SAME AMES SEAM? Phoenix Rising, Part Deux

On

June 20th, 2025. The window of the cell in the monastery where I currently reside, on the windswept Jutland coast, looks out over the Limfjord. This morning I walked along three miles of narrow beach, with the scents of salt, beach roses and cow shit mingling on the breeze and a millennium of marine exoskeletons whispering under my feet. And I remembered a debate I waged 16 years ago with the late, great Bruce Ames at a conference in Vejle, just a few miles to the south.

Bruce presented his theory about why cancer rates increase with age, which he said was due to the time-related accumulation of genetic errors and mutations. (This was subsequently amended to include an age-related decline in inhibitory and repair mechanisms). I had been immersing myself in Victoriana, and knew that the age distribution of cancer in the 19th century was very different, with peak frequency occurring between the ages of 40 and 50 and dropping off thereafter.

Bruce insisted that my data were wrong because they didn’t fit his beautiful theory. I was fairly certain, however, that the mid-Victorian data were correct, and have always believed that theory must yield to facts, so the debate was not particularly productive.

I did not and do not believe that Ames was entirely wrong. His theory fits the facts as seen in a modern, post-transitional and therefore dysnourished landscape, but is ahistoric; the mid-Victorians’ experience of cancer was very different to ours, as I have described elsewhere (1).

One of only two sub-groups of Victorians who experienced rates of cancer anything like ours were the chimneysweeps (2). These abused children were forced to climb naked into narrow chimney flues in order to clean them and were routinely covered in soot, which contains high levels of PAH carcinogens. They frequently developed scrotal cancer (2), and lived short and wretched lives.

In the dark satanic mills, mule spinners were also exposed to PAH compounds from shale oil that lubricated and burned on high-speed, hot-running spindles. The children who operated these devices were similarly prone to cancer (3).

In wider 19th century society, however, and in nature (4), cancer was and is rare.

If you compare similar socio-economic groups, and control for infant mortality, the mid-Victorians lived roughly as long as we do but did not fear cancer as we do because it was relatively uncommon, occurring at about 10% of the levels experienced today (1, 4). Their cancers appear to have been clinically different too, with different time lines (as mentioned above), and survival times matching or exceeding ours, even without modern diagnostic and therapeutic options (5).

Perhaps, then, we might usefully consider cancer from a different angle.

The prevailing construct runs something like this:

Mutations accumulate over time, cancer cells form, most die, a very small percentage of those persist and a small percentage of the surviving cancer cells become clinically significant. Once cancer has been diagnosed we fire magic bullets at it, from the murderous mustards and folate antagonists of the 1940’s and ‘50’s to today’s more specific checkpoint inhibitors, immune modulators, immunoconjugates and antibody–drug conjugates. These have somewhat improved therapeutic indices, but are still toxic!

Chemo generally produces initially positive effects, but resistance commonly emerges and is a frequent cause of treatment failure, along with the toxic effects of treatment.

It is no accident that this approach is very similar to the way in which we regard and treat infection, because at the core of the medical model is the concept of specificity. This is the justification for ‘magic bullets’, which have their roots in 19th century anti-microbial medicine, Louis Pasteur’s germ theory and Paul Ehrlich’s zauberkugels.

Potentially pathogenic microorganisms crowd around and inside us constantly. If / when they break through to become a clinical problem we attack them with antimicrobials. If all goes well the infection disappears, but here also – and increasingly – we often see treatment failure, due to antimicrobial resistance (6).

Although infectology still runs on broadly Pasteurian lines, there is growing acknowledgment of the relevance of Claude Bernard’s terrain theory. With the possible exception of gain-of-function bio-weapons (thank you Mr Fauci), for most pathogens the integrity of the host aka le terrain is important in determining whether clinical infection does occur, and how serious it will be.

Lifestyle factors are very relevant.

Chronic stress, lack of sleep and tobacco consumption compromise immune function. So do malnutrition, obesity, diabetes (see below) and other conditions such as chronic kidney disease (7), inter-related problems which are all increasing. Consider also the increasing use of immuno-suppressive drugs, from steroids to NSAIDs (8), and the negative impact of the Covid campaigns (9) and clot shots (10).

Many of these issues are aided, abetted and worsened by the immuno-disruptive effects of chronic inflammation (11, 12), dysbiosis (13) and failing blood glucose control (14), all of which are increasing.

The evidence base is complicated, as issues such as climate change, sexual behaviors, substance abuse, mass migratory patterns etc undoubtedly play a role here, but evidence of increasing infections is accumulating (15-17).

Factor in the reluctance of pharma companies to invest in new anti-microbials (18, 19) and the future looks bleak indeed (20), UNLESS public health authorities shift to a more Bernardian perspective. The case for facilitating prophylactic behaviors such as weight management, smoking cessation, eating an anti-inflammatory, eubiotic, and low-glycemic diet, and taking 1-3, 1-6 beta-glucan supplements seems self-evident.

For the sticklers: I am not here promoting terrain theory at the expense of germ theory. There is truth in both, as Covid demonstrated (21), a meta-truth which is increasingly being acknowledged (22).

Cancer is made more likely by most of the above lifestyle factors (ie 23-25), and oncology research has also started to explore le terrain. Some call this the ecology of cancer.

In 2019, a multi-disciplinary duo from the University of Utah published a fascinating paper entitled ‘Cancer Ecology and Evolution: Positive interactions and system vulnerability’ (26). In this paper Frederick Adler and Deborah Gordon argued that cancer cells are not invading species but more like native species in an ecosystem that have escaped control.

In a subsequent paper (27), Professor Adler emphasised the role of senescent cells in enabling the loss of local control, an idea which underlies the importance of senolytic therapies.

I read the 2019 paper with the guilty pleasure of bias confirmation, as Adler and Gordon’s thesis dovetails with a paper I published in 2023 (1), in complete ignorance of the Utah team’s work.

Like microbes, cancer cells and cancer-like cells are constantly forming and growing in our tissues (28). However, if all our defenses are operating as they were designed to do, the vast majority of cancerous cells are locked down or killed. This must be the case, as the number of clinical cancers is very much lower than the number of potentially cancerous cells found during screening of ‘healthy’ persons (28).

Many of the factors known to hold cancer cells in check are phytonutrients (1). Here is one reason why the ultraprocessed diet – which, together with our low energy lifestyles, has reduced our intakes of these plant-derived chemo-protective compounds – has been linked to increased risk of cancer (ie 29, 30). The data are admittedly noisy, due to variables such as regionally varied eating patterns and the ways in which UP foods are defined.

Foods are incredibly complex and the NOVA scheme, while workable, makes mechanistic analysis difficult (ie 31-33). Processed meats are associated with increased cancer risk, and there is a plausible nitrite link here (33) – but sugar-sweetened beverages? From a pharmacological perspective it is hard to see why confectionery, ice creams and the more extreme breakfast cereals would be any better, or why artificially sweetened beverages might pose a higher risk than sugar-sweetened ones (31).

Korean eating habits differ from the West, and provide a different nutritional backdrop. This population throws up somewhat different outcomes. Now NOVA scores are unrelated to mortality but increased all-cause mortality is linked to ultra-processed red meat and fish and oddly, among men, milk and soymilk consumption (34).

Too confusing.

I think it more useful to review the pathological drivers of cancer. These overlap to a considerable extent with those factors which, via impeding immune function, make infection more likely. Once again chronic inflammation (35), dysbiosis (36, 37) and failing or failed blood glucose control (38, 39) are all identified as making some or many cancers more likely.

The modern diet and lifestyle promote all the above, forcing us down an interlinking web of pathological processes which move inexorably towards catastrophe (40). Obesity, for example, a known risk factor for cancer, overlaps with chronic inflammation and impaired blood glucose control (41). Obesity also increases the risk of chronic kidney disease (CKD), which pushes us in the direction of cancer by a different but overlapping set of pathways (42).

Among the poisoned public, obesity is also closely linked to dybiosis (43). This increases the risk of CKD (44), opening yet another set of routes to the end-destination of cancer; and all of these conditions negatively affect the immune system (45-47), thereby damaging another major cancer defense.

In other words, le terrain has shifted from a traditionally cancer-hostile to a cancer-friendly configuration. The eco-system has degraded. Under these conditions a cell lacking self-control is not so likely to be checked or killed by the multi-cellular body’s multiple defenses, and more likely to emerge as a clinical problem. Or, as Adler and Gordon put it (26, 27), to escape local control.

In such poor terrain, as mutations continually accumulate, the chances of a selfish cell escaping control and progressing to a clinical cancer will increase indeed exponentially over time, as Ames described. Amongst the mid-Victorians, however, and in non-domesticated species, every person and animal was so well protected that cancer only emerged among the genetically predisposed (1), and those chronically exposed to very high levels of carcinogens.

If the modern diet and lifestyle are degrading our multiple defenses, and if cancer cells are developing randomly, then we should see cancers emerging not only in greater numbers but also earlier in life. Relatively ‘mild’ gene mutations that in a previous age would not have become clinically relevant, now emerge as clinical problems. If our defense systems have become dysfunctional, many of these cancers should present in more aggressive forms.

Since 1990, cancers in teens and young adults have doubled, with a steady increase in early onset cancers of the breast, colorectum, endometrium, esophagus, extrahepatic bile duct, gallbladder, head and neck, kidney, liver, bone marrow, pancreas, prostate, stomach and thyroid (48). Ames’ theory is looking increasingly dog-eared.

And those cancers seem to be becoming more aggressive (ie 49)

Specific factors are under investigation. Reduced intakes of dietary fiber, the wrong microbiota, insufficient exercise … but this is really just a hangover of magic bullet thinking. We could wait for the next-gen anti-cancer eco-drugs, which would be another magic bullet approach. Or we could stem the problem at its source.

According to the ecological model bequeathed to us via Claude Bernard, Walter Cannon, Frederick Adler and Deborah Gordon, I believe we must reconfigure our internal environments. We should re-wild ourselves (1, 50), and in this way re-exert multi-cellular control over our unruly single cells.

Coming soon: UPFs: Where NOVA does not go.

References:

  1. Clayton P, Channan-Khan A. ‘Back to the Future – A 19th Century Perspective on Cancer’.  (2024). Medical Research Archives, [online] 11(10). https://doi.org/10.18103/mra.v11i10.3658
  2. Chirurgical observations: relative to the cataract, the polypus of the nose, the cancer of the scrotum, the different kinds of ruptures, and the mortification of the toes and feet. Pott, Percivall. … 1714-1788. London: Printed, by T.J. Carnegy, for L. Hawes, W. Clarke, and R. Collins. MDCCLXXV 1775. Library Catalog; MMS ID 992825173406676; NLM Unique ID 2731593R
  3. Southam AH. OCCUPATIONAL CANCER OF MULE-SPINNERS. Br Med J. 1928 Sep 8;2(3531):437-8.
  4. https://drpaulclayton.eu/blog/petos-pets/
  5. Clayton P, Rowbotham J. How the mid-Victorians worked, ate and died. Int J Environ Res Public Health. 2009 Mar;6(3):1235-53. 
  6. Mancuso G, Midiri A, Gerace E, Biondo C. Bacterial Antibiotic Resistance: The Most Critical Pathogens. Pathogens. 2021 Oct 12;10(10):1310.
  7. Yang WS, Chang YC, Chang CH, Wu LC, Wang JL, Lin HH. The Association Between Body Mass Index and the Risk of Hospitalization and Mortality due to Infection: A Prospective Cohort Study. Open Forum Infect Dis. 2020 Oct 11;8(1):ofaa545.
  8. Bancos S, Bernard MP, Topham DJ, Phipps RP. Ibuprofen and other widely used non-steroidal anti-inflammatory drugs inhibit antibody production in human cells. Cell Immunol. 2009;258(1):18-28.
  9. Marcinkiewicz J. Increase in the incidence of invasive bacterial infections following the COVID-19 pandemic: potential links with decreased herd trained immunity – a novel concept in medicine. Pol Arch Intern Med. 2024 Sep 27;134(9):16794.
  10. Boretti A. mRNA vaccine boosters and impaired immune system response in immune compromised individuals: a narrative review. Clin Exp Med. 2024 Jan 27;24(1):23.
  11. Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019 Dec;25(12):1822-1832. 
  12. Drozd M, Pujades-Rodriguez M, Morgan AW, Lillie PJ, Witte KK, Kearney MT, Cubbon RM. Systemic Inflammation Is Associated With Future Risk of Fatal Infection: An Observational Cohort Study. J Infect Dis. 2022 Aug 26;226(3):554-562.
  13. Schlechte J, Zucoloto AZ, Yu IL, Doig CJ, Dunbar MJ, McCoy KD, McDonald B. Dysbiosis of a microbiota-immune metasystem in critical illness is associated with nosocomial infections. Nat Med. 2023 Apr;29(4):1017-1027. 
  14. Zhou K, Lansang MC. Diabetes Mellitus and Infection. Endotext, last updated June 30, 2024. https://www.ncbi.nlm.nih.gov/books/NBK569326/
  15. https://www.cdc.gov/ncird/whats-new/mycoplasma-pneumoniae-infections-have-been-increasing.html#:~:text=What%20CDC%20knows,months%2C%20peaking%20in%20late%20August.
  16. https://www.cdc.gov/ncird/whats-new/meningococcal-disease-cases-increasing-us.html#:~:text=CDC%20issued%20a%20health%20advisory%20notice,to%20date%20with%20meningococcal%20vaccination
  17. https://www.cdc.gov/media/releases/2023/p0320-cauris.html#:~:text=auris%20has%20spread%20in%20the,public%20health%20investigations%20suggest%20C.
  18. When Antibiotics Fail. Expert Panel on the Potential Socio-Economic Impacts of Antimicrobial Resistance in Canada (2019). https://cca-reports.ca/wp-content/uploads/2018/10/When-Antibiotics-Fail-1.pdf
  19. Talbot GH, Jezek A, Murray BE, Jones RN, Ebright RH, Nau GJ, Rodvold KA, Newland JG, Boucher HW; Infectious Diseases Society of America. The Infectious Diseases Society of America’s 10 × ’20 Initiative (10 New Systemic Antibacterial Agents US Food and Drug Administration Approved by 2020): Is 20 × ’20 a Possibility? Clin Infect Dis. 2019 Jun 18;69(1):1-11. 
  20. Bracing for Superbugs: Strengthening environmental action in the One Health response to antimicrobial resistance. UN Environment Report 7.2.2023. https://www.unep.org/resources/superbugs/environmental-action
  21. Athavale P, Kumar V, Clark J, Mondal S, Sur S. Differential Impact of COVID-19 Risk Factors on Ethnicities in the United States. Front Public Health. 2021 Dec 6;9:743003.
  22. Carlsson F, Råberg L. The germ theory revisited: A noncentric view on infection outcome. Proc Natl Acad Sci U S A. 2024 Apr 23;121(17):e2319605121.
  23. Lauby-Secretan B, Scoccianti C, Loomis D, Grosse Y, Bianchini F, Straif K; International Agency for Research on Cancer Handbook Working Group. Body Fatness and Cancer–Viewpoint of the IARC Working Group. N Engl J Med. 2016 Aug 25;375(8):794-8.
  24. Mei S, Deng Z, Chen Y, Ning D, Guo Y, Fan X, Wang R, Meng Y, Zhou Q, Tian X. Dysbiosis: The first hit for digestive system cancer. Front Physiol. 2022 Nov 22;13:1040991.
  25. Zhao H, Wu L, Yan G, Chen Y, Zhou M, Wu Y, Li Y. Inflammation and tumor progression: signaling pathways and targeted intervention. Signal Transduct Target Ther. 2021 Jul 12;6(1):263.
  26. Adler FR, Gordon DM. Cancer Ecology and Evolution: Positive interactions and system vulnerability. Curr Opin Syst Biol. 2019 Oct;17:1-7.
  27. Adler FR. A modelling framework for cancer ecology and evolution. J R Soc Interface. 2024 Jul;21(216):20240099. 
  28. Martincorena I, Roshan A, Gerstung M, Ellis P, Van Loo P, McLaren S, Wedge DC, Fullam A, Alexandrov LB, Tubio JM, Stebbings L, Menzies A, Widaa S, Stratton MR, Jones PH, Campbell PJ. High burden and pervasive positive selection of somatic mutations in normal human skin, Science 348 (2015) 880–886 (2015).
  29. Isaksen IM, Dankel SN. Ultra-processed food consumption and cancer risk: A systematic review and meta-analysis. Clin Nutr. 2023 Jun;42(6):919-928.
  30. Lian Y, Wang GP, Chen GQ, Chen HN, Zhang GY. Association between ultra-processed foods and risk of cancer: a systematic review and meta-analysis. Front Nutr. 2023 Jun 8;10:1175994.
  31. Taneri PE, Wehrli F, Roa-Díaz ZM, Itodo OA, Salvador D, Raeisi-Dehkordi H, Bally L, Minder B, Kiefte-de Jong JC, Laine JE, Bano A, Glisic M, Muka T. Association Between Ultra-Processed Food Intake and All-Cause Mortality: A Systematic Review and Meta-Analysis. Am J Epidemiol. 2022 Jun 27;191(7):1323-1335. 
  32. Visioli F, Del Rio D, Fogliano V, Marangoni F, Poli A. Ultra processed foods and cancer. Lancet Reg Health Eur. 2024 Feb 12;38:100863. 
  33. BLOG POST HOMO ULTRAPROCESSUS
  34. Kityo A, Lee SA. The intake of ultra-processed foods, all-cause, cancer and cardiovascular mortality in the Korean Genome and Epidemiology Study-Health Examinees (KoGES-HEXA) cohort. PLoS One. 2023 May 4;18(5):e0285314.
  35. Nigam M, Mishra AP, Deb VK, Dimri DB, Tiwari V, Bungau SG, Bungau AF, Radu AF. Evaluation of the association of chronic inflammation and cancer: Insights and implications. Biomed Pharmacother. 2023 Aug;164:115015.
  36. Biragyn A, Ferrucci L. Gut dysbiosis: a potential link between increased cancer risk in ageing and inflammaging. Lancet Oncol. 2018 Jun;19(6):e295-e304.
  37. Mei S, Deng Z, Chen Y, Ning D, Guo Y, Fan X, Wang R, Meng Y, Zhou Q, Tian X. Dysbiosis: The first hit for digestive system cancer. Front Physiol. 2022 Nov 22;13:1040991. 
  38. Chang WC, Hsieh TC, Hsu WL, Chang FL, Tsai HR, He MS. Diabetes and further risk of cancer: a nationwide population-based study. BMC Med. 2024 May 29;22(1):214. 
  39. Zhu B, Qu S. The Relationship Between Diabetes Mellitus and Cancers and Its Underlying Mechanisms. Front Endocrinol (Lausanne). 2022 Feb 11;13:800995.
  40. https://drpaulclayton.eu/blog/1516/
  41. Pati S, Irfan W, Jameel A, Ahmed S, Shahid RK. Obesity and Cancer: A Current Overview of Epidemiology, Pathogenesis, Outcomes, and Management. Cancers (Basel). 2023 Jan 12;15(2):485.
  42. Hu M, Wang Q, Liu B, Ma Q, Zhang T, Huang T, Lv Z, Wang R. Chronic Kidney Disease and Cancer: Inter-Relationships and Mechanisms. Front Cell Dev Biol. 2022 May 18;10:868715.
  43. Breton J, Galmiche M, Déchelotte P. Dysbiotic Gut Bacteria in Obesity: An Overview of the Metabolic Mechanisms and Therapeutic Perspectives of Next-Generation Probiotics. Microorganisms. 2022 Feb 16;10(2):452.
  44. Evenepoel P, Dejongh S, Verbeke K, Meijers B. The Role of Gut Dysbiosis in the Bone-Vascular Axis in Chronic Kidney Disease. Toxins (Basel). 2020 Apr 29;12(5):285.
  45. Piening A, Ebert E, Gottlieb C, Khojandi N, Kuehm LM, Hoft SG, Pyles KD, McCommis KS, DiPaolo RJ, Ferris ST, Alspach E, Teague RM. Obesity-related T cell dysfunction impairs immunosurveillance and increases cancer risk. Nat Commun. 2024 Apr 2;15(1):2835. 
  46. Espi M, Koppe L, Fouque D, Thaunat O. Chronic Kidney Disease-Associated Immune Dysfunctions: Impact of Protein-Bound Uremic Retention Solutes on Immune Cells. Toxins (Basel). 2020 May 6;12(5):300.
  47. Wiertsema SP, van Bergenhenegouwen J, Garssen J, Knippels LMJ. The Interplay between the Gut Microbiome and the Immune System in the Context of Infectious Diseases throughout Life and the Role of Nutrition in Optimizing Treatment Strategies. Nutrients. 2021 Mar 9;13(3):886.
  48. Ugai T, Sasamoto N, Lee HY, Ando M, Song M, Tamimi RM, Kawachi I, Campbell PT, Giovannucci EL, Weiderpass E, Rebbeck TR, Ogino S. Is early-onset cancer an emerging global epidemic? Current evidence and future implications. Nat Rev Clin Oncol. 2022 Oct;19(10):656-673.
  49. Siegel RL, Fedewa SA, Anderson WF, Miller KD, Ma J, Rosenberg PS, Jemal A. Colorectal Cancer Incidence Patterns in the United States, 1974-2013. J Natl Cancer Inst. 2017 Aug 1;109(8):djw322. 
  50. https://drpaulclayton.eu/blog/walking-in-the-uncanny-valley/
  1. Clayton P, Channan-Khan A. ‘Back to the Future – A 19th Century Perspective on Cancer’.  (2024). Medical Research Archives, [online] 11(10). https://doi.org/10.18103/mra.v11i10.3658
  2. Chirurgical observations: relative to the cataract, the polypus of the nose, the cancer of the scrotum, the different kinds of ruptures, and the mortification of the toes and feet. Pott, Percivall. … 1714-1788. London: Printed, by T.J. Carnegy, for L. Hawes, W. Clarke, and R. Collins. MDCCLXXV 1775. Library Catalog; MMS ID 992825173406676; NLM Unique ID 2731593R
  3. Southam AH. OCCUPATIONAL CANCER OF MULE-SPINNERS. Br Med J. 1928 Sep 8;2(3531):437-8.
  4. https://drpaulclayton.eu/blog/petos-pets/
  5. Clayton P, Rowbotham J. How the mid-Victorians worked, ate and died. Int J Environ Res Public Health. 2009 Mar;6(3):1235-53. 
  6. Mancuso G, Midiri A, Gerace E, Biondo C. Bacterial Antibiotic Resistance: The Most Critical Pathogens. Pathogens. 2021 Oct 12;10(10):1310.
  7. Yang WS, Chang YC, Chang CH, Wu LC, Wang JL, Lin HH. The Association Between Body Mass Index and the Risk of Hospitalization and Mortality due to Infection: A Prospective Cohort Study. Open Forum Infect Dis. 2020 Oct 11;8(1):ofaa545.
  8. Bancos S, Bernard MP, Topham DJ, Phipps RP. Ibuprofen and other widely used non-steroidal anti-inflammatory drugs inhibit antibody production in human cells. Cell Immunol. 2009;258(1):18-28.
  9. Marcinkiewicz J. Increase in the incidence of invasive bacterial infections following the COVID-19 pandemic: potential links with decreased herd trained immunity – a novel concept in medicine. Pol Arch Intern Med. 2024 Sep 27;134(9):16794.
  10. Boretti A. mRNA vaccine boosters and impaired immune system response in immune compromised individuals: a narrative review. Clin Exp Med. 2024 Jan 27;24(1):23.
  11. Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019 Dec;25(12):1822-1832. 
  12. Drozd M, Pujades-Rodriguez M, Morgan AW, Lillie PJ, Witte KK, Kearney MT, Cubbon RM. Systemic Inflammation Is Associated With Future Risk of Fatal Infection: An Observational Cohort Study. J Infect Dis. 2022 Aug 26;226(3):554-562.
  13. Schlechte J, Zucoloto AZ, Yu IL, Doig CJ, Dunbar MJ, McCoy KD, McDonald B. Dysbiosis of a microbiota-immune metasystem in critical illness is associated with nosocomial infections. Nat Med. 2023 Apr;29(4):1017-1027. 
  14. Zhou K, Lansang MC. Diabetes Mellitus and Infection. Endotext, last updated June 30, 2024. https://www.ncbi.nlm.nih.gov/books/NBK569326/
  15. https://www.cdc.gov/ncird/whats-new/mycoplasma-pneumoniae-infections-have-been-increasing.html#:~:text=What%20CDC%20knows,months%2C%20peaking%20in%20late%20August.
  16. https://www.cdc.gov/ncird/whats-new/meningococcal-disease-cases-increasing-us.html#:~:text=CDC%20issued%20a%20health%20advisory%20notice,to%20date%20with%20meningococcal%20vaccination
  17. https://www.cdc.gov/media/releases/2023/p0320-cauris.html#:~:text=auris%20has%20spread%20in%20the,public%20health%20investigations%20suggest%20C.
  18. When Antibiotics Fail. Expert Panel on the Potential Socio-Economic Impacts of Antimicrobial Resistance in Canada (2019). https://cca-reports.ca/wp-content/uploads/2018/10/When-Antibiotics-Fail-1.pdf
  19. Talbot GH, Jezek A, Murray BE, Jones RN, Ebright RH, Nau GJ, Rodvold KA, Newland JG, Boucher HW; Infectious Diseases Society of America. The Infectious Diseases Society of America’s 10 × ’20 Initiative (10 New Systemic Antibacterial Agents US Food and Drug Administration Approved by 2020): Is 20 × ’20 a Possibility? Clin Infect Dis. 2019 Jun 18;69(1):1-11. 
  20. Bracing for Superbugs: Strengthening environmental action in the One Health response to antimicrobial resistance. UN Environment Report 7.2.2023. https://www.unep.org/resources/superbugs/environmental-action
  21. Athavale P, Kumar V, Clark J, Mondal S, Sur S. Differential Impact of COVID-19 Risk Factors on Ethnicities in the United States. Front Public Health. 2021 Dec 6;9:743003.
  22. Carlsson F, Råberg L. The germ theory revisited: A noncentric view on infection outcome. Proc Natl Acad Sci U S A. 2024 Apr 23;121(17):e2319605121.
  23. Lauby-Secretan B, Scoccianti C, Loomis D, Grosse Y, Bianchini F, Straif K; International Agency for Research on Cancer Handbook Working Group. Body Fatness and Cancer–Viewpoint of the IARC Working Group. N Engl J Med. 2016 Aug 25;375(8):794-8.
  24. Mei S, Deng Z, Chen Y, Ning D, Guo Y, Fan X, Wang R, Meng Y, Zhou Q, Tian X. Dysbiosis: The first hit for digestive system cancer. Front Physiol. 2022 Nov 22;13:1040991.
  25. Zhao H, Wu L, Yan G, Chen Y, Zhou M, Wu Y, Li Y. Inflammation and tumor progression: signaling pathways and targeted intervention. Signal Transduct Target Ther. 2021 Jul 12;6(1):263.
  26. Adler FR, Gordon DM. Cancer Ecology and Evolution: Positive interactions and system vulnerability. Curr Opin Syst Biol. 2019 Oct;17:1-7.
  27. Adler FR. A modelling framework for cancer ecology and evolution. J R Soc Interface. 2024 Jul;21(216):20240099. 
  28. Martincorena I, Roshan A, Gerstung M, Ellis P, Van Loo P, McLaren S, Wedge DC, Fullam A, Alexandrov LB, Tubio JM, Stebbings L, Menzies A, Widaa S, Stratton MR, Jones PH, Campbell PJ. High burden and pervasive positive selection of somatic mutations in normal human skin, Science 348 (2015) 880–886 (2015).
  29. Isaksen IM, Dankel SN. Ultra-processed food consumption and cancer risk: A systematic review and meta-analysis. Clin Nutr. 2023 Jun;42(6):919-928.
  30. Lian Y, Wang GP, Chen GQ, Chen HN, Zhang GY. Association between ultra-processed foods and risk of cancer: a systematic review and meta-analysis. Front Nutr. 2023 Jun 8;10:1175994.
  31. Taneri PE, Wehrli F, Roa-Díaz ZM, Itodo OA, Salvador D, Raeisi-Dehkordi H, Bally L, Minder B, Kiefte-de Jong JC, Laine JE, Bano A, Glisic M, Muka T. Association Between Ultra-Processed Food Intake and All-Cause Mortality: A Systematic Review and Meta-Analysis. Am J Epidemiol. 2022 Jun 27;191(7):1323-1335. 
  32. Visioli F, Del Rio D, Fogliano V, Marangoni F, Poli A. Ultra processed foods and cancer. Lancet Reg Health Eur. 2024 Feb 12;38:100863. 
  33. BLOG POST HOMO ULTRAPROCESSUS
  34. Kityo A, Lee SA. The intake of ultra-processed foods, all-cause, cancer and cardiovascular mortality in the Korean Genome and Epidemiology Study-Health Examinees (KoGES-HEXA) cohort. PLoS One. 2023 May 4;18(5):e0285314.
  35. Nigam M, Mishra AP, Deb VK, Dimri DB, Tiwari V, Bungau SG, Bungau AF, Radu AF. Evaluation of the association of chronic inflammation and cancer: Insights and implications. Biomed Pharmacother. 2023 Aug;164:115015.
  36. Biragyn A, Ferrucci L. Gut dysbiosis: a potential link between increased cancer risk in ageing and inflammaging. Lancet Oncol. 2018 Jun;19(6):e295-e304.
  37. Mei S, Deng Z, Chen Y, Ning D, Guo Y, Fan X, Wang R, Meng Y, Zhou Q, Tian X. Dysbiosis: The first hit for digestive system cancer. Front Physiol. 2022 Nov 22;13:1040991. 
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