There is no firm evidence that stressors play a role in the development of cancer, but there is some evidence that it can facilitate the progression of the already existing disease.
Recent studies indicate that stress could facilitate growth of some cancers and even the development of metastases. These are mainly studies on animals which have also made it possible to identify various endocrine, cellular and molecular mechanisms that could be at the basis of these processes. The point was made by a recent review by Anabel Eckerling and her collaborators at Tel Aviv University’s Sagol School of Neuroscience and School of Psychological Sciences, and published in the journal Nature. Animal models have shown that stressors can favor many characteristic features of cancer, the review authors say. Furthermore the stress response can facilitate cancer growth and metastasis through a direct action on the molecular characteristics of the malignant tissue, on its microenvironment, on the antitumor immune activity and on other indirect modulators of cancer progression. On the other hand, if we move from the level of animal research to clinical research on humans, both epidemiological studies and clinical trials have generated somewhat uncertain results, indicating only a possible small effect, not necessarily significant, stress on cancer progression. As a result, current medical routines do not include measures designed to prevent stress responses as a means of improving cancer survival. Within the medical community this attitude seems to reflect a certain skepticism that stress is a significant biological factor in causing cancer and its progression.
The mechanisms
But what are the mechanisms by which stress could induce the development or growth of some forms of cancer? Regarding the initial transformation of normal tissue into cancer, the stress involved, for example, for the induction of a lower effectiveness of natural cellular repair processes. Furthermore, stress can reduce the body’s resistance to some types of viruses, called oncogenes, which are now known to be significantly involved in the initiation of about 15 percent of cancer cases. The human papillomavirus, the Epstein – Barr virus, the Kaposi herpesvirus associated with sarcoma and the hepatitis C and B viruses can be reactivated by both catecholamines and glucocorticoids, typical stress hormones. As for the rate of progression of a cancer that is already present, it is now accepted that catecholamines are able to promote the proliferation of cancer cells, their survival and migration to other tissues. In particular, the action of some social stressors has been studied in this sense, such as conflict with other people and loneliness. High circulating levels of norepinephrine (a catecholamine) can also stimulate the growth of the tumor innervation, which in turn can deliver more norepinephrine, in a dangerous vicious circle. Likewise, catecholamines can facilitate the development of blood vessels within the cancer, a decisive factor for its further growth. A phenomenon observed for example in ovarian, breast, pancreatic and colorectal cancer.
Stimulus to inflammatory processes
Another mechanism by which stress promotes cancer progression the stimulus to inflammatory processes and the inhibition of some fundamental joints of the immune system. Another area of research that he is trying to grasp any correlations between stress and cancer that of studies on large populations. The effect of stress on patient survival was studied, as well as stress dependent on individual factors, such as depression, isolation, lack of social support, and that dependent on factors not directly related to the individual, such as wars and climate change. Considering the discordant or small-scale effects that emerged from observational studies, and bearing in mind the heterogeneity of the research methodologies, the populations studied and the type of stressor considered, it remains uncertain whether stress can increase the incidence of cancer and to what extent it can really facilitate its progression say the review authors about the results from the epidemiological studies. Finally, the review authors also looked at clinical studies that evaluated the possible effect of psychosocial or psychopharmacological interventions on cancer progression, for example the use of anxiolytics and antidepressants. Also in this case it was not possible to draw definitive conclusions, due to the methodological difficulties associated with this type of investigation.
Results
In conclusion? Although the evidence that stress promotes cancer initiation is inconsistent, instead, there is strong evidence that stress can facilitate cancer progression through a modulation of several of its characteristic constitutive elements – say the authors of the review -. Molecular and systemic mechanisms that mediate these effects have been identified in animal studies and many of them have also been recognized in cancer patients. And what about the opportunity to start support programs for stress reduction in cancer patientsAnabel Eckerling and her collaborators state that stress management interventions should be tested in critical periods affecting cancer progression, especially in the short post-operative period and adjuvant treatments, by making comparisons with other periods and accompanying them with pharmacological interventions aimed at counteracting stress and inflammatory responses inevitably triggered by medical procedures. More multicenter experimental studies will be needed to evaluate the effects of long-distance treatments.
May 22, 2022 (change May 22, 2022 | 18:21)
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