeostatic Challenge: The Role of the Hypothalamus. (21Set21) N Francis et al. Trends Neurosci. 2021 Sep 21;44(11).   The role of epigenetics in cancer: From pathways to the clinic. (24Sept25) A A Almalki. J Family Med Prim Care 14(8).  Epigenetic Regulation of Development, Cellular Differentiation, and Disease Progression/Protection in Adults. (12Jun22) R J Ryznar et al. Cells11(12).

[13] What is a ‘cancer gene’…. (25Feb26 ) S Diepstraten et al. The Conversation.  Genetic landscape of cancer…. (17Aug25) A Karnwal et al. Clin Transl Oncol 28.   Tumor initiation and early tumorigenesis…. (19Jun24) S Zhang  et al. Sig Trans Tar Ther. 9 (149).    

[14] The role of epigenetics in cancer: From pathways to the clinic. (24Sept25) A A Almalki et al. J Family Med Prim Care.14(8).   

[15] How Diet Influences Gene Expression Through Epigenetic Mechanisms. (2026) V Kumar Malesu et al. News Med Lifesciences.  Restoring Epigenetic Reprogramming with Diet and Exercise to Improve Health-Related Metabolic Diseases. (7Feb23) M J Abraham et al. Biomolecules 13(2),

[16] The Telomere Effect. (2017) E Blackburn.

[17] Early Life Stress and the Onset of Obesity: Proof of MicroRNAs’ Involvement Through Modulation of Serotonin and Dopamine Systems’ Homeostasis. (28Jul2008)G A Tavares et al. Front Physiol.11.

[18] The role of telomere and telomerase in cancer and novel therapeutic target…. (14Feb25) T Baylie et al. Front. Oncol.15.

[19]  Role of telomere length in human carcinogenesis. (22May2023) A Tsatsakis et al. Int J Oncol. 63(1). TERT links telomere length to cancer risk by integrating genomic instability and immune modulation. (30Sept25) J Zhao et al. Discov Onc 16. The Effect of Cancer Treatments on Telomere Length…. (28Sept18) L Gallicchio et al. J Natl Cancer Inst 110(10). 

[20] Genetic determinants of telomere length and cancer risk. (Feb20) C P Nelson et al. Cur Opin in Genetics & Dev.  Telomere Length Dynamics and the Evolution of Cancer Genome Architecture. (6Feb18) K Cleal et al. Int J Mol Sci. 2018 Feb 6;19(2).