Cytomegalovirus and Bladder Cancer: Can We Trust the Data?

CAUSATION 🌍 International Journal of Science Impressum: Causation International Journal Of Science Chief-Editor / V. i. S. d. P.: Ilija Barukˇ ci´ c Hegelitzer Str. 22 DE-26409 Wittmund-Ardorf (Germany) ©Editorial Team: Editorial Team mWebsite: www.causation.eu kE-Mail: [email protected] TPhone: +(49) 4466 - 333 Year: 2026; Volume: 23; Issue: 2; pp. 5–21. BReceived: November 30, 2025 VAccepted: November 30, 2025 ¥Published: November 30, 2025 iDeutsche Nationalbibliothek Frankfurt YISSN: 1863-9542 DOI:10.5281/zenodo.17770705 !Find in: Zenodo Orcid Academia ... Cytomegalovirus and Bladder Cancer: Can We Trust the Data? Research article Ilija Barukˇ ci´ c1 1Internist, Horandstrasse, 26441 Jever, Germany *Correspondence: E-Mail: [email protected]; Tel: +49-4466-333; Fax: +49-4466-333. 6 Abstract Background: The relationship between cytomegalovirus (CMV) infection and bladder cancer pathogenesis remains incompletely characterized. This re-analysis investigates the potential necessary condition relationship between CMV seropositivity and bladder cancer carcinogenesis. Material and methods: We performed a secondary analysis of a subset of data originally published by Geris et al. Advanced statistical methods were applied, with a specific focus on testing the necessary condition hypothesis. The analysis centered on the relationship between CMV IgG serostatus and subsequent bladder cancer diagnosis in a large transplant cohort. Results: Our re-analysis demonstrates that CMV IgG seropositivity appears to be a necessary condition for bladder cancer development. The statistical evidence supporting this conclusion is exceptionally strong (p=1.10 ×10−58), indicating an absence of bladder cancer cases among individuals without CMV exposure, as determined by serum CMV IgG serology. Conclusion: These findings suggest that CMV infection may play a fundamental etiological role in bladder cancer pathogenesis. The consistent absence of bladder cancer in CMV-seronegative individuals provides strong evidence that CMV seropositivity acts as a necessary condition in the causal pathway of bladder carcinogenesis. This compelling relationship warrants further systematic investigation to elucidate the underlying biological mechanisms. Keywords: Cause; Effect; Causal relationship k; Causality; Causation ©Reviewer 1: None/Author. §Reviewer 2: None. §Reviewer 3: None. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 7 1. Introduction Bladder cancer represents a significant global health issue, ranking as the tenth most commonly diagnosed cancer worldwide. The disease demonstrates a strong male predominance, with men being approximately four times more likely to develop bladder cancer than women. Incidence rates 1are generally higher in developed nations, and age serves as a major risk factor, with the majority of cases diagnosed in individuals over 65 years old. Aetiology and Risk Factors The primary cause of bladder cancer is still unknown. Various risk factors 2,3like chronic exposure to carcinogens that undergo renal excretion and subsequent storage in urine are discussed in literature. Tobacco smoking constitutes the single most important risk factor, accounting for approximately 50% of all cases. Occupational exposure to aromatic amines and polycyclic aromatic hydrocarbons–prevalent in the dye, rubber, and paint industries–represents another well-established causative factor. Additional risk factors include chronic urinary tract infections, schistosomiasis (a leading cause of squamous cell carcinoma in endemic regions), prior pelvic radiation, and specific chemotherapeutic agents such as cyclophosphamide. Clinical Presentation The hallmark symptom of bladder cancer is gross or microscopic haematuria, typically painless in nature. Irritative voiding symptoms, including urinary frequency, urgency, and dysuria, may also manifest, particularly in carcinoma in situ (CIS). Advanced disease can present with flank pain secondary to ureteral obstruction or symptoms related to metastatic spread (e.g., bone pain). Diagnostic Work-up •Clinical History & Physical Examination: Focus on risk factors, haematuria, and voiding symptoms •Urine Tests: Urinalysis (detection of haematuria); Cytology (high specificity for high-grade lesions, limited sensitivity) 1Jubber I, Ong S, Bukavina L, Black PC, Comp´ erat E, Kamat AM, Kiemeney L, Lawrentschuk N, Lerner SP, Meeks JJ, Moch H, Necchi A, Panebianco V, Sridhar SS, Znaor A, Catto JWF, Cumberbatch MG. Epidemiology of Bladder Cancer in 2023: A Systematic Review of Risk Factors. Eur Urol. 2023 Aug;84(2):176-190. doi: 10.1016/j.eururo.2023.03.029. Epub 2023 May 16. PMID: 37198015. 2Jankovi´ c S, Radosavljevi´ c V. Risk factors for bladder cancer. Tumori. 2007 Jan-Feb;93(1):4-12. doi: 10.1177/030089160709300102. PMID: 17455864. 3Alouini S. Risk Factors Associated with Urothelial Bladder Cancer. Int J Environ Res Public Health. 2024 Jul 22;21(7):954. doi: 10.3390/ijerph21070954. PMID: 39063530; PMCID: PMC11277468. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 8 •Imaging: CT Urography (gold standard for upper tract evaluation and staging); Ultrasound (assessment of hydronephrosis and renal masses) •Primary Diagnostic Procedure: Cystoscopy (direct tumor visualization) followed by Transurethral Resection of Bladder Tumor (TURBT). TURBT serves dual purposes: diagnostic confirmation (histology, grading, muscle invasion assessment) and therapeutic intervention for non-muscle-invasive disease Therapy Treatment strategies 4of bladder cancer are fundamentally determined by disease staging from TURBT, primarily distinguishing non-muscle-invasive (NMIBC) from muscle-invasive (MIBC) disease. Non-Muscle-Invasive Bladder Cancer (NMIBC) •Initial Treatment: Complete TURBT •Risk-Adapted Adjuvant Therapy: Single post-TURBT instillation of intravesical chemotherapy for low-risk tumors. For intermediate and high-risk tumors, including CIS, induction and maintenance courses of Bacillus Calmette-Gu´ erin (BCG) immunotherapy represent the standard of care to reduce recurrence and progression rates •High-Risk Unresponsive Disease: Radical cystectomy is recommended for BCG-unresponsive high-risk NMIBC, with intravesical chemotherapy serving as an alternative option Muscle-Invasive Bladder Cancer (MIBC) •Standard Curative Approach: Radical Cystectomy with pelvic lymph node dissection, preceded by neoadjuvant cisplatin-based combination chemotherapy in eligible patients to enhance overall survival •Bladder Preservation: For carefully selected, motivated patients with solitary tumors, Trimodality Therapy (TMT) presents a viable option, involving thorough TURBT followed by concurrent radiosensitizing chemotherapy and external beam radiotherapy •Metastatic Disease: Treatment is primarily systemic. First-line therapy consists of cisplatinbased chemotherapy. For cisplatin-ineligible patients, immunotherapy with checkpoint inhibitors 4Flaig TW, Spiess PE, Abern M, Agarwal N, Bangs R, Buyyounouski MK, Chan K, Chang SS, Chang P, Friedlander T, Greenberg RE, Guru KA, Herr HW, Hoffman-Censits J, Kaimakliotis H, Kishan AU, Kundu S, Lele SM, Mamtani R, Mian OY, Michalski J, Montgomery JS, Parikh M, Patterson A, Peyton C, Plimack ER, Preston MA, Richards K, Sexton WJ, Siefker-Radtke AO, Stewart T, Sundi D, Tollefson M, Tward J, Wright JL, Cassara CJ, Gurski LA. NCCN Guidelines®Insights: Bladder Cancer, Version 3.2024. J Natl Compr Canc Netw. 2024 May;22(4):216-225. doi: 10.6004/jnccn.2024.0024. PMID: 38754471. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 9 (e.g., pembrolizumab) represents a key alternative. Second-line and subsequent therapies include immunotherapy, targeted agents (e.g., Erdafitinib for FGFR-altered tumors), and antibody-drug conjugates (e.g., enfortumab vedotin) Theoretically, the risk for urological malignancies may be related to exposure to infectious agents5, including cytomegalovirus. In this investigation, we aim to further examine the relationship between cytomegalovirus and bladder cancer. Cytomegalovirus history The history (Riley Jr,1997) of human cytomegalovirus (CMV) with corresponding back and forth is quite turbulent. Moritz Wilhelm Hugo Ribbert (1855-1920) was the first to document large inclusionbearing cells in the kidneys of an infant (Ribbert,1904). It didn’t take long and Goodpasture and Talbert suggested in 1921 that the ‘cytomegalia’could be due to a viral agent (Goodpasture and Talbot,1921). In 1950, Smith and Vellios showed that a ‘cytomegalia’infection may occur even in utero (Smith and Vellios,1950). Finally, with considerable effort, Smith (Smith,1956) in 1956, Rowe and coworkers (Wallace et al.,1956) in 1956, and Weller et al (Weller et al.,1957) in 1957 independently of each other succeeded in isolating human ‘cytomegalia’strains. In the end, in 1960, Weller and coworkers (Weller et al.,1960) coined the term ‘cytomegalovirus’. Human cytomegalovirus or human (Lefkowitz et al.,2018) herpesvirus-5 (HHV-5), is a doublestranded deoxyribonucleic (Watson and Crick,1953) acid (DNA) virus consisting of two unique regions and a member of the viral family known as herpesviruses or herpesviridae. The highly complex eukaryotic CMV(see Razonable et al.,2002) with its intrinsic ability to induce cell enlargement, or cytomegalia, encodes approximately for 200 genes (Bankier et al.,1991) and is the largest (Dioverti and Razonable,2016) of the herpesviruses. Meanwhile, the complete genetic content of various viruses like Epstein-Barr (Baer et al.,1984) virus (EBV), varicella zoster (Davison and Scott,1986) virus (VZV), the herpes simplex (McGeoch et al.,1988) virus type 1 (HSV-1) and of other (Johnson et al., 1991) viruses has been determined. In point of fact, scientist succeeded in sequencing (Chee et al., 1990) CMV too. CMV infects more than 60% of adults (Cannon et al.,2010) with an increase in the population’s seroprevalence (Staras et al.,2006,2008;Bate et al.,2010;Lachmann et al.,2018) with increasing age (Gupta and Shorman,2017). In fact, children 6-11-year-old are 36.3% CMV positive. As known, CMV seroprevalence (Zuhair et al.,2019) is increasing gradually with age and can be found in those aged >=80 years in more than 90.8% of cases (Staras et al.,2006). CMV infection results from a primary CMV infection in previously CMV uninfected individuals or from reactivation of latent CMV acquired in early life. CMV PCR or CMV pp65 antigen testing of blood are of help to identify CMV replication or (systemic or site-specific) CMV viral load. After recovery of a primary CMV infection, CMV remains dormant within the myeloid cells of the host over long periods with more or less a frequent viral reactivation. Nonetheless, a CMV infection(Chen et al.,2019) with clinical 5Gazzaniga P, Vercillo R, Gradilone A, Silvestri I, Gandini O, Napolitano M, Giuliani L, Fioravanti A, Gallucci M, Aglian` o AM. Prevalence of papillomavirus, Epstein-Barr virus, cytomegalovirus, and herpes simplex virus type 2 in urinary bladder cancer. J Med Virol. 1998 Aug;55(4):262-7. doi: 10.1002/(sici)1096-9071(199808)55:4¡262::aid-jmv2¿3.0.co;2-z. PMID: 9661833. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 10 manifestations ranging from asymptomatic to life-threatening states makes it difficult to manage this infection effectively with today’s very meager (cidofovir, foscarnet, ganciclovir, valganciclovir et cetera) possibilities (Mozaffar et al.,2018;Bartlett et al.,2018). Meanwhile, it was possible to detect CMV mRNA, CMV DNA, and/or CMV antigens in tumour tissues and to provide seroepidemiologic evidence of CMV infection in the etiology of several human malignancies (Michaelis et al.,2009;Cinatl et al., 2004). Cytomegalovirus epidemiology The epidemiology, pathogenesis, and diagnosis of CMV infection and disease might be found in greater detail elsewhere. CMV infects more than 60% of adults (Staras et al.,2006) with an increase in the population’s seroprevalence (Staras et al.,2006,2008;Bate et al.,2010;Lachmann et al.,2018) with increasing age (Bate et al.,2010;Wang et al.,2017;Fang et al.,2009;Gupta and Shorman, 2017). In fact, CMV-IgG seroprevalence among U.S. children 1 to 5 years (2011 to 2012) indicating a (previous) CMV infection has been about 20.7% children (Lanzieri et al.,2015), while 6-11-yearold (Staras et al.,2006) patients are 36.3% CMV positive. As known, CMV seroprevalence (Zuhair et al.,2019) is increasing gradually with age and can be found in those aged >=80 years in more than 90.8% of cases (Staras et al.,2006). After recovery of a primary CMV infection, CMV remains dormant within the myeloid cells of the host over long periods with more or less a frequent viral reactivation. Nonetheless, a CMV infection(Chen et al.,2019) with clinical manifestations ranging from asymptomatic to life-threatening states makes it difficult to manage this infection effectively with today’s very meager (cidofovir, foscarnet, ganciclovir, valganciclovir et cetera) possibilities (Mozaffar et al.,2018;Bartlett et al.,2018). Meanwhile, it was possible to detect CMV mRNA, CMV DNA, and/or CMV antigens in tumour tissues and to provide seroepidemiologic evidence of CMV infection in the etiology of several human malignancies (Michaelis et al.,2009;Cinatl et al.,2004). Previous studies have provided some evidence of higher anti CMV antibody levels in patients with chronic obstructive pulmonary(Tan et al.,2016) disease (COPD). And much more than this. Nenna et al.(Nenna et al.,2020) were able to determine a strong relationship between CMV serology and the risk of dying from COPD. According to Nenna et al., CMV serology was associated with cancer mortality too. Furthermore, the study group of Balthesen et al. (Balthesen et al.,1993) found that the lungs are one major organ site of cytomegalovirus latency and recurrence. Thus far, theoretically, a possible (causal) relationship between CMV and lung (Ferlay et al.,2019) cancer (LC) does not seem completely out of question. The epidemiology, pathogenesis, and diagnosis of CMV infection and disease might be found in greater detail elsewhere. The prevalence of CMV infection increases (Bate et al.,2010;Wang et al.,2017;Fang et al.,2009) with age. Cytomegalovirus Treatment Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 11 At this occasion, let us discuss view aspects of the treatment of a CMV infection. Various drugs are used, among them intravenous (i.v.) ganciclovir (GCV), oral valganciclovir (VGC), foscarnet (FOS), cidofovir (CDV), artesunate (Efferth et al.,2008), maribavir (MBV), and leflunomide. However, under circumstances, where there are no anti-viral medications effective against CMV, one option physicians could use is the reduction of immunosuppression. 6 A highly effective CMV vaccine(Gerna and Lilleri,2019) is not available. Leflunomide Leflunomide is a drug with excellent antiviral activity against cytomegalovirus (CMV) and considerably less expensive than intravenous ganciclovir. Leflunomide as a drug appears to inhibit virion assembly rather than DNA synthesis. 7CMV DNA was cleared from the blood at an average of 1 month. 8 A Leflunomide loading dose of 100 mg of leflunomide once daily on days 1-3 is given orally and then 20 mg once daily orally for 3 months. CMV-Ig (Cytotect) Several studies 9reported the utility of CMV-Ig as an agent for the treatment of CMV infection or disease. Lautenschlager et al. 10 used CMV-Ig (Cytotect) at 2 ml/kg/day to treat CMV disease and reported success in 23 of 24 cases. 6Tobin JO’H. Cytomegalovirus infection. In: Weatherall DJ, Ledingham JGG, Warrell DA, editors. Oxford textbook of medicine. 2. Oxford: Oxford University Press; 1987. pp. 5.76–5.80. ISBN-10: 0192615513 7Chacko B, John GT. Leflunomide for cytomegalovirus: bench to bedside. Transpl Infect Dis. 2012 Apr;14(2):111-20. doi: 10.1111/j.1399-3062.2011.00682.x. Epub 2011 Oct 9. PMID: 22093814. 8John GT, Manivannan J, Chandy S, Peter S, Jacob CK. Leflunomide therapy for cytomegalovirus disease in renal allograft recipients. Transplantation. 2004 May 15;77(9):1460-1. doi: 10.1097/01.tp.0000122185.64004.89. PMID: 15167608. 9Snydman DR. Cytomegalovirus immunoglobulins in the prevention and treatment of cytomegalovirus disease. Rev Infect Dis. 1990 Sep-Oct;12 Suppl 7:S839-48. doi: 10.1093/clinids/12.supplement 7.s839. PMID: 2173113. 10Lautenschlager I, Ahonen J, Eklund B, H¨ ockerstedt K, Salmela K, Isoniemi H, Korsb¨ ack C, Suni J, H¨ ayry P. Hyperimmune globulin therapy of clinical cytomegalovirus infection in renal allograft recipients. Scand J Infect Dis. 1989;21(2):139-43. doi: 10.3109/00365548909039960. PMID: 2543060. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 12 2. Material and methods The study of Gries et al. In the cohort study by Geris et al.11, after various exclusions, 247,318 solid organ transplantation (SOT) recipients were included in the final analysis. The CMV negative (R−/D−) group of 41,518 patients comprising seronegative recipients (R−) who received an organ from a seronegative donor (D−) serves as the critical reference group for analyzing the relationship between cytomegalovirus (CMV) serostatus and post-transplant malignancy risk. This group is considered to have the “baseline” or “normal” risk for this study. However, it is necessary to highlight one of the most important methodological limitations of this study–the problem of subsequent CMV exposure. The study deliberately uses only the CMV status at the time of transplantation as the exposure. Regular CMV tests during the post-transplantation period (e.g., for monitoring viremia) are often not completely or consistently documented in such large national registries. In other words, in this study, the “exposure” (the risk factor) is not an (active) CMV infection at the time of cancer diagnosis. The authors state, among other things: “The primary limitation of our study is the lack of data for CMV infection or disease following transplantation, which would allow for better characterization of the role of CMV in development of cancer.” The CMV serostatus was available at the time of transplantation and was treated as static. However, a patient in the R−/D−group (classified as “non-exposed”) could have become infected with CMV after transplantation (e.g., through blood transfusions and other sources) and developed cancer. A patient classified as CMV negative who later developed cancer was nevertheless incorrectly assigned to the “non-exposed” group (R−/D−) due to the study design. This study design leads to cancer cases being incorrectly recorded in the “non-exposed” group (R−/D−) that should appear in the CMV-positive group. The study design leads to an underestimation of the association between CMV and cancer. 11Geris JM, Spector LG, Pfeiffer RM, Limaye AP, Yu KJ, Engels EA. Cancer risk associated with cytomegalovirus infection among solid organ transplant recipients in the United States. Cancer. 2022;128(22):3985-3994. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 13 We performed an extensive statistical re-analysis of the cohort data from Geris et al. using advanced statistical 12 methods (see Barukˇ ci´ c,1989,2019,2005,2016,2021,2024). Table 1. Relationship: CMV IgG positive and Bladder cancer (Study of Geris et al. , 2022 ). Bladder cancer YES NO CMV IgG positive YES 272 205528 205800 NO 42 41476 41518 314 247004 247318 Statistical Analysis. Causal relationship k = 0,00325441 P Value (one sided right tailed) (HGD) = 0,05833136 p (SINE) = 0,99983018 p (SINE) approx.= 1-(c/B)) >0,86624204 p (SINE) approx.= 1-(c/(Not A))) >0,99898839 P Values. P Value (one sided right tailed) (HGD) = 0,05833136 ˜χ2(SINE— Not At) = 0,04 ˜χ2(SINE— Bt) = 5,62 P Value (SINE) = 0,00017387 P Value (one sided right tailed) (Poisson) = 1,09805E-58 ;H0:p≤0,999 Proportions. (a/N) ×100 = ( 272 / 247318 ) ×100 = 0,11 % (b/N) ×100 = ( 205528 / 247318 ) ×100 = 83,10 % (c/N) ×100 = ( 42 / 247318 ) ×100 = 0,02 % (d/N) ×100 = ( 41476 / 247318 ) ×100 = 16,77 % (a/A) ×100 = ( 272 / 205800 ) ×100 = 0,13 % (b/A) ×100 =( 205528 / 205800 ) ×100 = 99,87 % (c/ not A) ×100 =( 42 / 41518 ) ×100 = 0,10 % (d/ not A) ×100 =( 41476 / 41518 ) ×100 = 99,90 % (a/B) ×100 =( 272 / 314 ) ×100 = 86,62 % (c/B) ×100 =( 42 / 314 ) ×100 = 13,38 % (b/ not B) ×100 =( 205528 / 247004 ) ×100 = 83,21 % (d/ not B) ×100 =( 41476 / 247004 ) ×100 = 16,79 % (A/N) ×100 =( 205800 / 247318 ) ×100 = 83,21 % ( not A/N) ×100 =( 41518 / 247318 ) ×100 = 16,79 % (B/N) ×100 =( 314 / 247318 ) ×100 = 0,13 % ( not B/N) ×100 =( 247004 / 247318 ) ×100 = 99,87 % Additional statistical measures. Relative risk (RR). RR (necessary condition) = 1,30650377 RR (sufficient condition) = 1,04105158 Other statistical measures. Odds ratio (OR) = 1,30690940 Index of relationship (IOR) = 0,04099732 Study design. p(IOU)= 0,16660332 p(IOI)= 0,83085744 12Barukˇ ci´ c I. The causal relationship. *MATEC Web Conf*. 2021;336:09032. doi:10.1051/matecconf/202133609032. Published online February 15, 2021. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 20 Associated Data Copyright Copyright ©November 30, 2025 by Ilija Barukˇ ci´ c, Horandstrasse, Jever, Germany. All Rights Reserved. Alle Rechte vorbehalten. Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21 21 ©2026 Ilija Barukˇ ci´ ca,b,c,d,e,f,g,h,i,j,k, l,mIlija Barukˇ ci´ c, Chief-Editor, Jever, Germany, November 30, 2025. All rights reserved. Alle Rechte vorbehalten. This is an open access article which can be downloaded under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0). I was born October, 1st 1961 in Novo Selo, Bosnia and Herzegovina, former Yogoslavia. I am of Croatian origin. From 1982-1989 C.E., I studied human medicine at the University of Hamburg, Germany. Meanwhile, I am working as a specialist of internal medicine. My basic field of research since my high school days at the Wirtschaftsgymnasium Bruchsal, Baden W¨urttemberg, Germany is the mathematization of the relationship between a cause and an effect valid without any restriction under any circumstances including the conditions of classical logic, probability theory, quantum mechanics, special and general theory of relativity, human medicine et cetera. I endeavour to investigate positions of quantum mechanics, relativity theory, mathematics et cetera, only insofar as these positions put into question or endanger the general validity of the principle of causality. ahttps://orcid.org/0000-0002-6988-2780 bhttps://www.webofscience.com/wos/author/record/ 1972920 chttps://www.scopus.com/authid/detail.uri?authorId= 37099674500 dhttps://www.scopus.com/authid/detail.uri?authorId= 54974181600 ehttps://www.mendeley.com/search/?authorFullName= Ilija%20Baruk%C4%8Di%C4%87&page=1&query=Barukcic& sortBy=relevance fhttps://www.researchgate.net/profile/ Ilija-Barukcic-2 ghttps://zenodo.org/search?page=1&size=20&q= keywords:%22Baruk%C4%8Di%C4%87%22&sort=mostviewed hhttps://zenodo.org/search?page=1&size=20&q= keywords:%22Baruk%C4%8Di%C4%87,%20Conference%22 ihttps://twitter.com/ilijabarukcic?lang=de jhttps://twitter.com/Causation_Journ khttps://vixra.org/author/ilija_barukcic lhttps://www.youtube.com/channel/ UCwf3w1IngcukIOOjpw8HTwg mhttps://portal.dnb.de/opac/showNextResultSite? currentResultId=%22Barukcic%22%26any¤tPosition= 30 Causation ISSN: 1863-9542 https://www.doi.org/10.5281/zenodo.17770705 Volume 23, Issue 2, 5–21