The Case of Cancer of the Prostate

March 15, 2023 Health & Healing No Comments

The influence of the mind on cancer needs to be treated cautiously. In both directions, one should avoid wrong impressions stemming from personal/cultural biases rather than science. Also, one should respect the present-day state of scientific knowledge. Will the yet unknown be filled by the ‘bodyless mind’ or the ‘mindless body’?

See also: Psychological impact on cancer

If you have cancer, please don’t let anything make you feel guilty. Instead of this, you can take responsibility for your well-being.

In this text, CaP = Carcinoma (cancer) of the prostate.

Some related background

CaP is one of the most frequently diagnosed cancers in males and, due to this, one with the highest cancer-related mortality in the US (30.000 yearly), Europe (85.000 yearly), and worldwide (300.000 yearly, prospected to rise to 500.000 by 2030). [34, 39, 45] Nevertheless, relatively few men with histological CaP become symptomatic and/or are diagnosed even after many years. [49]

About PSA (prostate-specific antigen): “although PSA levels are typically treated as an indicator of potential disease, the relationship between PSA and prostate cancer is in fact far from clear. … Up to 25% of men with PSA below a cut point of 4 ng/ml probably have prostate cancer. … PSA levels are known to vary considerably and are affected by a range of factors unrelated to prostatic disease such as prostate size, physical exercise, and ejaculation.” [2] Notwithstanding, a “rising level of prostate-specific antigen (PSA), after primary surgery or radiation therapy, is the hallmark of recurrent prostate cancer and is often the earliest sign of extraprostatic spread in patients who are otherwise asymptomatic. [29]

Some quotes from PubMed journal articles (= high-level medical science)

  • In a study on 4105 Swedish men, the findings “show a significant association between prostate cancer-specific mortality and perceived stress as measured by the Cohen Stress Scale in patients initially diagnosed with localized, non-metastatic prostate cancer.” [12] The ratio of influence on mortality between low and high stress in this study was 1.66.
  • Glucocorticoid hormones such as cortisol also mediate stress pathways and have been found to have a role in prostate cancer progression in ex vivo human prostate cancer cell models. [12]
  • The experiments presented above demonstrated that in 2 distinct in vivo models of prostate cancer, C42 xenografts and prostates of Hi-Myc mice, behavioral stress activated the adrenaline/ADRB2/PKA/BAD antiapoptotic signaling pathway, which in turn reduced therapeutic sensitivity and accelerated prostate cancer development. These data introduce behavioral stress as a new environmental component contributing to prostate cancer pathogenesis [5]
  • For more quotes, see below this text.

There is no mind without body or body without mind.

This puts the question in this text’s subtitle in the proper perspective. Mind=body ― no doubt or bias. Therefore, we can start with the following threesome of questions:

  • Is a significant influence of the mind on CaP possible? YES!
  • Is it probable? As we will see, this is also a yes! (No capitals, though, much is unknown.)
  • Is it scientifically proven? This is a difficult question, as science is a difficult undertaking. With this text, you may get an idea of where we are right now.

We can proceed on this note, but first, some things about the complexity of what we are dealing with.

Cancer, a complex phenomenon

Many people still think cancer is just an issue of one cell starting to behave (very) badly, proliferating into a cancerous tumor ― something like a human body that also starts with one cell.

Cancer is so complex that these people are right and wrong at the same time.

We all continually have many cells misbehaving this way. Almost all of these cells are cleared away. Much of this happens by a natural, ‘programmed’ process of attrition (called ‘apoptosis’) from within the cells themselves or through the complex working of the immune system. This is only one part of the complexity of the phenomenon ‘cancer.’ Apoptosis is vital in the causation of CaP, as well as in immunogenic, chemotherapeutic, and radiotherapeutic resistance. Some mechanisms of apoptosis may even turn the immune system into a collaborator of cancer growth. [22]

Stress, another complex phenomenon

Many people still think stress is something like a blob that can be measured on a simple scale from little stress to much stress.

More realistic is to see stress as a universe of complexity, calling not for stress management but stressional intelligence. Acute stress is, in many ways, different from chronic stress. Then there is a diverse influence of acute-upon-chronic stress. Low to moderate stress is different from high-degree stress, with even well-documented reverse antitumor effects. [5] There is consciously versus non-consciously felt stress. Most of all, there is a vast complexity in the depth of meaning of stress, also as a cause of health or disease. Intermingled with this is the influence of negative expectations and (re)appraisals on stress complications.

Also physiologically, the influence of stress is super-complex. For instance: the HPA (hypothalamic–pituitary–adrenal) axis leading to cortisol production, or changes in the adrenal medulla leading to adrenalin release. A heightened level of cortisol is not equal to distress as such. In one study, there was no influence of cortisol nor of controllable life events on PSA heightening. Still, there was an influence of both together. In addition, there was an influence of uncontrollable life events. [3]

Most interesting is how this physiology (cortisol, adrenaline…) is ‘master-minded’ by, well, the mind. In a profound way, it all starts with the latter. This also shows there may be a substantial positive influence if only we know how to.

We are not interested in the effect of stress-as-a-blob ― especially since several types of stress may cancel out each other’s effects. We are mainly interested in how to prevent diseases such as CaP, and, if possible, how to help heal them or keep them stable ― ideally, until no longer relevant. The latter is particularly interesting for CaP, and probably within our means.

Different pathways of stress → CaP

One type of stress may exert an influence through many physiological pathways toward cancer. Also, many types of stress may have the same path of influence. One type may block/enhance another type.

One of many interesting pathways is the inflammatory response implicated in many diseases – including the progression of some cancers [22] – while also having an exceedingly complex relationship with stress. Equally interesting is that stress can alter the expression of cancer-related genes in the prostates of rats. [11]

An interestingly probable mind → CaP pathway is apoptosis as mentioned above. In my view, this also leads to directions we can (therefore, direly need to) investigate how to turn this into hands-on ways for positively using the mind.

Of rats and mice (and humans, indirectly)

The little guys (male rats and mice) can be put under stressful conditions that are ethically impossible in the human case. The little ones also have prostates. Science has been done on them with clear results. So, YES, a significant influence of the mind on CaP is possible, probable, and even proven (in these cases).

This research has gone even further, elucidating some of the factual physiological pathways in mind → CaP, such as adrenaline-dependent apoptosis-related. [5] In this study, the effect was prevented by beta-2-antagonists. This may also be relevant for humans. One study “found an 18% decrease in prostate cancer incidence among users of beta-blockers.” [7]

There is also indirect evidence in humans, such as mind factors leading to higher levels of PSA. In one study, “men with ‘possible’ clinical depression at initial PSA testing (n = 519/4886) were 23% more likely to have a diagnosis of prostate cancer.” [2]

Why are there mixed results of science on mind → CaP in humans?

Several studies do not find a relation between psychosocial factors and the subsequent risk of CaP. [18, 23] We shouldn’t discard these, but try to understand the mixed results.

Theoretically, the reason for positive results may be bad science showing an influence where there is none: few subjects, confirmatory-biased or otherwise selective reporting, etc. ― pretty much pandemic in science (which doesn’t make the scientific effort less important, only more challenging to conduct and interpret). Of course, part of the ‘bad’ science isn’t so bad as it is ethically impossible to perform in better ways ― at least presently.

Mind-related factors make experimental science even more challenging (for instance, the problematic conceptualization of ‘stress’ as mentioned above). These challenges make some researchers disparagingly critical of any mind → body influence, which is a logical error. Not seeing something doesn’t mean it’s not there. A more nuanced assumption is that “much needs to be learned at the more basic biobehavioral level about the impact of stress or psychological factors on tumor biology before even considering whether large clinical trials [about psychosocial interventions] are warranted.” [42]

Otherwise put, the complexity (see above) indicates an absolute need for better science ― especially but certainly not exclusively mind-related. The present-day RCT-related science isn’t good enough to indiscriminately warrant much more of the same in this domain. Bringing too much simplicity in the field may obfuscate rather than clarify. We can and should surmount this.


It’s one thing to know about influences and another to act upon this through positive interventions ― before or after diagnosis. Nevertheless, it has been done, primarily because of conventional treatment’s many possible side effects ― including urinary incontinence and sexual dysfunction. In an extension of the Prostate Cancer Lifestyle Trial over 2 years, patients were encouraged to adopt a low-fat, plant-based diet, to exercise and practice stress management, and to attend group support sessions. The conclusion was that, with no increase in risk, “patients with early-stage prostate cancer choosing active surveillance might be able to avoid or delay conventional treatment for at least 2 years by making changes in their diet and lifestyle.” [25]

Contrary to this, there is little good news concerning psychotherapeutic interventions, as already pointed out. Also, there is discord about whether psychosocial interventions relieve distress in typical cancer patients above what can be brought non-specifically (a good talk with a good friend). [43] This should not be surprising, given the minor success of psychotherapeutic methodologies in other domains. As to psychotherapy in psychosomatics, we have barely begun scratching the surface, beneath which lies something pretty different. Meanwhile, the absence of any psychotherapeutic effect proves nothing else. The gap between what is and what is possible remains vast.


Starting from mind=body, there is a fundamental difference between AURELIS and conceptual psychotherapy. From the same start, one can envision a profound effectiveness of AURELIS even where none is seen in the field of psychotherapy. Of course, this needs to be scientifically proven.

In any case, the more complex patterns can be investigated, the clearer the causative correlations are bound to be. However, such patterns are notoriously difficult to investigate and replicate in present-day RCTs, leading to an automatic trade-off between complexity and internal consistency. This means that in such studies, we can either not see it or not properly investigate it. To be able to fully surmount this conundrum, A.I. tools are necessary.

A dream tool is video coach-bot Lisa. As a pattern recognizer, Lisa will be able to discern in the above-mentioned complexity any existing influence as well as how to make this a positive one. This has two lines of advantages:

  • Lisa will be able to help many people directly through her coaching.
  • Lisa-science will clarify these patterns so that people can take care of them outside of any coaching.

Altogether, I dare predict this will also have a clear consequence on the scientific field of mind → CaP (and many other health issues).

Wanted, dead or alive: Lisa and Lisa-science.

More quotes from PubMed journal articles

  • We are at the very beginning of understanding complex stress-cancer interactions, with multifaceted responses to stress that affect cancer cells, tumor microenvironment, and the organism overall. There is a vast body of literature on psychological disorders experienced by cancer patients (54), and yet very little is known about the changes in the ‘endocrinome’ of cancer patients caused by behavioral stress. [5]
  • These results [in mice] demonstrate interactions between prostate tumors and the psychosocial environment mediated by activation of an adrenaline/ADRB2/ PKA/BAD antiapoptotic signaling pathway.” [5]
  • Considering that prostate cancer diagnosis increases stress and anxiety levels, activation of a stress-induced antiapoptotic pathway may lead to a vicious cycle of stress and cancer progression. [5]
  • While this study cannot prescribe specific interventions, it does affirm previous studies’ recommendations [concerning mind → CaP] to target improvements in QoL. [12]
  • To date, preclinical studies have gradually uncovered the promotive effects of psychological distress on tumor hallmarks. In contrast, eustress may exert suppressive effects on tumorigenesis and beneficial effects on tumor treatment, which brings a practicable means and psychosocial perspective to cancer treatment. However, the underlying mechanisms remain incompletely understood. [8]
  • … complex interaction between social and psychological factors, and related biobehavioral processes (see Figure 1). Previous evidence of the independent effect of these factors on prostate cancer risk factors points to the crucial need to comprehensively examine how these factors may interactively impact prostate cancer risk. For instance, while findings on the association between SES and prostate cancer incidence were mixed, psychological factors may help in part to explain how this relationship varies by race. [6]
  • Perceived stress variables were associated with increased risk of prostate cancer among non-Hispanic white men, but not among non-Hispanic black men. … The reasons underlying this difference by racial/ethnic group are unclear. [17]
  • A recent meta-analysis of over 150 studies found that psychosocial factors are reliably
  • predictive of cancer prognosis, not cancer-onset, independent of initial tumor stage and other confounders. [3]
  • These results are consistent with the generalized conclusion from multiple studies which have shown that stress does not affect cancer incidence but contributes to increased mortality from already established cancers. [7]
  • These findings in animal models led us to propose that more attention should be given to analysis of interactions among stress, activation of the hypothalamic–pituitary–adrenal axis and ADRB2 signaling in prostate cancer progression in men. In fact, in 20% of prostate cancer patients, we observed increases of epinephrine over 1 nmol l-1, a concentration that has been sufficient to activate the anti-apoptotic signaling pathway in tissue culture and in mouse prostates. [7]
  • To our knowledge, this is the first semi-prospective case-control study to investigate whether harmony-seeking personality is related to the occurrence of prostate cancer. Type 1 personality, classified by the SIRI33, was significantly associated with the presence of prostate cancer. [1]
  • [In patients with metastatic hormone-refractory prostate cancer,] “those with better baseline Health-Related Quality of Life (HRQL) have better predicted survival, time to disease progression and pain prognosis than those with worse HRQL.” [39] ― note: Here, causation can run both ways.
  • Our findings suggest that the intervention we employed [a plant-based diet, in combination with stress reduction] may have resulted in a slowing of disease progression and, in a few patients, possibly disease reversal. … contribute to a growing literature that suggests that in at least some circumstances, cancer may be partly reversible… Over the course of the 6-month intervention, there was a significant decrease in the rate of PSA rise from the prestudy period. Four of 10 patients experienced an absolute reduction in their PSA levels, suggesting the possibility of at least some degree of disease remission. … increase in median PSA doubling time, … from 11.9 months (prestudy) to 112.3 months (intervention) [29]
  • In summary, this study [of 318 men participating in a prostate-specific antigen (PSA) screening program] provides support for the possibility that both perceived stress and social support are factors in prostate disease. Longitudinal studies of these and other psychosocial factors are necessary to confirm the findings, and studies with disease outcomes will offer the best evidence of the associations. [37]
  • Only a small portion of the men diagnosed with prostate cancer will die of the disease, even when diagnosed with high-risk prostate cancer. … Given the long natural history of prostate cancer and evidence that a diagnosis of prostate cancer or high-risk prostate cancer is not often predictive of death from prostate cancer because of competing causes of mortality,2 the evaluation of death from prostate cancer and death from all causes is particularly pertinent. [26]
  • Over 90% of all deaths from cancer are not due to the primary tumor, which often can be successfully treated, but are due to the metastases. [28]
  • After radical prostatectomy or radiation therapy, unfortunately, about 35% of patients will undergo a recurrence of the disease within 10 years of primary treatment. … About a third of those will develop radiological or pathological evidence of metastatic spread to bone or visceral organs within the first 5 years of detection of the recurrence. [29]
  • [In a small group of 30 participants:] Pathway analysis identified significant modulation of biological processes that have critical roles in tumorigenesis, including protein metabolism and modification, intracellular protein traffic, and protein phosphorylation (all P < 0.05). Intensive nutrition and lifestyle changes [including stress management techniques] may modulate gene expression in the prostate. Understanding the prostate molecular response to comprehensive lifestyle changes may strengthen efforts to develop effective prevention and treatment. [30]
  • If an agent can slow the growth of existing cancer cells, it remains plausible that they may be effective as an adjunct to surgery, radiation, or chemotherapy. … Second, the timelines along the ontogeny of these cancers is so long (decades) that an agent with the capacity to slow this process would be of tremendous benefit. [24]


These are the relevant articles read for this text, of which not all have been referenced within the text itself:

1: Kumano H, Haseme E, Fujimoto H, Matsuoka N, Yoshiuchi K, Uchitomi Y, Akechi T, Nakano T, Kobayashi M, Agari I, Kuboki T. Harmony seeking and the risk of prostate cancer: a prebioptic study. J Psychosom Res. 2005 Sep;59(3):167-74. doi: 10.1016/j.jpsychores.2005.04.006. PMID: 16198190.

2: Turner EL, Lane JA, Metcalfe C, Down L, Donovan JL, Hamdy F, Neal D, Vedhara K. Psychological distress and prostate specific antigen levels in men with and without prostate cancer. Brain Behav Immun. 2009 Nov;23(8):1073-8. doi: 10.1016/j.bbi.2009.01.009. Epub 2009 Jan 22. PMID: 19486654.

3: Gidron Y, Fabre B, Grosman H, Nolazco C, Mesch V, Mazza O, Berg G. Life events, cortisol and levels of prostate specific antigen: a story of synergism. Psychoneuroendocrinology. 2011 Jul;36(6):874-80. doi: 10.1016/j.psyneuen.2010.11.011. Epub 2010 Dec 30. PMID: 21194845.

4: Woods-Burnham L, Stiel L, Martinez SR, Sanchez-Hernandez ES, Ruckle HC, Almaguel FG, Stern MC, Roberts LR, Williams DR, Montgomery S, Casiano CA. Psychosocial Stress, Glucocorticoid Signaling, and Prostate Cancer Health Disparities in African American Men. Cancer Health Disparities. 2020;4: PMID: 35252767; PMCID: PMC8896511.

5: Hassan S, Karpova Y, Baiz D, Yancey D, Pullikuth A, Flores A, Register T, Cline JM, D’Agostino R Jr, Danial N, Datta SR, Kulik G. Behavioral stress accelerates prostate cancer development in mice. J Clin Invest. 2013 Feb;123(2):874-86. doi: 10.1172/JCI63324. Epub 2013 Jan 25. PMID: 23348742; PMCID: PMC3561807.

6: Cuevas AG, Trudel-Fitzgerald C, Cofie L, Zaitsu M, Allen J, Williams DR. Placing prostate cancer disparities within a psychosocial context: challenges and opportunities for future research. Cancer Causes Control. 2019 May;30(5):443-456. doi: 10.1007/s10552-019-01159-1. Epub 2019 Mar 22. PMID: 30903484; PMCID: PMC6484832.

7: Kulik G. Targeting psychoemotional stress to treat prostate cancer. Asian J Androl. 2013 May;15(3):362-3. doi: 10.1038/aja.2013.30. Epub 2013 Apr 15. PMID: 23584381; PMCID: PMC3739661.

8: Wu Y, Zhou L, Zhang X, Yang X, Niedermann G, Xue J. Psychological distress and eustress in cancer and cancer treatment: Advances and perspectives. Sci Adv. 2022 Nov 25;8(47):eabq7982. doi: 10.1126/sciadv.abq7982. Epub 2022 Nov 23. PMID: 36417542; PMCID: PMC9683699.

9: Nagaraja AS, Armaiz-Pena GN, Lutgendorf SK, Sood AK. Why stress is BAD for cancer patients. J Clin Invest. 2013 Feb;123(2):558-60. doi: 10.1172/JCI67887. Epub 2013 Jan 25. PMID: 23348736; PMCID: PMC3561841.

10: Mohan A, Huybrechts I, Michels N. Psychosocial stress and cancer risk: a narrative review. Eur J Cancer Prev. 2022 Nov 1;31(6):585-599. doi: 10.1097/CEJ.0000000000000752. Epub 2022 Mar 29. PMID: 35352705.

11: Flores IE, Sierra-Fonseca JA, Davalos O, Saenz LA, Castellanos MM, Zavala JK, Gosselink KL. Stress alters the expression of cancer-related genes in the prostate. BMC Cancer. 2017 Sep 5;17(1):621. doi: 10.1186/s12885-017-3635-4. PMID: 28874141; PMCID: PMC5583991.

12: Jan M, Bonn SE, Sjölander A, Wiklund F, Stattin P, Holmberg E, Grönberg H, Bälter K. The roles of stress and social support in prostate cancer mortality. Scand J Urol. 2016;50(1):47-55. doi: 10.3109/21681805.2015.1079796. Epub 2015 Sep 7. PMID: 26343525.

13: Sharpley CF, Christie DRH, Bitsika V, Agnew LL, Andronicos NM, McMillan ME, Richards TM. Neurobiological and psychological evidence of chronic stress in prostate cancer patients. Eur J Cancer Care (Engl). 2017 Nov;26(6). doi: 10.1111/ecc.12671. Epub 2017 Mar 2. PMID: 28252237.

14: Coker AL, Sanderson M, Ellison GL, Fadden MK. Stress, coping, social support, and prostate cancer risk among older African American and Caucasian men. Ethn Dis. 2006 Autumn;16(4):978-87. PMID: 17061756.

15: Watts S, Leydon G, Birch B, Prescott P, Lai L, Eardley S, Lewith G. Depression and anxiety in prostate cancer: a systematic review and meta-analysis of prevalence rates. BMJ Open. 2014 Mar 13;4(3):e003901. doi: 10.1136/bmjopen-2013-003901. PMID: 24625637; PMCID: PMC3963074.

16: Ellison GL, Coker AL, Hebert JR, Sanderson SM, Royal CD, Weinrich SP. Psychosocial stress and prostate cancer: a theoretical model. Ethn Dis. 2001 Autumn;11(3):484-95. PMID: 11572415.

17: Kantor ED, Haneuse S, Valdimarsdóttir UA, Williams DR, Signorello LB, Rider JR. Socioenvironmental adversity and risk of prostate cancer in non-Hispanic black and white men. Cancer Causes Control. 2019 Sep;30(9):997-1007. doi: 10.1007/s10552-019-01196-w. Epub 2019 Jul 1. PMID: 31264140; PMCID: PMC6744283.

18: Heikkilä K, Nyberg ST, Theorell T, Fransson EI, Alfredsson L, Bjorner JB, Bonenfant S, Borritz M, Bouillon K, Burr H, Dragano N, Geuskens GA, Goldberg M, Hamer M, Hooftman WE, Houtman IL, Joensuu M, Knutsson A, Koskenvuo M, Koskinen A, Kouvonen A, Madsen IE, Magnusson Hanson LL, Marmot MG, Nielsen ML, Nordin M, Oksanen T, Pentti J, Salo P, Rugulies R, Steptoe A, Suominen S, Vahtera J, Virtanen M, Väänänen A, Westerholm P, Westerlund H, Zins M, Ferrie JE, Singh-Manoux A, Batty GD, Kivimäki M; IPD-Work Consortium. Work stress and risk of cancer: meta-analysis of 5700 incident cancer events in 116,000 European men and women. BMJ. 2013 Feb 7;346:f165. doi: 10.1136/bmj.f165. PMID: 23393080; PMCID: PMC3567204.

19: Metcalfe C, Davey Smith G, Macleod J, Hart C. The role of self-reported stress in the development of breast cancer and prostate cancer: a prospective cohort study of employed males and females with 30 years of follow-up. Eur J Cancer. 2007 Apr;43(6):1060-5. doi: 10.1016/j.ejca.2007.01.027. Epub 2007 Mar 1. PMID: 17336053.

20: Cohen L, Fouladi RT, Babaian RJ, Bhadkamkar VA, Par ker PA, Taylor CC, Smith MA, Gritz ER, Basen-Engquist K. Cancer worry is associated with abnormal prostate-specific antigen levels in men participating in a community screening program. Cancer Epidemiol Biomarkers Prev. 2003 Jul;12(7):610-7. PMID: 12869399.

21: Antoni MH, Lutgendorf SK, Cole SW, Dhabhar FS, Sephton SE, McDonald PG, Stefanek M, Sood AK. The influence of bio-behavioural factors on tumour biology: pathways and mechanisms. Nat Rev Cancer. 2006 Mar;6(3):240-8. doi: 10.1038/nrc1820. PMID: 16498446; PMCID: PMC3146042.

22: McKenzie S, Kyprianou N. Apoptosis evasion: the role of survival pathways in prostate cancer progression and therapeutic resistance. J Cell Biochem. 2006 Jan 1;97(1):18-32. doi: 10.1002/jcb.20634. PMID: 16216007; PMCID: PMC2274918.

23: Nielsen NR, Kristensen TS, Zhang ZF, Strandberg-Larsen K, Schnohr P, Grønbaek M. Sociodemographic status, stress, and risk of prostate cancer. A prospective cohort study. Ann Epidemiol. 2007 Jul;17(7):498-502. doi: 10.1016/j.annepidem.2007.02.001. Epub 2007 Apr 19. PMID: 17448677.

24: Fleshner N, Zlotta AR. Prostate cancer prevention: past, present, and future. Cancer. 2007 Nov 1;110(9):1889-99. doi: 10.1002/cncr.23009. PMID: 17893870.

25: Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008 Dec;72(6):1319-23. doi: 10.1016/j.urology.2008.04.050. Epub 2008 Jul 7. PMID: 18602144.

26: Tang P, Sun L, Uhlman MA, Polascik TJ, Freedland SJ, Moul JW. Baseline PSA as a predictor of prostate cancer-specific mortality over the past 2 decades: Duke University experience. Cancer. 2010 Oct 15;116(20):4711-7. doi: 10.1002/cncr.25447. PMID: 20589748.

27: Grytli HH, Fagerland MW, Fosså SD, Taskén KA, Håheim LL. Use of β-blockers is associated with prostate cancer-specific survival in prostate cancer patients on androgen deprivation therapy. Prostate. 2013 Feb 15;73(3):250-60. doi: 10.1002/pros.22564. Epub 2012 Jul 20. PMID: 22821802.

28: Palm D, Lang K, Niggemann B, Drell TL 4th, Masur K, Zaenker KS, Entschladen F. The norepinephrine-driven metastasis development of PC-3 human prostate cancer cells in BALB/c nude mice is inhibited by beta-blockers. Int J Cancer. 2006 Jun 1;118(11):2744-9. doi: 10.1002/ijc.21723. PMID: 16381019.

29: Saxe GA, Major JM, Nguyen JY, Freeman KM, Downs TM, Salem CE. Potential attenuation of disease progression in recurrent prostate cancer with plant-based diet and stress reduction. Integr Cancer Ther. 2006 Sep;5(3):206-13. doi: 10.1177/1534735406292042. PMID: 16880425.

30: Ornish D, Magbanua MJ, Weidner G, Weinberg V, Kemp C, Green C, Mattie MD, Marlin R, Simko J, Shinohara K, Haqq CM, Carroll PR. Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A. 2008 Jun 17;105(24):8369-74. doi: 10.1073/pnas.0803080105. Epub 2008 Jun 16. PMID: 18559852; PMCID: PMC2430265.

31: Miller HC. Stress prostatitis. Urology. 1988 Dec;32(6):507-10. doi: 10.1016/s0090-4295(98)90030-9. PMID: 3201657.

32: Sastry KS, Karpova Y, Prokopovich S, Smith AJ, Essau B, Gersappe A, Carson JP, Weber MJ, Register TC, Chen YQ, Penn RB, Kulik G. Epinephrine protects cancer cells from apoptosis via activation of cAMP-dependent protein kinase and BAD phosphorylation. J Biol Chem. 2007 May 11;282(19):14094-100. doi: 10.1074/jbc.M611370200. Epub 2007 Mar 12. PMID: 17353197.

33: Ben-Eliyahu S, Page GG, Schleifer SJ. Stress, NK cells, and cancer: Still a promissory note. Brain Behav Immun. 2007 Oct;21(7):881-7. doi: 10.1016/j.bbi.2007.06.008. Epub 2007 Jul 26. PMID: 17662574.

34: Center               Jemal A, Lortet-Tieulent J, Ward E, Ferlay J, Brawley O, Bray F. International variation in prostate cancer incidence and mortality rates. Eur Urol. 2012 Jun;61(6):1079-92. doi: 10.1016/j.eururo.2012.02.054. Epub 2012 Mar 8. PMID: 22424666.

35: Braun DP, Gupta D, Staren ED. Predicting survival in prostate cancer: the role of quality of life assessment. Support Care Cancer. 2012 Jun;20(6):1267-74. doi: 10.1007/s00520-011-1213-x. Epub 2011 Jun 28. PMID: 21710307; PMCID: PMC3342489.

36: Lis CG, Gupta D, Grutsch JF. Patient satisfaction with health-related quality of life: implications for prognosis in prostate cancer. Clin Genitourin Cancer. 2008 Sep;6(2):91-6. doi: 10.3816/CGC.2008.n.014. PMID: 18824431.

37: Stone AA, Mezzacappa ES, Donatone BA, Gonder M. Psychosocial stress and social support are associated with prostate-specific antigen levels in men: results from a community screening program. Health Psychol. 1999 Sep;18(5):482-6. doi: 10.1037//0278-6133.18.5.482. PMID: 10519464.

38: Collette L, van Andel G, Bottomley A, Oosterhof GO, Albrecht W, de Reijke TM, Fossà SD. Is baseline quality of life useful for predicting survival with hormone-refractory prostate cancer? A pooled analysis of three studies of the European Organisation for Research and Treatment of Cancer Genitourinary Group. J Clin Oncol. 2004 Oct 1;22(19):3877-85. doi: 10.1200/JCO.2004.07.089. PMID: 15459209.

39: Sullivan PW, Nelson JB, Mulani PM, Sleep D. Quality of life as a potential predictor for morbidity and mortality in patients with metastatic hormone-refractory prostate cancer. Qual Life Res. 2006 Oct;15(8):1297-306. doi: 10.1007/s11136-006-0003-2. Epub 2006 Aug 10. PMID: 16830258.

40: Zhao XY, Malloy PJ, Krishnan AV, Swami S, Navone NM, Peehl DM, Feldman D. Glucocorticoids can promote androgen-independent growth of prostate cancer cells through a mutated androgen receptor. Nat Med. 2000 Jun;6(6):703-6. doi: 10.1038/76287. Erratum in: Nat Med 2000 Aug;6(8):939. PMID: 10835690.

41: Boesen EH, Johansen C. Impact of psychotherapy on cancer survival: time to move on? Curr Opin Oncol. 2008 Jul;20(4):372-7. doi: 10.1097/CCO.0b013e3283021690. PMID: 18525330.

42: Stefanek ME, Palmer SC, Thombs BD, Coyne JC. Finding what is not there: unwarranted claims of an effect of psychosocial intervention on recurrence and survival. Cancer. 2009 Dec 15;115(24):5612-6. doi: 10.1002/cncr.24671. PMID: 19834959.

43: Coyne JC, Lepore SJ, Palmer SC. Efficacy of psychosocial interventions in cancer care: evidence is weaker than it first looks. Ann Behav Med. 2006 Oct;32(2):104-10. doi: 10.1207/s15324796abm3202_5. PMID: 16972805.

44: Coyne JC, Hanisch LJ, Palmer SC. Psychotherapy does not promote survival (Kissane et al., 2007): now what? Psychooncology. 2007 Nov;16(11):1050-2. doi: 10.1002/pon.1285. PMID: 17937383.

45: Tao ZQ, Shi AM, Wang KX, Zhang WD. Epidemiology of prostate cancer: current status. Eur Rev Med Pharmacol Sci. 2015;19(5):805-12. PMID: 25807434.

46: Garssen B. Psychological factors and cancer development: evidence after 30 years of research. Clin Psychol Rev. 2004 Jul;24(3):315-38. doi: 10.1016/j.cpr.2004.01.002. PMID: 15245834.

47: Chida Y, Hamer M, Wardle J, Steptoe A. Do stress-related psychosocial factors contribute to cancer incidence and survival? Nat Clin Pract Oncol. 2008 Aug;5(8):466-75. doi: 10.1038/ncponc1134. Epub 2008 May 20. PMID: 18493231.

48: Denaro N, Tomasello L and Russi EG. Cancer and stress: what’s matter? from epidemiology: the psychologist and oncologist point of view. J Cancer Ther Res. 2014; 3:6.

49: Stamatiou K, Alevizos A, Agapitos E, Sofras F. Incidence of impalpable carcinoma of the prostate and of non-malignant and precarcinomatous lesions in Greek male population: an autopsy study. Prostate. 2006 Sep 1;66(12):1319-28. doi: 10.1002/pros.20339. PMID: 16688747.

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