Introduction
1. M. A. Martinez-Gonzalez, A. Sanchez-Tainta, D. Corella, et al., “A provegetarian food pattern and reduction in total mortality in the Prevencion con Dieta Mediterranea (PREDIMED) study,” American Journal of Clinical Nutrition 100, no. 1 (July 2014): 320S–28S, Erratum, Supplement, American Journal of Clinical Nutrition 100, no. 6 (December 2014): 1605.
2. V. Er, J. A. Lane, R. M. Martin, et al., “Adherence to dietary and lifestyle recommendations and prostate cancer risk in the prostate testing for cancer and treatment (ProtecT) trial,” Cancer Epidemiology, Biomarkers and Prevention 23, no. 10 (October 2014): 206–77.
3. P. F. Innominato, D. Spiegel, A. Ulusakarya, et al., “Subjective sleep and overall survival in chemotherapy-naive patients with metastatic colorectal cancer,” Sleep Medicine 16, no. 3 (March 2015): 391–98.
4. P. F. Innominato, S. Giacchetti, G. A. Bjarnason, et al., “Prediction of overall survival through circadian rest-activity monitoring during chemotherapy for metastatic colorectal cancer,” International Journal of Cancer 131, no. 11 (December 2012): 2684–92.
5. P. Cormie, E. M. Zopf, X. Zhang, K. H. Schmitz, “The impact of exercise on cancer mortality, recurrence, and treatment-related adverse effects,” Epidemiologic Reviews 39, no. 1 (January 2017): 71–92.
6. B. Bortolato, T. N. Hyphantis, S. Valpione, et al., “Depression in cancer: the many biobehavioral pathways driving tumor progression,” Cancer Treatment Reviews 52 (January 2017): 58–70.
7. B. L. Andersen, H. C. Yang, W. B. Farrar, et al., “Psychologic intervention improves survival for breast cancer patients: a randomized clinical trial,” Cancer 113, no. 12 (December 2008): 3450–58.
8. J. C. Pairon, P. Andujar, M. Rinaldo, et al., “Asbestos exposure, pleural plaques, and the risk of death from lung cancer,” American Journal of Respiratory and Critical Care Medicine 190, no. 12 (December 2014): 1413–20.
9. I. A. Ojajarvi, T. J. Partanen, A. Ahlbom, et al., “Occupational exposures and pancreatic cancer: a meta-analysis,” Occupational and Environmental Medicine 57, no. 5 (May 2000): 316–24.
10. D. Servan-Schreiber, Anticancer: A New Way of Life (New York: Viking, 2009).
11. B. Arun, T. Austin, G. V. Babiera, et al., “A comprehensive lifestyle randomized clinical trial: design and initial patient experience,” Integrative Cancer Therapies 16, no. 1 (March 2017): 3–20.
12. M. L. McCullough, A. V. Patel, L. H. Kushi, et al., “Following cancer prevention guidelines reduces risk of cancer, cardiovascular disease, and all-cause mortality,” Cancer Epidemiology, Biomarkers and Prevention 20, no. 6 (June 2011): 1089–97.
13. L. J. Rasmussen-Torvik, C. M. Shay, J. G. Abramson, et al., “Ideal cardiovascular health is inversely associated with incident cancer: the atherosclerosis risk in communities study,” Circulation 127, no. 12 (March 2013): 1270–75.
PART ONE: THE ANTICANCER AGE
Chapter One: The Anticancer Revolution
1. American Institute for Cancer Research, “Nearly 50% of the most common cancers can be prevented,” 2017, www.aicr.org/learn-more-about-cancer/infographics/nearly-50-infographic.html.
2. T. Lohse, D. Faeh, M. Bopp, S. Rohrmann, “Adherence to the cancer prevention recommendations of the World Cancer Research Fund/American Institute for Cancer Research and Mortality: a census-linked cohort,” American Journal of Clinical Nutrition 104, no. 3 (September 2016): 678–85.
3. G. C. Kabat, C. E. Matthews, V. Kamensky, A. R. Hollenbeck, T. E. Rhan, “Adherence to cancer prevention guidelines and cancer incidence, cancer mortality, and total mortality: a prospective cohort study,” American Journal of Clinical Nutrition 101, no. 3 (March 2015): 558–69.
4. R. L. Siegel, K. D. Miller, A. Jemal, “Cancer statistics, 2017,” CA: A Cancer Journal for Clinicians 67, no. 1 (January 2017): 7–30.
5. D. Hanahan, R. A. Weinberg, “Hallmarks of cancer: the next generation,” Cell 144, no. 5 (March 2011): 646–74.
6. G. A. Thomas, B. Cartmel, M. Harrigan, et al., “The effect of exercise on body composition and bone mineral density in breast cancer survivors taking aromatase inhibitors,” Obesity 25, no. 2 (February 2017): 346–51.
7. M. Inoue-Choi, K. Robien, D. Lazovich, “Adherence to the WCRF/AICR guidelines for cancer prevention is associated with lower mortality among older female cancer survivors,” Cancer Epidemiology Biomarkers & Prevention 22, no. 5 (May 2013): 792–802.
8. P. Cormie, E. M. Zopf, X. Zhang, K. H. Schmitz, “The impact of exercise on cancer mortality, recurrence, and treatment-related adverse effects,” Epidemiologic Reviews 39, no. 1 (January 2017): 71–92.
9. S. Wu, S. Powers, W. Zhu, Y. A. Hannun, “Substantial contribution of extrinsic risk factors to cancer development,” Nature 529, no. 7584 (January 2016): 43–47.
10. World Health Organization, “Cancer,” February 2017, www.who.int/mediacentre/factsheets/fs297/en.
11. American Cancer Society, Cancer Facts & Figures 2017 (Atlanta: American Cancer Society, 2017).
12. M. C. White, D. M. Holman, J. E. Boehm, et al., “Age and cancer risk: a potentially modifiable relationship,” American Journal of Preventive Medicine 46, no. 3 Supplement 1 (March 2014): S7–15.
13. R. L. Siegel, S. A. Fedewa, W. F. Anderson et al., “Colorectal cancer incidence patterns in the United States, 1974–2013,” Journal of the National Cancer Institute 109, no. 8 (August 2017).
14. M. R. Cooperberg, J. M. Broering, P. R. Carroll, “Time trends and local variation in primary treatment of localized prostate cancer,” Journal of Clinical Oncology 28, no. 7 (March 2010): 1117–23.
15. L. J. Esserman, Y. Shieh, E. J. Rutgers, et al., “Impact of mammographic screening on the detection of good and poor prognosis breast cancers,” Breast Cancer Research and Treatment 130, no. 3 (December 2011): 725–34.
16. D. Katz, “True health initiative, 2017,” www.truehealthinitiative.org.
17. J. M. McGinnis, W. H. Foege, “Actual causes of death in the United States,” Journal of the American Medical Association 270, no. 18 (November 1993): 2207–12.
18. A. H. Mokdad, J. S. Marks, D. F. Stroup, J. L. Gerberding, “Actual causes of death in the United States, 2000,” Journal of the American Medical Association 291, no. 10 (March 2004): 1238–45.
19. M. Song, E. Giovannucci, “Preventable incidence and mortality of carcinoma associated with lifestyle factors among white adults in the United States,” Journal of the American Medical Association Oncology 2, no. 9 (September 2016): 1154–61.
20. G. A. Colditz, S. Sutcliffe, “The preventability of cancer: Stacking the deck,” Journal of the American Medical Association Oncology 2, no. 9 (September 2016): 1131–33.
21. M. Greger, G. Stone, How Not to Die: Discover the Foods Scientifically Proven to Prevent and Reverse Disease (New York: Flatiron Books, 2015).
22. Surgeon General’s Advisory Committee on Smoking and Health, United States, Public Health Service, Office of the Surgeon General, United States, “Smoking and health: report of the advisory committee of the surgeon general of the public health service,” Public Health Service, Office of the Surgeon General, 1964, www.profiles.nlm.nih.gov/NN/B/B/M/Q.
23. F. Islami, L. A. Torre, A. Jemal, “Global trends of lung cancer mortality and smoking prevalence,” Translational Lung Cancer Research 4, no. 4 (August 2015): 327–38.
24. Australian Bureau of Statistics, “National health survey: First results, 2014–15: Smoking,” www.abs.gov.au/ausstats/abs@.nsf/Lookup/bySubject/4364.0.55.001~2014-15~Main Features~Smoking~24.
25. T. Goldman, “Health policy brief: tobacco taxes,” Health Affairs, September 19, 2016, www.healthaffairs.org/healthpolicybriefs/brief.php?brief_id=163.
26. K. Lunze, L. Migliorini, “Tobacco control in the Russian Federation—a policy analysis,” BMC Public Health 13 (January 2013): 64.
27. M. B. Drummond, D. Upson, “Electronic cigarettes: potential harms and benefits,” Annals of the American Thoracic Society 11, no. 2 (February 2014): 236–42.
28. D. Hammond, J. L. Reid, A. G. Cole, S. T. Leatherdale, “Electronic cigarette use and smoking initiation among youth: longitudinal cohort study,” Canadian Medical Association Journal 189, no. 43 (October 2017): E1328–36.
29. P. Anand, A. B. Kunnumakara, C. Sundaram, et al., “Cancer is a preventable disease that requires major lifestyle changes,” Pharmaceutical Research 25, no. 9 (September 2008): 2097–116.
30. D. Chan, “Where do the millions of cancer research dollars go every year?,” Slate, February 7, 2013, www. /blogs/quora/2013/02/07/where_do_the_millions_of_cancer_research_dollars_go_every_year.html.
31. V. Bouvard, D. Loomis, K. Z. Guyton, et al., “Carcinogenicity of consumption of red and processed meat,” The Lancet Oncology 16, no. 16 (October 2015): 1599–1600.
32. Y. Jiang, Y. Pan, P. R. Rhea, et al., “A sucrose-enriched diet promotes tumorigenesis in mammary gland in part through the 12-lipoxygenase pathway,” Cancer Research 76, no. 1 (January 2016): 24–29.
33. Q. Yang, Z. Zhang, E. W. Gregg, et al., “Added sugar intake and cardiovascular diseases mortality among U.S. adults,” Journal of the American Medical Association Internal Medicine 174, no. 4 (April 2014): 516–24.
34. W. E. Barrington, E. White, “Mortality outcomes associated with intake of fast-food items and sugar-sweetened drinks among older adults in the Vitamins and Lifestyle (VITAL) study,” Public Health Nutrition 19, no. 18 (December 2016): 3319–26.
35. R. Shavelle, K. Vavra-Musser, J. Lee, J. Brooks, “Life expectancy in pleural and peritoneal mesothelioma,” Lung Cancer International 2017 (January 2017): 2782590.
36. S. J. Gould, “The median isn’t the message,” UMass Amherst, www.people.umass.edu/biep540w/pdf/Stephen%20Jay%20Gould.pdf.
37. K. D. Miller, R. L. Siegel, C. C. Lin, et al., “Cancer treatment and survivorship statistics, 2016,” CA: A Cancer Journal for Clinicians 66, no. 4 (July 2016): 271–89.
38. P. S. Rosenberg, K. A. Barker, W. F. Anderson, “Estrogen receptor status and the future burden of invasive and in situ breast cancers in the United States,” JNCI Journal of the National Cancer Institute 107, no. 9 (June 2015).
Chapter Two: Our Healing Powers
1. D. Ornish, G. Weidner, W. R. Fair, et al., “Intensive lifestyle changes may affect the progression of prostate cancer,” Journal of Urology 174, no. 3 (September 2005): 1065–69; discussion 1069–70.
2. D. Romaguera, E. Gracia-Lavedan, A. Molinuevo, et al., “Adherence to nutrition-based cancer prevention guidelines and breast, prostate and colorectal cancer risk in the MCC-Spain case-control study,” International Journal of Cancer 141, no. 1 (July 2017): 83–93.
3. N. Jankovic, A. Geelen, R. M. Winkels, et al., “Adherence to the WCRF/AICR dietary recommendations for cancer prevention and risk of cancer in elderly from Europe and the United States: a meta-analysis within the CHANCES Project,” Cancer Epidemiology, Biomarkers and Prevention 26, no. 1 (January 2017): 136–44.
4. P. P. Bao, G. M. Zhao, X. O. Shu et al., “Modifiable lifestyle factors and triple-negative breast cancer survival: a population-based prospective study,” Epidemiology 26, no. 6 (November 2015): 909–16.
5. C. A. Thomson, M. L. McCullough, B. C. Wertheim, et al., “Nutrition and physical activity cancer prevention guidelines, cancer risk, and mortality in the women’s health initiative,” Cancer Prevention Research 7, no. 1 (January 2014): 42–53.
6. T. Lohse, D. Faeh, M. Bopp, S. Rohrmann, “Adherence to the cancer prevention recommendations of the World Cancer Research Fund/American Institute for Cancer Research and Mortality: a census-linked cohort,” American Journal of Clinical Nutrition 104, no. 3 (September 2016): 678–85.
7. P. Jallinoja, P. Absetz, R. Kuronen, et al., “The dilemma of patient responsibility for lifestyle change: perceptions among primary care physicians and nurses,” Scandinavian Journal of Primary Health Care 25, no. 4 (December 2007): 244–49.
8. K. M. Adams, M. Kohlmeier, S. H. Zeisel, “Nutrition education in U.S. medical schools: latest update of a national survey,” Academic Medicine 85, no. 9 (September 2010): 1537–42.
9. M. Zajenkowski, K. S. Jankowski, D. Kołata, “Let’s dance—feel better! Mood changes following dancing in different situations,” European Journal of Sport Science 15, no. 7 (October 2015): 640–46.
10. V. N. Salimpoor, M. Benovoy, K. Larcher, A. Dagher, R. J. Zatorre, “Anatomically distinct dopamine release during anticipation and experience of peak emotion to music,” Nature Neuroscience 14, no. 2 (February 2011): 257–62.
11. K. Hojan, E. Kwiatkowska-Borowczyk, E. Leporowska, et al., “Physical exercise for functional capacity, blood immune function, fatigue, and quality of life in high-risk prostate cancer patients during radiotherapy: a prospective, randomized clinical study,” European Journal of Physical & Rehabilitation Medicine 52, no. 4 (August 2016): 489–501.
12. K. S. Courneya, C. M. Friedenreich, C. Franco-Villalobos, et al., “Effects of supervised exercise on progression-free survival in lymphoma patients: an exploratory follow-up of the help trial,” Cancer Causes and Control 26, no. 2 (February 2015): 269–76.
13. T. Bouillet, X. Bigard, C. Brami, et al., “Role of physical activity and sport in oncology: scientific commission of the National Federation Sport and Cancer Cami,” Critical Reviews in Oncology-Hematology 94, no. 1 (April 2015): 74–86.
14. E. M. Zopf, W. Bloch, S. Machtens, et al., “Effects of a 15-month supervised exercise program on physical and psychological outcomes in prostate cancer patients following prostatectomy: the prorehab study,” Integrative Cancer Therapies 14, no. 5 (September 2015): 409–18.
15. G. Zhu, X. Zhang, Y. Wang, et al., “Effects of exercise intervention in breast cancer survivors: a meta-analysis of 33 randomized controlled trials,” OncoTargets and Therapy 9 (April 2016): 2153–68.
16. C. Catsburg, A. B. Miller, T. E. Rohan, “Adherence to cancer prevention guidelines and risk of breast cancer,” International Journal of Cancer 135, no. 10 (November 2014): 2444–52.
17. M. Inoue-Choi, D. Lazovich, A. E. Prizment, K. Robien, “Adherence to the World Cancer Research Fund/American Institute for Cancer Research recommendations for cancer prevention is associated with better health-related quality of life among elderly female cancer survivors,” Journal of Clinical Oncology 31, no. 14 (May 2013): 1758–66.
18. M. Inoue-Choi, K. Robien, D. Lazovich, “Adherence to the WCRF/AICR guidelines for cancer prevention is associated with lower mortality among older female cancer survivors,” Cancer Epidemiology Biomarkers & Prevention 22, no. 5 (May 2013): 792–802.
19. American Cancer Society, “ACS guidelines on nutrition and physical activity for cancer prevention,” February 5, 2016, www.cancer.org/healthy/eat-healthy-get-active/acs-guidelines-nutrition-physical-activity-cancer-prevention.html.
20. American Institute for Cancer Research, “Recommendations for cancer prevention,” 2017, www.aicr.org/reduce-your-cancer-risk/recommendations-for-cancer-prevention.
21. N. Makarem, Y. Lin, E. V. Bandera, P. F. Jacques, N. Parekh, “Concordance with World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) guidelines for cancer prevention and obesity-related cancer risk in the framingham offspring cohort (1991–2008),” Cancer Causes and Control 26, no. 2 (February 2015): 277–86.
22. A. C. Vergnaud, D. Romaguera, P. H. Peeters, et al., “Adherence to the World Cancer Research Fund/American Institute for Cancer Research guidelines and risk of death in Europe: results from the European Prospective Investigation into nutrition and cancer cohort study,” American Journal of Clinical Nutrition 97, no. 5 (May 2013): 1107–20.
23. J. J. Prochaska, J. O. Prochaska, “A review of multiple health behavior change interventions for primary prevention,” American Journal of Lifestyle Medicine 5, no. 3 (May 2011).
24. S. U. Maier, A. B. Makwana, T. A. Hare, “Acute stress impairs self-control in goal-directed choice by altering multiple functional connections within the brain’s decision circuits,” Neuron 87, no. 3 (August 2015): 621–31.
25. W. E. Barrington, S. A. Beresford, B. A. McGregor, E. White, “Perceived stress and eating behaviors by sex, obesity status, and stress vulnerability: findings from the vitamins and lifestyle (vital) study,” Journal of the Academy of Nutrition and Dietetics 114, no. 11 (November 2014): 1791–99.
26. A. W. Y. Leung, R. S. M. Chan, M. M. M. Sea, J. Woo, “An overview of factors associated with adherence to lifestyle modification programs for weight management in adults,” International Journal of Environmental Research and Public Health 14, no. 8 (August 2017): 922.
27. T. Asadollahi, S. Khakpour, F. Ahmadi, et al., “Effectiveness of mindfulness training and dietary regime on weight loss in obese people,” Journal of Medicine and Life 8, no. 4 (December 2015): 114–24.
28. D. J. Hyman, V. N. Pavlik, W. C. Taylor, G. K. Goodrick, L. Moye, “Simultaneous vs sequential counseling for multiple behavior change,” Archives of Internal Medicine 167, no. 11 (June 2007): 1152–58.
29. B. Spring, A. King, S. Pagoto, L. Van Horn, J. Fisher, “Fostering multiple healthy lifestyle behaviors for primary prevention of cancer,” American Psychologist 70, no. 2 (March 2015): 75–90.
30. M. A. Lerner, “Difference Between Healing and Curing,” Awaken.org, February 7, 2015, www.awaken.org/read/view.php?tid=1066.
31. D. J. Hauser, N. Schwarz, “The war on prevention: bellicose cancer metaphors hurt (some) prevention intentions,” Personality Health 14, no. 8 (August 2017): 922.
32. D. Servan-Schreiber, Anticancer: A New Way of Life (New York: Viking, 2009).
33. S. K. Lutgendorf, K. De Geest, D. Bender, et al., “Social influences on clinical outcomes of patients with ovarian cancer,” Journal of Clinical Oncology 30, no. 23 (August 2012): 2885–90.
34. Anticancer Lifestyle Foundation, “Anticancer lifestyle program,” 2017, www.anti cancerlifestyle.org.
35. P. J. Goodwin, R. T. Chlebowski, “Obesity and cancer: insights for clinicians,” Journal of Clinical Oncology 34, no. 35 (December 2016): 4197–202.
36. P. Cormie, E. M. Zopf, X. Zhang, K. H. Schmitz, “The impact of exercise on cancer mortality, recurrence, and treatment-related adverse effects,” Epidemiologic Reviews 39, no. 1 (January 2017): 71–92.
37. M. L. McCullough, A. V. Patel, L. H. Kushi, et al., “Following cancer prevention guidelines reduces risk of cancer, cardiovascular disease, and all-cause mortality,” Cancer Epidemiology, Biomarkers and Prevention 20, no. 6 (June 2011): 1089–97.
38. P. F. Innominato, D. Spiegel, A. Ulusakarya, et al., “Subjective sleep and overall survival in chemotherapy-naive patients with metastatic colorectal cancer,” Sleep Medicine 16, no. 3 (March 2015): 391–98.
39. M. Jan, S. E. Bonn, A. Sjolander, et al., “The roles of stress and social support in prostate cancer mortality,” Scandinavian Journal of Urology 50, no. 1 (August 2016): 47–55.
Chapter Three: What Causes Cancer, Anyway?
1. Hanahan, R. A. Weinberg, “Hallmarks of cancer: the next generation,” Cell 144, no. 5 (March 2011): 646–74.
2. S. Wu, S. Powers, W. Zhu, Y. A. Hannun, “Substantial contribution of extrinsic risk factors to cancer development,” Nature 529, no. 7584 (January 2016): 43–47.
3. C. Tomasetti, B. Vogelstein, “Variation in cancer risk among tissues can be explained by the number of stem cell divisions,” Science 347, no. 6217 (January 2015): 78.
4. C. Tomasetti, L. Li, B. Vogelstein, “Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention,” Science 355, no. 6331 (March 2017): 1330.
5. American Institute for Cancer Research, “The AICR 2015 cancer risk awareness survey report,” 2015, www.aicr.org/assets/docs/pdf/education/aicr-awareness-report-2015.pdf.
6. J. E. Garber, K. Offit, “Hereditary cancer predisposition syndromes,” Journal of Clinical Oncology 23, no. 2 (January 2005): 276–92.
7. P. Lichtenstein, N. V. Holm, P. K. Verkasalo, et al., “Environmental and heritable factors in the causation of cancer—analyses of cohorts of twins from Sweden, Denmark, and Finland,” New England Journal of Medicine 343, no. 2 (July 2000): 78–85.
8. National Cancer Institute, “BRCA1 and BRCA2: cancer risk and genetic testing,” April 1, 2015, www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet-q9.
9. American Institute for Cancer Research, “Nearly 50% of the most common cancers can be prevented,” 2017, www.aicr.org/learn-more-about-cancer/infographics/nearly-50-infographic.html.
10. International Agency for Research on Cancer, “IARC monographs of the evaluation of carcenogenic risks to humans,” World Health Organization, 2017, www.monographs.iarc.fr.
11. Centers for Disease Control and Prevention, “Agency for toxic substances and disease registry,” November 27, 2017, www.atsdr.cdc.gov.
12. American Association for Cancer Research, “AACR cancer progress report. Preventing cancer: understanding risk factors,” www.cancerprogressreport.org/Pages/cpr17-preventing-cancer.aspx.
13. P. Anand, A. B. Kunnumakara, C. Sundaram, et al., “Cancer is a preventable disease that requires major lifestyle changes,” Pharmaceutical Research 25, no. 9 (September 2008): 2097–116.
14. National Toxicology Program, “Report on carcinogens, fourteenth edition,” U.S. Department of Health and Human Services, Public Health Service, 2016b.
15. N. K. LoConte, A. M. Brewster, J. S. Kaur, J. K. Merrill, A. J. Alberg, “Alcohol and cancer: a statement of the American Society of Clinical Oncology,” Journal of Clinical Oncology (November 2017): JCO2017761155.
16. D. E. Nelson, D. W. Jarman, J. Rehm, et al., “Alcohol-attributable cancer deaths and years of potential life lost in the United States,” American Journal of Public Health 103, no. 4 (April 2013): 641–48.
17. World Health Organization, “Tobacco Free Initiative (TFI): fact sheet about health benefits of smoking cessation,” 2017, www.who.int/tobacco/quitting/benefits/en.
18. A. Parsons, A. Daley, R. Begh, P. Aveyard, “Influence of smoking cessation after diagnosis of early stage lung cancer on prognosis: systematic review of observational studies with meta-analysis,” BMJ 340 (January 2010).
19. G. Poschl, H. K. Seitz, “Alcohol and cancer,” Alcohol and Alcoholism 39, no. 3 (June 2004): 155–65.
20. H. Kuper, A. Tzonou, E. Kaklamani, et al., “Tobacco smoking, alcohol consumption and their interaction in the causation of hepatocellular carcinoma,” International Journal of Cancer 85, no. 4 (February 2000): 498–502.
21. A. Prabhu, K. O. Obi, J. H. Rubenstein, “The synergistic effects of alcohol and tobacco consumption on the risk of esophageal squamous cell carcinoma: a meta-analysis,” American Journal of Gastroenterology 109, no. 6 (June 2014): 822–27.
22. M. Hashibe, P. Brennan, S. C. Chuang, et al., “Interaction between tobacco and alcohol use and the risk of head and neck cancer: pooled analysis in the inhance consortium,” Cancer Epidemiology, Biomarkers & Prevention 18, no. 2 (February 2009): 541–50.
23. T. Lohse, D. Faeh, M. Bopp, S. Rohrmann, “Adherence to the cancer prevention recommendations of the World Cancer Research Fund/American Institute for Cancer Research and Mortality: a census-linked cohort,” American Journal of Clinical Nutrition 104, no. 3 (September 2016): 678–85.
24. A. C. Vergnaud, D. Romaguera, P. H. Peeters, et al., “Adherence to the World Cancer Research Fund/American Institute for Cancer Research guidelines and risk of death in Europe: results from the European Prospective Investigation into nutrition and cancer cohort study,” American Journal of Clinical Nutrition 97, no. 5 (May 2013): 1107–20.
25. M. Inoue-Choi, K. Robien, D. Lazovich, “Adherence to the WCRF/AICR guidelines for cancer prevention is associated with lower mortality among older female cancer survivors,” Cancer Epidemiology Biomarkers & Prevention 22, no. 5 (May 2013): 792–802.
26. G. C. Kabat, C. E. Matthews, V. Kamensky, A. R. Hollenbeck, T. E. Rohan, “Adherence to cancer prevention guidelines and cancer incidence, cancer mortality, and total mortality: a prospective cohort study,” American Journal of Clinical Nutrition 101, no. 3 (March 2015): 558–69.
27. C. A. Thomson, M. L. McCullough, B. C. Wertheim, et al., “Nutrition and physical activity cancer prevention guidelines, cancer risk, and mortality in the Women’s Health Initiative,” Cancer Prevention Research 7, no. 1 (January 2014): 42–53.
28. C. Catsburg, A. B. Miller, T. E. Rohan, “Adherence to cancer prevention guidelines and risk of breast cancer,” International Journal of Cancer 135, no. 10 (November 2014): 2444–52.
29. A. Nerurkar, “What a Happy Cell Looks Like,” February 10, 2015, www.theatlantic.com/health/archive/2015/02/what-a-happy-cell-looks-like/385000.
Chapter Four: A Cell’s Quest for Immortality
1. E. Bianconi, A. Piovesan, F. Facchin, et al., “An estimation of the number of cells in the human body,” Annals of Human Biology 40, no. 6 (December 2013): 463–71.
2. X. Dai, L. Xiang, T. Li, et al., “Cancer hallmarks, biomarkers and breast cancer molecular subtypes,” Journal of Cancer 10, no. 7 (2016): 1281–94.
3. D. Hanahan, R. A. Weinberg, “Hallmarks of cancer: the next generation,” Cell 144, no. 5 (March 2011): 646–74.
4. J. R. Aunan, W. C. Cho, K. Soreide, “The biology of aging and cancer: a brief overview of shared and divergent molecular hallmarks,” Aging and Disease 8, no. 5 (October 2017): 628–42.
5. B. Vogelstein, N. Papadopoulos, V. E. Velculescu, et al., “Cancer genome landscapes,” Science 339, no. 6127 (March 2013): 1546–58.
6. American Cancer Society, Cancer Facts & Figures 2017 (Atlanta: American Cancer Society, 2017c).
7. X. Han, J. Wang, Y. Sun, “Circulating tumor DNA as biomarkers for cancer detection,” Genomics, Proteomics & Bioinformatics 15, no. 2 (April 2017): 59–72.
8. J. Irudayara, “Research could lead to test strips for early cervical cancer detection,” March 28, 2017, www.purdue.edu/newsroom/releases/2017/Q1/research-could-lead-to-test-strips-for-early-cervical-cancer-detection.html.
9. For a wonderful history on cancer and cancer treatment, see: S. Mukhergee, The Emperor of All Maladies: A Biography of Cancer (New York: Simon and Shuster, 2011).
10. H. S. Ahn, H. J. Kim, H. G. Welch, “Korea’s thyroid-cancer ‘epidemic’—screening and overdiagnosis,” New England Journal of Medicine 371, no. 19 (November 2014): 1765–67.
11. J. H. Hayes, M. J. Barry, “Screening for prostate cancer with the prostate-specific antigen test: a review of current evidence,” Journal of the American Medical Association 311, no. 11 (March 2014): 1143–49.
12. M. R. Cooperberg, J. M. Broering, P. R. Carroll, “Time trends and local variation in primary treatment of localized prostate cancer,” Journal of Clinical Oncology 28, no. 7 (March 2010): 1117–23.
13. American Cancer Society, “Watchful waiting or active surveillance for prostate cancer,” March 11, 2016, www.cancer.org/cancer/prostate-cancer/treating/watchful-waiting.html.
14. T. J. Wilt, M. K. Brawer, K. M. Jones, et al., “Radical prostatectomy versus observation for localized prostate cancer,” New England Journal of Medicine 367, no. 3 (July 2012): 203–13.
15. J. Hegarty, P. V. Beirne, E. Walsh, et al., “Radical prostatectomy versus watchful waiting for prostate cancer,” Cochrane Database of Systematic Reviews, no. 11 (November 2010): Cd006590.
16. D. A. Barocas, J. Alvarez, M. J. Resnick, et al., “Association between radiation therapy, surgery, or observation for localized prostate cancer and patient-reported outcomes after 3 years,” Journal of the American Medical Association 317, no. 11 (March 2017): 1126–40.
17. J. C. Hu, L. Kwan, C. S. Saigal, M. S. Litwin, “Regret in men treated for localized prostate cancer,” Journal of Urology 169, no. 6 (June 2003): 2279–83.
18. E. J. Groen, L. E. Elshof, L. L. Visser, et al., “Finding the balance between over- and under-treatment of ductal carcinoma in situ (dcis),” The Breast 31, Supplement C (February 2017): 274–83.
19. J. R. Benson, I. Jatoi, M. Toi, “Treatment of low-risk ductal carcinoma in situ: is nothing better than something?,” The Lancet Oncology 17, no. 10 (October 2016): e442–51.
20. L. M. Youngwirth, J. C. Boughey, E. S. Hwang, “Surgery versus monitoring and endocrine therapy for low-risk dcis: the COMET Trial,” Bulletin of the American College of Surgeons 102, no. 1 (January 2017): 62–63.
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24. National Cancer Institute, “National Cancer Act of 1971,” February 16, 2016, www.cancer.gov/about-nci/legislative/history/national-cancer-act-1971.
25. National Human Genome Research Institute, “All about the Human Genome Project (HGP),” October 1, 2015, www.genome.gov/10001772/all-about-the-human-genome-project-hgp.
26. D. Hanahan, R. A. Weinberg, “The hallmarks of cancer,” Cell 100, no. 1 (January 2000): 57–70.
27. S. K. Lutgendorf, K. DeGeest, L. Dahmoush, et al., “Social isolation is associated with elevated tumor norepinephrine in ovarian carcinoma patients,” Brain, Behavior, and Immunity 25, no. 2 (February 2011): 250–55.
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29. Z. Zhang, L. L. Atwell, P. E. Farris, E. Ho, J. Shannon, “Associations between cruciferous vegetable intake and selected biomarkers among women scheduled for breast biopsies,” Public Health Nutrition 19, no. 7 (May 2016): 1288–95.
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33. S. K. Lutgendorf, E. L. Johnsen, B. Cooper, et al., “Vascular endothelial growth factor and social support in patients with ovarian carcinoma,” Cancer 95 (August 2002): 808–15.
34. J. M. Saxton, E. J. Scott, A. J. Daley, et al., “Effects of an exercise and hypocaloric healthy eating intervention on indices of psychological health status, hypothalamic-pituitary-adrenal axis regulation and immune function after early-stage breast cancer: a randomised controlled trial,” Breast Cancer Research 16, no. 2 (April 2014): R39.
35. G. Fisher, T. C. Hyatt, G. R. Hunter, et al., “Effect of diet with and without exercise training on markers of inflammation and fat distribution in overweight women,” Obesity 19, no. 6 (December 2011): 1131–36.
36. I. Imayama, C. M. Ulrich, C. M. Alfano, et al., “Effects of a caloric restriction weight loss diet and exercise on inflammatory biomarkers in overweight/obese postmenopausal women: a randomized controlled trial,” Cancer Research 72, no. 9 (May 2012): 2314–26.
37. S. B. Jones, G. A. Thomas, S. D. Hesselsweet, et al., “Effect of exercise on markers of inflammation in breast cancer survivors: the Yale exercise and survivorship study,” Cancer Prevention Research 6, no. 2 (December 2013).
38. F. K. Tabung, T. T. Fung, J. E. Chavarro, et al., “Associations between adherence to the world cancer research fund/American institute for cancer research cancer prevention recommendations and biomarkers of inflammation, hormonal, and insulin response,” International Journal of Cancer 140, no. 4 (February 2017): 764–76.
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41. A. Ruiz-Casado, A. Martin-Ruiz, L. M. Perez, et al., “Exercise and the hallmarks of cancer,” Trends Cancer 3, no. 6 (June 2017): 423–41.
42. G. J. Koelwyn, D. F. Quail, X. Zhang, R. M. White, L. W. Jones, “Exercise-dependent regulation of the tumour microenvironment,” Nature Reviews: Cancer 17, no. 10 (September 2017): 620–32.
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44. W. Demark-Wahnefried, T. J. Polascik, S. L. George, et al., “Flaxseed supplementation (not dietary fat restriction) reduces prostate cancer proliferation rates in men presurgery,” Cancer Epidemiology Biomarkers & Prevention 17, no. 12 (December 2008): 3577–87.
45. R. Valdes-Ramos, A. D. Benitez-Arciniega, “Nutrition and immunity in cancer,” British Journal of Nutrition 98, Supplement 1 (October 2007): S127–132.
46. Y. Cao, R. Langer, “A review of Judah Folkman’s remarkable achievements in biomedicine,” Proceedings of the National Academy of Sciences of the United States of America 105, no. 36 (September 2008): 13203–05.
47. G. H. Lyman, H. L. Moses, “Biomarker tests for molecularly targeted therapies: laying the foundation and fulfilling the dream,” Journal of Clinical Oncology 34, no. 17 (June 2016): 2061–66.
48. S. C. Sodergren, E. Copson, A. White, et al., “Systematic review of the side effects associated with anti-her2-targeted therapies used in the treatment of breast cancer, on behalf of the eortc quality of life group,” Targeted Oncology 11, no. 3 (June 2016): 277–92.
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51. N. Shibata, K. Nagai, Y. Morita, et al., “Development of protein degradation inducers of androgen receptor by conjugation of androgen receptor ligands and inhibitor of apoptosis protein ligands,” Journal of Medicinal Chemistry (June 2017).
52. D. Li, Q. Fu, M. Li, et al., “Primary tumor site and anti-EGFR monoclonal antibody benefit in metastatic colorectal cancer: a meta-analysis,” Future Oncology 13, no. 12 (May 2017): 1115–27.
53. M. P. Pinto, G. I. Owen, I. Retamal, M. Garrido, “Angiogenesis inhibitors in early development for gastric cancer,” Expert Opinion Investigational Drugs 26, no. 9 (September 2017): 1007–17.
54. L. E. Fulbright, M. Ellermann, J. C. Arthur, “The microbiome and the hallmarks of cancer,” PLoS Pathogens 13, no. 9 (September 2017): e1006480.
55. V. Gopalakrishnan, C. N. Spencer, L. Nezi, et al., “Gut microbiome modulates response to anti-PD-1 immunotherapy in melanoma patients,” Science (November 2017).
56. A. A. Hibberd, A. Lyra, A. C. Ouwehand, et al., “Intestinal microbiota is altered in patients with colon cancer and modified by probiotic intervention,” BMJ Open Gastroenterol 4, no. 1 (July 2017): e000145.
57. L. E. Wroblewski, R. M. Peek, K. T. Wilson, “Helicobacter pylori and gastric cancer: factors that modulate disease risk,” Clinical Microbiology Reviews 23, no. 4 (October 2010): 713–39.
58. G. Zeller, J. Tap, A. Y. Voigt, et al., “Potential of fecal microbiota for early-stage detection of colorectal cancer,” Molecular Systems Biology 10, no. 11 (November 2014): 766.
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60. C. J. Tokheim, N. Papadopoulos, K. W. Kinzler, B. Vogelstein, R. Karchin, “Evaluating the evaluation of cancer driver genes,” Proceedings of the National Academy of Sciences of the United States of America 113, no. 50 (December 2016): 14330–35.
61. A. L. Wilson, M. Plebanski, A. N. Stephens, “New trends in anti-cancer therapy: combining conventional chemotherapeutics with novel immunomodulators,” Current Medicinal Chemistry (August 2017).
62. National Cancer Institute, “Human papillomavirus (HPV) vaccines,” November 2, 2016, www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hpv-vaccine-fact-sheet.
63. L. E. Markowitz, S. Hariri, C. Lin, et al., “Reduction in human papillomavirus (HPV) prevalence among young women following HPV vaccine introduction in the United States, National Health and Nutrition Examination Surveys, 2003–2010,” Journal of Infectious Diseases 208, no. 3 (August 2013): 385–93.
64. American Cancer Society, “American Cancer Society recommendations for human papillomavirus (HPV) vaccine use,” July 19, 2016, www.cancer.org/cancer/cancer-causes/infectious-agents/hpv/acs-recommendations-for-hpv-vaccine-use.html.
65. American Cancer Society, “American Cancer Society endorses two-dose regimen for HPV vaccination: guideline updated to reflect recent federal recommendation,” ScienceDaily, February 7, 2017, www.sciencedaily.com/releases/2017/02/170207092811.htm.
66. S. R. Husain, J. Han, P. Au, K. Shannon, R. K. Puri, “Gene therapy for cancer: regulatory considerations for approval,” Cancer Gene Therapy 22, no. 12 (December 2015): 554–63.
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Chapter Five: The Epigenetics of Prevention
1. S. Wu, S. Powers, W. Zhu, Y. A. Hannun, “Substantial contribution of extrinsic risk factors to cancer development,” Nature 529, no. 7584 (January 2016): 43–47.
2. M. Gerlinger, A. J. Rowan, S. Horswell, et al., “Intratumor heterogeneity and branched evolution revealed by multiregion sequencing,” New England Journal of Medicine 366, no. 10 (March 2012): 883–92.
3. D. Ornish, J. Lin, J. M. Chan, et al., “Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study,” The Lancet Oncology 14, no. 11 (October 2013): 1112–20.
4. D. Ornish, M. J. Magbanua, G. Weidner, et al., “Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention,” Proceedings of the National Academy of Sciences of the United States of America 105, no. 24 (June 2008): 8369–74.
5. W. Demark-Wahnefried, E. A. Platz, J. A. Ligibel, et al., “The role of obesity in cancer survival and recurrence,” Cancer Epidemiology, Biomarkers & Prevention 21, no. 8 (June 2012): 1244–59.
6. L. Delgado-Cruzata, W. Zhang, J. A. McDonald, et al., “Dietary modifications, weight loss, and changes in metabolic markers affect global DNA methylation in Hispanic, African American, and Afro-Caribbean breast cancer survivors,” Journal of Nutrition 145, no. 4 (April 2015): 783–90.
7. Z. Li, W. J. Aronson, J. R. Arteaga, et al., “Feasibility of a low-fat/high-fiber diet intervention with soy supplementation in prostate cancer patients after prostatectomy,” European Journal of Clinical Nutrition 62, no. 4 (April 2008): 526–36.
8. S. K. Lutgendorf, K. DeGeest, L. Dahmoush, et al., “Social isolation is associated with elevated tumor norepinephrine in ovarian carcinoma patients,” Brain, Behavior, and Immunity 25, no. 2 (February 2011): 250–55.
9. Y. C. Yang, M. K. McClintock, M. Kozloski, T. Li, “Social isolation and adult mortality: the role of chronic inflammation and sex differences,” Journal of Health and Social Behavior 54, no. 2 (June 2013): 183–203.
10. E. Motevaseli, A. Dianatpour, S. Ghafouri-Fard, “The role of probiotics in cancer treatment: emphasis on their in vivo and in vitro anti-metastatic effects,” International Journal of Molecular Cellular Medicine 6, no. 2 (Spring 2017): 66–76.
11. K. L. Chen, P. Jung, E. Kulkoyluoglu-Cotul, et al., “Impact of diet and nutrition on cancer hallmarks,” Journal of Cancer Prevention & Current Research 7, no. 4 (February 2017): 00240.
12. A. Ruiz-Casado, A. Martin-Ruiz, L. M. Perez, et al., “Exercise and the hallmarks of cancer,” Trends in Cancer 3, no. 6 (June 2017): 423–41.
13. L. Cohen, S. W. Cole, A. K. Sood, et al., “Depressive symptoms and cortisol rhythmicity predict survival in patients with renal cell carcinoma: role of inflammatory signaling,” PloS One 7, no. 8 (August 2012): e42324.
14. J. Lin, J. A. Blalock, M. Chen, et al., “Depressive symptoms and short telomere length are associated with increased mortality in bladder cancer patients,” Cancer Epidemiology, Biomarkers & Prevention 24, no. 2 (February 2015): 336–43.
15. L. E. Carlson, T. L. Beattie, J. Giese-Davis, et al., “Mindfulness-based cancer recovery and supportive-expressive therapy maintain telomere length relative to controls in distressed breast cancer survivors,” Cancer 121, no. 3 (February 2015): 476–84.
16. M. R. Irwin, R. Olmstead, E. C. Breen, et al., “Tai chi, cellular inflammation, and transcriptome dynamics in breast cancer survivors with insomnia: a randomized controlled trial,” Journal of the National Cancer Institute Monographs 2014, no. 50 (November 2014): 295–301.
17. M. K. Bhasin, J. A. Dusek, B. H. Chang, et al., “Relaxation response induces temporal transcriptome changes in energy metabolism, insulin secretion and inflammatory pathways,” PloS One 8, no. 5 (May 2013): e62817.
18. S. W. Cole, “Human social genomics,” Plos Genetics 10, no. 8 (August 2014): e1004601.
19. S. W. Cole, L. C. Hawkley, J. M. Arevalo, et al., “Social regulation of gene expression in human leukocytes,” Genome Biology 8, no. 9 (September 2007): R189.
20. S. W. Cole, M. E. Levine, J. M. Arevalo, et al., “Loneliness, eudaimonia, and the human conserved transcriptional response to adversity,” Psychoneuroendocrinology 6 (December 2015): 11–17.
21. S. W. Cole, G. Conti, J. M. Arevalo, et al., “Transcriptional modulation of the developing immune system early life social adversity,” Proceedings of the National Academy of Sciences of the United States of America 109, no. 50 (December 2012): 20578–83.
22. V. J. Felitti, R. F. Anda, D. Nordenberg, et al., “Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The adverse childhood experiences (ACE) study,” American Journal of Preventive Medicine 14, no. 4 (May 1998): 245–58.
23. M. Kelly-Irving, B. Lepage, D. Dedieu, et al., “Childhood adversity as a risk for cancer: findings from the 1958 British birth cohort study,” BMC Public Health 13 (August 2013): 767.
24. K. Hughes, M. A. Bellis, K. A. Hardcastle, et al., “The effect of multiple adverse childhood experiences on health: a systematic review and meta-analysis,” The Lancet Public Health 2, no. 8 (August 2017): e356–66.
25. M. H. Antoni, S. K. Lutgendorf, B. Blomberg, et al., “Cognitive-behavioral stress management reverses anxiety-related leukocyte transcriptional dynamics,” Biological Psychiatry 71, no. 4 (February 2012a): 366–72.
26. BLUEPRINT Epigenome, “A blueprint of haemtopoietic epigenomes,” 2017, www.blueprint-epigenome.eu.
27. Johns Hopkins University School of Medicine, “Center for the Epigenetics of Common Human Disease,” 2017, www.hopkinsmedicine.org/epigenetics/index.html.
28. Cancer Quest, “Interview with Dr. Jean-Pierre Issa,” 2016, www.cancerquest.org/media-center/cancer-research-interviews/dr-jean-pierre-issa.
29. R. Yehuda, L. M. Bierer, “Transgenerational transmission of cortisol and PTSD risk,” Progress in Brain Research 167 (November 2008): 121–35.
30. R. Yehuda, N. P. Daskalakis, L. M. Bierer, et al., “Holocaust exposure induced intergenerational effects on fkbp5 methylation,” Biological Psychiatry 80, no. 5 (September 2016): 372–80.
31. M. P. Groot, R. Kooke, N. Knoben, et al., “Effects of multi-generational stress exposure and offspring environment on the expression and persistence of transgenerational effects in arabidopsis thaliana,” PloS One 11, no. 3 (March 2016): e0151566.
32. A. Klosin, E. Casas, C. Hidalgo-Carcedo, T. Vavouri, B. Lehner, “Transgenerational transmission of environmental information in C. elegans,” Science 356, no. 6335 (April 2017): 320–23.
33. B. M. Herrera, S. Keildson, C. M. Lindgren, “Genetics and epigenetics of obesity,” Maturitas 69, no. 1 (May 2011): 41–49.
34. M. V. Veenendaal, R. C. Painter, S. R. de Rooij, et al., “Transgenerational effects of prenatal exposure to the 1944–45 Dutch famine,” BJOG: An International Journal of Obstetrics and Gynaecology 120, no. 5 (April 2013): 548–53.
35. E. H. Blackburn, E. S. Epel, “Telomeres and adversity: too toxic to ignore,” Nature 490, no. 7419 (October 2012): 169–71.
36. K. Rogers, “Epigenetics: a turning point in our understanding of heredity,” Scientific American, January 16, 2012, www.blogs.scientificamerican.com/guest-blog/epigenetics-a-turning-point-in-our-understanding-of-heredity/#.
37. American Cancer Society, “DES exposure: questions and answers,” June 10, 2015, www.cancer.org/cancer/cancer-causes/medical-treatments/des-exposure.html.
38. L. Titus-Ernstoff, R. Troisi, E. E. Hatch, et al., “Offspring of women exposed in utero to diethylstilbestrol (DES): a preliminary report of benign and malignant pathology in the third generation,” Epidemiology 19, no. 2 (March 2008): 251–57.
39. M. K. Skinner, M. Manikkam, C. Guerrero-Bosagna, “Epigenetic transgenerational actions of environmental factors in disease etiology,” Trends in Endocrinology and Metabolism 21, no. 4 (April 2010): 214–22.
40. F. Perera, J. Herbstman, “Prenatal environmental exposures, epigenetics, and disease,” Reproductive Toxicology 31, no. 3 (January 2011): 363–73.
41. J. M. Gray, S. Rasanayagam, C. Engel, J. Rizzo, “State of the evidence 2017: an update on the connection between breast cancer and the environment,” Environmental Health 16, no. 1 (September 2017): 94.
42. Z. M. Zhao, B. Zhao, Y. Bai, et al., “Early and multiple origins of metastatic lineages within primary tumors,” Proceedings of the National Academy of Sciences of the United States of America 113, no. 8 (February 2016): 2140–45.
43. Z. Kashef, “Yale study examines evolution of cancer,” YaleNews, February 8, 2016, www.news.yale.edu/2016/02/08/yale-study-examines-evolution-cancer.
Chapter Six: Synergy and the Mix of Six
1. S. W. Cole, A. S. Nagaraja, S. K. Lutgendorf, P. A. Green, A. K. Sood, “Sympathetic nervous system regulation of the tumour microenvironment,” Nature Reviews: Cancer 15, no. 9 (September 2015): 563–72.
2. S. K. Lutgendorf, B. L. Andersen, “Biobehavioral approaches to cancer progression and survival: mechanisms and interventions,” American Psychologist 70, no. 2 (March 2015): 186–97.
3. C. P. Fagundes, K. W. Murdock, D. A. Chirinos, P. A. Green, “Biobehavioral pathways to cancer incidence, progression, and quality of life,” Current Directions in Psychological Science (November 2017).
4. R. J. Davidson, B. S. McEwen, “Social influences on neuroplasticity: stress and interventions to promote well-being,” Nature Neuroscience 15, no. 5 (April 2012): 689–95.
5. S. Sephton, D. Spiegel, “Circadian disruption in cancer: a neuroendocrine-immune pathway from stress to disease?,” Brain, Behavior, and Immunity 17, no. 5 (October 2003): 321–28.
6. M. R. Irwin, “Why sleep is important for health: a psychoneuroimmunology perspective,” Annual Review of Psychology 66, no. 1 (January 2015): 143–72.
7. M. R. Irwin, R. Olmstead, J. E. Carroll, “Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis of cohort studies and experimental sleep deprivation,” Biological Psychiatry 80, no. 1 (July 2016): 40–52.
8. I. M. Lee, E. J. Shiroma, F. Lobelo, et al., “Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy,” The Lancet 380, no. 9838 (July 2012): 219–29.
9. L. Cohen, A. Jefferies, “Comprehensive lifestyle change: harnessing synergy to improve cancer outcomes,” Journal of the National Cancer Institute Monographs, no. 52 (November 2017).
10. D. Romaguera, E. Gracia-Lavedan, A. Molinuevo, et al., “Adherence to nutrition-based cancer prevention guidelines and breast, prostate and colorectal cancer risk in the MCC-Spain case-control study,” International Journal of Cancer 141, no. 1 (July 2017): 83–93.
11. F. Bravi, J. Polesel, W. Garavello, et al., “Adherence to the World Cancer Research Fund/American Institute for Cancer research recommendations and head and neck cancers risk,” Oral Oncology 6 (January 2017): 59–64.
12. A. C. Vergnaud, D. Romaguera, P. H. Peeters, et al., “Adherence to the World Cancer Research Fund/American Institute for Cancer Research guidelines and risk of death in Europe: results from the European Prospective Investigation into nutrition and cancer cohort study,” American Journal of Clinical Nutrition 97, no. 5 (May 2013): 1107–20.
13. B. L. Andersen, W. B. Farrar, D. M. Golden-Kreutz, et al., “Psychological, behavioral, and immune changes after a psychological intervention: a clinical trial,” Journal of Clinical Oncology 22, no. 17 (September 2004): 3570–80.
14. B. L. Andersen, H. C. Yang, W. B. Farrar, et al., “Psychologic intervention improves survival for breast cancer patients: a randomized clinical trial,” Cancer 113, no. 12 (December 2008): 3450–58.
15. B. L. Andersen, L. M. Thornton, C. L. Shapiro, et al., “Biobehavioral, immune, and health benefits following recurrence for psychological intervention participants,” Clinical Cancer Research 16, no. 12 (June 2010): 3270–78.
16. B. L. Andersen, W. B. Farrar, D. Golden-Kreutz, et al., “Distress reduction from a psychological intervention contributes to improved health for cancer patients,” Brain, Behavior, and Immunity 21, no. 7 (October 2007): 953–61.
17. B. L. Andersen, R. A. Shelby, D. M. Golden-Kreutz, “RCT of a psychological intervention for patients with cancer: I. Mechanisms of change,” Journal of Consulting and Clinical Psychology 75, no. 6 (December 2007): 927–38.
18. D. Ornish, G. Weidner, W. R. Fair, et al., “Intensive lifestyle changes may affect the progression of prostate cancer,” Journal of Urology 174, no. 3 (September 2005): 1065–69; discussion 1069–70.
19. D. Ornish, J. Lin, J. M. Chan, et al., “Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study,” The Lancet Oncology 14, no. 11 (October 2013): 1112–20.
20. D. Ornish, M. J. Magbanua, G. Weidner, et al., “Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention,” Proceedings of the National Academy of Sciences of the United States of America 105, no. 24 (June 2008): 8369–74.
21. D. Lemanne, K. I. Block, B. R. Kressel, V. P. Sukhatme, J. D. White, “A case of complete and durable molecular remission of chronic lymphocytic leukemia following treatment with epigallocatechin-3-gallate, an extract of green tea,” Cureus 7, no. 12 (December 2015): e441.
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PART TWO: THE MIX OF SIX
Chapter Seven: The Foundation Is Love and Social Support
1. N. D. Anderson, T. Damianakis, E. Kroger, et al., “The benefits associated with volunteering among seniors: a critical review and recommendations for future research,” Psychological Bulletin 140, no. 6 (November 2014): 1505–33.
2. M. A. Okun, E. W. Yeung, S. Brown, “Volunteering by older adults and risk of mortality: a meta-analysis,” Psychology and Aging 28, no. 2 (June 2013): 564–77.
3. C. E. Jenkinson, A. P. Dickens, K. Jones, et al., “Is volunteering a public health intervention? A systematic review and meta-analysis of the health and survival of volunteers,” BMC Public Health 13, no. 1 (August 2013): 773.
4. L. Ayalon, “Volunteering as a predictor of all-cause mortality: what aspects of volunteering really matter?,” International Psychogeriatrics 20, no. 5 (October 2008): 1000–1013.
5. B. E. Kok, K. A. Coffey, M. A. Cohn, et al., “How positive emotions build physical health: perceived positive social connections account for the upward spiral between positive emotions and vagal tone,” Psychological Science 24, no. 7 (July 2013): 1123–32.
6. J. Dyavanapalli, O. Dergacheva, X. Wang, D. Mendelowitz, “Parasympathetic vagal control of cardiac function,” Current Hypertension Reports 18, no. 3 (March 2016): 22.
7. S. W. Porges, J. A. Doussard-Roosevelt, A. K. Maiti, “Vagal tone and the physiological regulation of emotion,” Monographs of the Society for Research in Child Development 59, no. 2–3 (February 1994): 167–86.
8. L. S. Smith, P. A. Dmochowski, D. W. Muir, B. S. Kisilevsky, “Estimated cardiac vagal tone predicts fetal responses to mother’s and stranger’s voices,” Developmental Psychobiology 49, no. 5 (July 2007): 543–47.
9. J. F. Thayer, S. S. Yamamoto, J. F. Brosschot, “The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors,” International Journal of Cardiology 141, no. 2 (May 2010): 122–31.
10. J. M. Dekker, E. G. Schouten, P. Klootwijk, et al., “Heart rate variability from short electrocardiographic recordings predicts mortality from all causes in middle-aged and elderly men: the Zutphen study,” American Journal of Epidemiology 145, no. 10 (May 1997): 899–908.
11. X. Zhou, Z. Ma, L. Zhang, et al., “Heart rate variability in the prediction of survival in patients with cancer: a systematic review and meta-analysis,” Journal of Psychosomatic Research 89 (October 2016): 20–25.
12. A. Kogan, C. Oveis, E. W. Carr, et al., “Vagal activity is quadratically related to prosocial traits, prosocial emotions, and observer perceptions of prosociality,” Journal of Personality and Social Psychology 107, no. 6 (December 2014): 1051–63.
13. B. H. Gottlieb, E. D. Wachala, “Cancer support groups: a critical review of empirical studies,” Psycho-Oncology 16, no. 5 (May 2007): 379–400.
14. L. M. Hoey, S. C. Ieropoli, V. M. White, M. Jefford, “Systematic review of peer-support programs for people with cancer,” Patient Education and Counseling 70, no. 3 (March 2008): 315–37.
15. B. Nausheen, Y. Gidron, R. Peveler, R. Moss-Morris, “Social support and cancer progression: a systematic review,” Journal of Psychosomatic Research 67, no. 5 (November 2009): 403–15.
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59. S. W. Cole, M. E. Levine, J. M. Arevalo, et al., “Loneliness, eudaimonia, and the human conserved transcriptional response to adversity,” Psychoneuroendocrinology 62 (December 2015): 11–17.
60. G. M. Slavich, S. W. Cole, “The emerging field of human social genomics,” Clinical Psychological Science 1, no. 3 (July 2013): 331–48.
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62. S. W. Cole, “Social regulation of human gene expression: mechanisms and implications for public health,” American Journal of Public Health 103, Supplement 1 (October 2013): S84–92.
63. S. K. Lutgendorf, K. DeGeest, C. Y. Sung, et al., “Depression, social support, and beta-adrenergic transcription control in human ovarian cancer,” Brain, Behavior, and Immunity 23, no. 2 (February 2009): 176–83.
64. S. K. Lutgendorf, P. H. Thaker, J. M. Arevalo, et al., “Biobehavioral modulation of the exosome transcriptome in ovarian carcinoma,” Cancer (November 2017).
65. D. R. Jutagir, B. B. Blomberg, C. S. Carver, et al., “Social well-being is associated with less pro-inflammatory and pro-metastatic leukocyte gene expression in women after surgery for breast cancer,” Breast Cancer Research and Treatment 165, no. 1 (August 2017): 169–80.
66. J. M. Knight, J. D. Rizzo, B. R. Logan, et al., “Low socioeconomic status, adverse gene expression profiles, and clinical outcomes in hematopoietic stem cell transplant recipients,” Clinical Cancer Research 22, no. 1 (January 2016): 69–78.
67. S. W. Cole, L. C. Hawkley, J. M. Arevalo, et al., “Social regulation of gene expression in human leukocytes,” Genome Biology 8, no. 9 (September 2007): R189.
68. I. Barrera, D. Spiegel, “Review of psychotherapeutic interventions on depression in cancer patients and their impact on disease progression,” International Review of Psychiatry 26, no. 1 (February 2014): 31–43.
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76. A. J. Cunningham, “Group psychological therapy: an integral part of care for cancer patients,” Integrative Cancer Therapies 1, no. 1 (March 2002): 67–75; discussion 75.
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The Anticancer Living Guide to Love and Social Support
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Chapter Eight: Stress and Resilience
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61. L. Cohen, S. W. Cole, A. K. Sood, et al., “Depressive symptoms and cortisol rhythmicity predict survival in patients with renal cell carcinoma: role of inflammatory signaling,” PloS One 7, no. 8 (August 2012): e42324.
62. S. W. Cole, M. E. Levine, J. M. Arevalo, et al., “Loneliness, eudaimonia, and the human conserved transcriptional response to adversity,” Psychoneuroendocrinology 62 (December 2015): 11–17.
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The Anticancer Living Guide to Stress Reduction
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3. More about Molly’s Meditation: Molly M. gained tremendous knowledge from the program Alistair Cunningham developed in Toronto, Canada, called the Healing Journey Program. Program material is available online at www.healingjourney.ca. She practices a combination of relaxation, imagery, and meditation that includes calling up her ancestors and enlisting their help to prevent cancer cells from growing and spreading within her body. Molly is quick to point out that her visual imagery—for example, imagining leprechauns (from the lore of her Irish grandmother) cutting the blood supply to every tumor cell, cauterizing the cells, and then corking them so they cannot spread messages to the rest of her body that they need more blood—doesn’t work for everyone.
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Chapter Nine: The Need for Rest and Recovery
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The Anticancer Living Guide to Better Sleep
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Chapter Ten: Moving for Wellness
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7. S. Gujral, H. Aizenstein, C. F. Reynolds, M. A. Butters, K. I. Erickson, “Exercise effects on depression: possible neural mechanisms,” General Hospital Psychiatry 49 (November 2017): 2–10.
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15. U. Ladabaum, A. Mannalithara, P. A. Myer, G. Singh, “Obesity, abdominal obesity, physical activity, and caloric intake in U.S. adults: 1988 to 2010,” American Journal of Medicine 127, no. 8 (August 2014): 717–27.
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18. V. F. Gladwell, D. K. Brown, C. Wood, G. R. Sandercock, J. L. Barton, “The great outdoors: how a green exercise environment can benefit all,” Extreme Physiology & Medicine 2 (January 2013): 3.
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20. B. J. Park, Y. Tsunetsugu, T. Kasetani, T. Kagawa, Y. Miyazaki, “The physiological effects of shinrin-yoku (taking in the forest atmosphere or forest bathing): evidence from field experiments in 24 forests across Japan,” Environmental Health and Preventive Medicine 15, no. 1 (January 2010): 18–26.
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23. Centers for Disease Control and Prevention, “New CDC report: more than 100 million Americans have diabetes or prediabetes,” July 18, 2017, www.cdc.gov/media/releases/2017/p0718-diabetes-report.html.
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30. M. J. Ormsbee, C. M. Prado, J. Z. Ilich, et al., “Osteosarcopenic obesity: the role of bone, muscle, and fat on health,” Journal of Cachexia, Sarcopenia, and Muscle 5, no. 3 (September 2014): 183–92.
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41. K. S. Courneya, D. C. McKenzie, J. R. Mackey, et al., “Effects of exercise dose and type during breast cancer chemotherapy: multicenter randomized trial,” Journal of the National Cancer Institute 105, no. 23 (December 2013): 1821–32.
42. A. S. Betof, C. D. Lascola, D. Weitzel, et al., “Modulation of murine breast tumor vascularity, hypoxia and chemotherapeutic response by exercise,” Journal of the National Cancer Institute 107, no. 5 (May 2015).
43. S. C. Moore, I. M. Lee, E. Weiderpass, et al., “Association of leisure-time physical activity with risk of 26 types of cancer in 1.44 million adults,” Journal of the American Medical Association Internal Medicine 176, no. 6 (June 2016): 816–25.
44. National Cancer Institute, “Physical activity and cancer,” January 27, 2017, www.cancer.gov/about-cancer/causes-prevention/risk/obesity/physical-activity-fact-sheet.
45. K. Y. Wolin, Y. Yan, G. A. Colditz, I. M. Lee, “Physical activity and colon cancer prevention: a meta-analysis,” British Journal of Cancer 100, no. 4 (February 2009): 611–16.
46. American Institute for Cancer Research, “Getting up from your desk can put the ‘breaks’ on cancer,” November 3, 2011, www.aicr.org/press/press-releases/getting-up-from-your-desk.html.
47. Y. Wu, D. Zhang, S. Kang, “Physical activity and risk of breast cancer: a meta-analysis of prospective studies,” Breast Cancer Research and Treatment 137, no. 3 (February 2013): 869–82.
48. A. H. Eliassen, S. E. Hankinson, B. Rosner, M. D. Holmes, W. C. Willett, “Physical activity and risk of breast cancer among postmenopausal women,” Archives of Internal Medicine 170, no. 19 (October 2010): 1758–64.
49. J. S. Hildebrand, S. M. Gapstur, P. T. Campbell, M. M. Gaudet, A. V. Patel, “Recreational physical activity and leisure-time sitting in relation to postmenopausal breast cancer risk,” Cancer Epidemiology, Biomarkers & Prevention 22, no. 10 (October 2013): 1906–12.
50. A. Fournier, G. Dos Santos, G. Guillas, et al., “Recent recreational physical activity and breast cancer risk in postmenopausal women in the E3N cohort,” Cancer Epidemiology, Biomarkers & Prevention 23, no. 9 (September 2014): 1893–1902.
51. D. Schmid, G. Behrens, M. Keimling, et al., “A systematic review and meta-analysis of physical activity and endometrial cancer risk,” European Journal of Epidemiology 30, no. 5 (May 2015): 397–412.
52. M. Du, P. Kraft, A. H. Eliassen, et al., “Physical activity and risk of endometrial adenocarcinoma in the Nurses’ Health Study,” International Journal of Cancer 134, no. 11 (June 2014): 2707–16.
53. C. Friedenreich, A. Cust, P. H. Lahmann, et al., “Physical activity and risk of endometrial cancer: the European prospective investigation into cancer and nutrition,” International Journal of Cancer 121, no. 2 (July 2007): 347–55.
54. K. S. Courneya, C. M. Friedenreich, R. D. Reid, et al., “Predictors of follow-up exercise behavior 6 months after a randomized trial of exercise training during breast cancer chemotherapy,” Breast Cancer Research and Treatment 114, no. 1 (March 2009): 179–87.
55. K. S. Courneya, D. C. McKenzie, J. R. Mackey, et al., “Moderators of the effects of exercise training in breast cancer patients receiving chemotherapy: a randomized controlled trial,” Cancer 112, no. 8 (April 2008): 1845–53.
56. R. Ballard-Barbash, C. M. Friedenreich, K. S. Courneya, et al., “Physical activity, biomarkers, and disease outcomes in cancer survivors: a systematic review,” Journal of the National Cancer Institute 104, no. 11 (June 2012): 815–40.
57. K. M. Mustian, C. M. Alfano, C. Heckler, et al., “Comparison of pharmaceutical, psychological, and exercise treatments for cancer-related fatigue: a meta-analysis,” Journal of the American Medical Association Oncology 3, no. 7 (July 2017): 961–68.
58. M. G. Sweegers, T. M. Altenburg, M. J. Chinapaw, et al., “Which exercise prescriptions improve quality of life and physical function in patients with cancer during and following treatment? A systematic review and meta-analysis of randomised controlled trials,” British Journal of Sports Medicine (September 2017).
59. C. M. Friedenreich, H. K. Neilson, M. S. Farris, K. S. Courneya, “Physical activity and cancer outcomes: a precision medicine approach,” Clinical Cancer Research 22, no. 19 (October 2016): 4766–75.
60. W. Demark-Wahnefried, E. A. Platz, J. A. Ligibel, et al., “The role of obesity in cancer survival and recurrence,” Cancer Epidemiology, Biomarkers & Prevention 21, no. 8 (June 2012): 1244–59.
61. H. Arem, S. C. Moore, Y. Park, et al., “Physical activity and cancer-specific mortality in the NIH-AARP Diet and Health Study cohort,” International Journal of Cancer 135, no. 2 (July 2014): 423–31.
62. S. E. Bonn, A. Sjolander, Y. T. Lagerros, et al., “Physical activity and survival among men diagnosed with prostate cancer,” Cancer Epidemiology, Biomarkers & Prevention 24, no. 1 (January 2015): 57–64.
63. H. Arem, R. M. Pfeiffer, E. A. Engels, et al., “Pre- and postdiagnosis physical activity, television viewing, and mortality among patients with colorectal cancer in the National Institutes of Health-AARP Diet and Health Study,” Journal of Clinical Oncology 33, no. 2 (January 2015): 180–88.
64. M. Fitzmaurice, “Exercising key to cancer battle, world expert tells Ulster University,” December 7, 2015, www.belfastlive.co.uk/news/health/exercising-key-cancer-battle-world-10564610.
65. H. K. Sanoff, A. M. Deal, J. Krishnamurthy, et al., “Effect of cytotoxic chemotherapy on markers of molecular age in patients with breast cancer,” Journal of the National Cancer Institute 106, no. 4 (April 2014): dju057.
66. L. W. Jones, L. A. Habel, E. Weltzien, et al., “Exercise and risk of cardiovascular events in women with nonmetastatic breast cancer,” Journal of Clinical Oncology 34, no. 23 (August 2016): 2743–49.
67. L. W. Jones, D. R. Fels, M. West, et al., “Modulation of circulating angiogenic factors and tumor biology by aerobic training in breast cancer patients receiving neoadjuvant chemotherapy,” Cancer Prevention Research 6, no. 9 (September 2013): 925–37.
68. W. E. Hornsby, P. S. Douglas, M. J. West, et al., “Safety and efficacy of aerobic training in operable breast cancer patients receiving neoadjuvant chemotherapy: a phase ii randomized trial,” Acta Oncologica 53, no. 1 (January 2014): 65–74.
69. J. F. Meneses-Echavez, E. G. Jimenez, J. S. Rio-Valle, et al., “The insulin-like growth factor system is modulated by exercise in breast cancer survivors: a systematic review and meta-analysis,” BMC Cancer 16, no. 1 (August 2016): 682.
70. J. F. Meneses-Echavez, J. E. Correa-Bautista, E. Gonzalez-Jimenez, et al., “The effect of exercise training on mediators of inflammation in breast cancer survivors: a systematic review with meta-analysis,” Cancer Epidemiology, Biomarkers & Prevention 25, no. 7 (July 2016): 1009–17.
71. R. Ballard-Barbash, C. M. Friedenreich, K. S. Courneya, et al., “Physical activity, biomarkers, and disease outcomes in cancer survivors: a systematic review,” Journal of the National Cancer Institute 104, no. 11 (June 2012): 815–40.
72. A. Ruiz-Casado, A. Martin-Ruiz, L. M. Perez, et al., “Exercise and the hallmarks of cancer,” Trends Cancer 3, no. 6 (June 2017): 423–41.
73. G. J. Koelwyn, D. F. Quail, X. Zhang, R. M. White, L. W. Jones, “Exercise-dependent regulation of the tumour microenvironment,” Nature Reviews: Cancer 17, no. 10 (September 2017): 620–32.
74. G. J. Koelwyn, E. Wennerberg, S. Demaria, L. W. Jones, “Exercise in regulation of inflammation-immune axis function in cancer initiation and progression,” Oncology 29, no. 12 (December 2015): 908–20, 922.
75. O. K. Glass, B. A. Inman, G. Broadwater, et al., “Effect of aerobic training on the host systemic milieu in patients with solid tumours: an exploratory correlative study,” British Journal of Cancer 112, no. 5 (March 2015): 825–31.
76. M. J. M. Magbanua, E. L. Richman, E. V. Sosa, et al., “Physical activity and prostate gene expression in men with low risk prostate cancer,” Cancer Causes & Control 25, no. 4 (February 2014): 515–23.
77. M. E. Lindholm, F. Marabita, D. Gomez-Cabrero, et al., “An integrative analysis reveals coordinated reprogramming of the epigenome and the transcriptome in human skeletal muscle after training,” Epigenetics 9, no. 12 (December 2014): 1557–69.
78. K. A. Ashcraft, R. M. Peace, A. S. Betof, M. W. Dewhirst, L. W. Jones, “Efficacy and mechanisms of aerobic exercise on cancer initiation, progression, and metastasis: a critical systematic review of in vivo preclinical data,” Cancer Research 76, no. 14 (July 2016): 4032–50.
79. V. K. Verma, V. Singh, M. P. Singh, S. M. Singh, “Effect of physical exercise on tumor growth regulating factors of tumor microenvironment: Implications in exercise-dependent tumor growth retardation,” Immunopharmacology and Immunotoxicology 31, no. 2 (June 2009): 274–82.
80. L. W. Jones, B. L. Viglianti, J. A. Tashjian, et al., “Effect of aerobic exercise on tumor physiology in an animal model of human breast cancer,” Journal of Applied Physiology 108, no. 2 (February 2010): 343–48.
81. G. J. Koelwyn, D. F. Quail, X. Zhang, R. M. White, L. W. Jones, “Exercise-dependent regulation of the tumour microenvironment,” Nature Reviews: Cancer 17, no. 10 (September 2017): 620–32.
82. Dialogue Blog from the Wilmot Cancer Institute, “Exercise and cancer research: Setting new standards, giving patients control,” June 19, 2017, www.urmc.rochester.edu/cancer-institute/newsroom/dialogue-blog/june-2017/exercise-and-cancerresearch-settingnew-standard.aspx.
83. K. M. Mustian, L. K. Sprod, M. Janelsins, L. J. Peppone, S. Mohile, “Exercise recommendations for cancer-related fatigue, cognitive impairment, sleep problems, depression, pain, anxiety, and physical dysfunction: a review,” Oncolology Hematology Review 8, no. 2 (January 2012): 81–88.
84. K. M. Mustian, J. A. Katula, H. Zhao, “A pilot study to assess the influence of tai chi chuan on functional capacity among breast cancer survivors,” Journal of Supportive Oncology 4, no. 3 (March 2006): 139–45.
85. K. M. Mustian, O. G. Palesh, S. A. Flecksteiner, “Tai chi chuan for breast cancer survivors,” Medicine and Sport Science 52 (May 2008): 209–17.
86. L. K. Sprod, I. D. Fernandez, M. C. Janelsins, et al., “Effects of yoga on cancer-related fatigue and global side-effect burden in older cancer survivors,” Journal of Geriatric Oncology 6, no. 1 (January 2015): 8–14.
87. K. M. Mustian, L. K. Sprod, M. Janelsins, et al., “Multicenter, randomized controlled trial of yoga for sleep quality among cancer survivors,” Journal of Clinical Oncology 31, no. 26 (September 2013): 3233–41.
88. B. Oh, P. N. Butow, B. A. Mullan, et al., “Effect of medical qigong on cognitive function, quality of life, and a biomarker of inflammation in cancer patients: a randomized controlled trial,” Supportive Care in Cancer 20, no. 6 (June 2012): 1235–42.
89. B. Oh, P. Butow, B. Mullan, et al., “A critical review of the effects of medical qigong on quality of life, immune function, and survival in cancer patients,” Integrative Cancer Therapies 11, no. 2 (June 2012): 101–10.
90. K. M. Mustian, L. Peppone, T. V. Darling, et al., “A 4-week home-based aerobic and resistance exercise program during radiation therapy: a pilot randomized clinical trial,” Journal of Supportive Oncology 7, no. 5 (September–October 2009): 158–67.
91. National Comprehensive Cancer Network (NCCN), “Exercising during cancer treatment,” 2017, www.nccn.org/patients/resources/life_with_cancer/exercise.aspx.
92. L. W. Jones, “Precision oncology framework for investigation of exercise as treatment for cancer,” Journal of Clinical Oncology 33, no. 35 (December 2015): 4134–37.
93. D. Cohan, “Foundation for embodied medicine,” 2017, www.embodiedmedicine.org
94. O. H. Zahrt, A. J. Crum, “Perceived physical activity and mortality: evidence from three nationally representative U.S. Samples,” Health Psychology 36, no. 11 (November 2017): 1017–25.
95. D. Buettner, The Blue Zones: 9 Lessons for Living Longer from the People Who’ve Lived the Longest (Washington, D.C.: National Geographic, 2012).
96. American Cancer Society, “ACS guidelines on nutrition and physical activity for cancer prevention,” February 5, 2016, www.cancer.org/healthy/eat-healthy-get-active/acs-guidelines-nutrition-physical-activity-cancer-prevention.html.
97. For a great book on this topic, see G. Reynolds, The First 20 Minutes: Surprising Science Reveals How We Can Exercise Better, Train Smarter, Live Longer (New York: Penguin, 2013).
98. J. B. Gillen, B. J. Martin, M. J. MacInnis, et al., “Twelve weeks of sprint interval training improves indices of cardiometabolic health similar to traditional endurance training despite a five-fold lower exercise volume and time commitment,” PloS One 11, no. 4 (April 2016): e0154075.
99. D. M. Bhammar, S. S. Angadi, G. A. Gaesser, “Effects of fractionized and continuous exercise on 24-h ambulatory blood pressure,” Medicine and Science in Sports and Exercise 44, no. 12 (December 2012): 2270–76.
100. B. M. F. M. Duvivier, N. C. Schaper, M. A. Bremers, et al., “Minimal intensity physical activity (standing and walking) of longer duration improves insulin action and plasma lipids more than shorter periods of moderate to vigorous exercise (cycling) in sedentary subjects when energy expenditure is comparable,” PloS One 8, no. 2 (February 2013): e55542.
101. E. I. Fishman, J. A. Steeves, V. Zipunnikov, et al., “Association between objectively measured physical activity and mortality in nhanes,” Medicine and Science in Sports and Exercise 48, no. 7 (July 2016): 1303–11.
102. L. Liu, Y. Shi, T. Li, et al., “Leisure time physical activity and cancer risk: evaluation of the WHO’s recommendation based on 126 high-quality epidemiological studies,” British Journal of Sports Medicine 50, no. 6 (March 2016): 372.
103. C. M. Phillips, C. B. Dillon, I. J. Perry, “Does replacing sedentary behaviour with light or moderate to vigorous physical activity modulate inflammatory status in adults?,” International Journal of Behavioral Nutrition and Physical Activity 14 (October 2017): 138.
104. H. Arem, S. C. Moore, A. Patel, et al., “Leisure time physical activity and mortality: a detailed pooled analysis of the dose-response relationship,” Journal of the American Medical Association Internal Medicine 175, no. 6 (June 2015): 959–67.
105. G. Canales, “Blue Cure,” July 11, 2013, www.bluecure.org/gabe-canales.
Chapter Eleven: Food as Medicine
1. U.S. Department of Health and Human Services and U.S. Department of Agriculture,” 2015–2020 dietary guidelines for Americans, 8th ed.,” December 2015, www.health.gov/dietaryguidelines/2015/guidelines.
2. M. H. Carlsen, B. L. Halvorsen, K. Holte, et al., “The total antioxidant content of more than 3100 foods, beverages, spices, herbs and supplements used worldwide,” Nutrition Journal 9 (January 2010): 3.
3. M. Greger, “Antioxidant content of 3,139 foods,” www.nutritionfacts.org/video/antioxidant-content-of-3139-foods.
4. G. Diesing, “How a rooftop garden, local farming helped one hospital boost patient satisfaction,” June 6, 2016, www.hhnmag.com/articles/7218-how-a-rooftop-garden-local-farming-helped-one-hospital-boost-patient-satisfaction.
5. D. M. Klurfeld, D. Kritchevsky, “The Western diet: an examination of its relationship with chronic disease,” Journal of the American College of Nutrition 5, no. 5 (January 1986): 477–85.
6. A. Jemal, M. M. Center, C. DeSantis, E. M. Ward, “Global patterns of cancer incidence and mortality rates and trends,” Cancer Epidemiology, Biomarkers & Prevention 19, no. 8 (August 2010): 1893–07.
7. L. Sharp, D. Donnelly, A. Hegarty, et al., “Risk of several cancers is higher in urban areas after adjusting for socioeconomic status. Results from a two-country population-based study of 18 common cancers,” Journal of Urban Health: Bulletin of the New York Academy of Medicine 91, no. 3 (January 2014): 510–25.
8. L. A. Torre, R. L. Siegel, E. M. Ward, A. Jemal, “Global cancer incidence and mortality rates and trends—an update,” Cancer Epidemiology, Biomarkers & Prevention 25, no. 1 (January 2016): 16–27.
9. S. J. D. O’Keefe, J. V. Li, L. Lahti, et al., “Fat, fiber and cancer risk in African Americans and rural Africans,” Nature Communications 6 (April 2015): 6342.
10. Y. Fan, X. Jin, C. Man, Z. Gao, X. Wang, “Meta-analysis of the association between the inflammatory potential of diet and colorectal cancer risk,” Oncotarget 8, no. 35 (August 2017): 59592–600.
11. Human Microbiome Project Consortium, “A framework for human microbiome research,” Nature 486, no. 7402 (June 2012a): 215–21.
12. P. J. Turnbaugh, R. E. Ley, M. Hamady, et al., “The human microbiome project: exploring the microbial part of ourselves in a changing world,” Nature 449, no. 7164 (October 2007): 804.
13. National Human Genome Research Institute, “The Human Genome Project,” October 1, 2015, www.genome.gov/10001772/all-about-the-human-genome-project-hgp.
14. A. B. Hall, A. C. Tolonen, R. J. Xavier, “Human genetic variation and the gut microbiome in disease,” Nature Reviews: Genetics 18, no. 11 (November 2017): 690–99.
15. A. B. Shreiner, J. Y. Kao, V. B. Young, “The gut microbiome in health and in disease,” Current Opinion in Gastroenterology 31, no. 1 (January 2015): 69–75.
16. Institute of Medicine (US) Food Forum, “Influence of the Microbiome on the Metabolism of Diet and Dietary Components,” in The Human Microbiome, Diet, and Health: Workshop Summary (Washington, D.C.: National Academies Press, 2013).
17. W. S. Garrett, “Cancer and the microbiota,” Science 348, no. 6230 (April 2015): 80–86.
18. J. A. Segre, “MICROBIOME. Microbial growth dynamics and human disease,” Science 349, no. 6252 (September 2015): 1058–59.
19. L. Zitvogel, M. Ayyoub, B. Routy, G. Kroemer, “Microbiome and anticancer immunosurveillance,” Cell 165, no. 2 (April 2016): 276–87.
20. R. F. Schwabe, C. Jobin, “The microbiome and cancer,” Nature Reviews: Cancer 13, no. 11 (October 2013): 800–12.
21. More details on the microbiome: In some cases the specific bacterial species are better understood and characterized. For example, in colon cancer patients the bacterial diversity was similar or slightly reduced in cancer patients compared to matched controls, and the composition of the microbiome was commonly driven by high prevalence and levels of fusobacterium and porphyromonas, as well as lower levels of ruminococcus in feces from colon cancer patients. However, because these and other studies are observational studies, the link between the microbiome as a causative factor remains unclear in human studies.
22. R. Francescone, V. Hou, S. I. Grivennikov, “Microbiome, inflammation and cancer,” Cancer Journal 20, no. 3 (May–June 2014): 181–89.
23. S. V. Rajagopala, S. Vashee, L. M. Oldfield, et al., “The human microbiome and cancer,” Cancer Prevention Research 10, no. 4 (April 2017): 226–34.
24. N. Shi, N. Li, X. Duan, H. Niu, “Interaction between the gut microbiome and mucosal immune system,” Military Medical Research 4 (May 2017): 14.
25. Y. Belkaid, Timothy W. Hand, “Role of the microbiota in immunity and inflammation,” Cell 157, no. 1 (March 2014): 121–41.
26. H. J. Wu, E. Wu, “The role of gut microbiota in immune homeostasis and autoimmunity,” Gut Microbes 3, no. 1 (January–February 2012): 4–14.
27. V. Gopalakrishnan, C. N. Spencer, L. Nezi, et al., “Gut microbiome modulates response to anti-PD-1 immunotherapy in melanoma patients,” Science (November 2017).
28. M. Glick-Bauer, M.-C. Yeh, “The health advantage of a vegan diet: exploring the gut microbiota connection,” Nutrients 6, no. 11 (October 2014): 4822–38.
29. J. L. Sonnenburg, F. Backhed, “Diet-microbiota interactions as moderators of human metabolism,” Nature 535, no. 7610 (July 2016): 56–64.
30. V. K. Ridaura, J. J. Faith, F. E. Rey, et al., “Gut microbiota from twins discordant for obesity modulate metabolism in mice,” Science 341, no. 6150 (September 2013): 1241214.
31. D. Servan-Schreiber, Anticancer: A New Way of Life (New York: Viking, 2009).
32. Y. Barak, D. Fridman, “Impact of mediterranean diet on cancer: focused literature review,” Cancer Genomics & Proteomics 14, no. 6 (November–December 2017): 403–8.
33. L. Schwingshackl, C. Schwedhelm, C. Galbete, G. Hoffmann, “Adherence to mediterranean diet and risk of cancer: an updated systematic review and meta-analysis,” Nutrients 9, no. 10 (September 2017).
34. L. Schwingshackl, G. Hoffmann, “Does a Mediterranean-type diet reduce cancer risk?,” Current Nutrition Reports 5 (September 2016): 9–17.
35. H. E. Bloomfield, E. Koeller, N. Greer, et al., “Effects on health outcomes of a Mediterranean diet with no restriction on fat intake: a systematic review and meta-analysis,” Annals of Internal Medicine 165, no. 7 (October 2016): 491–500.
36. M. Dinu, G. Pagliai, A. Casini, F. Sofi, “Mediterranean diet and multiple health outcomes: an umbrella review of meta-analyses of observational studies and randomised trials,” European Journal of Clinical Nutrition (May 2017).
37. Y. S. Aridi, J. L. Walker, O. R. L. Wright, “The association between the Mediterranean dietary pattern and cognitive health: a systematic review,” Nutrients 9, no. 7 (June 2017).
38. M. Filomeno, C. Bosetti, E. Bidoli, et al., “Mediterranean diet and risk of endometrial cancer: a pooled analysis of three Italian case-control studies,” British Journal of Cancer 112, no. 11 (May 2015): 1816–21.
39. P. A. van den Brandt, M. Schulpen, “Mediterranean diet adherence and risk of postmenopausal breast cancer: results of a cohort study and meta-analysis,” International Journal of Cancer 140, no. 10 (May 2017): 2220–31.
40. National Cancer Institute, “Vitamin D and cancer prevention,” October 21, 2013, www.cancer.gov/about-cancer/causes-prevention/risk/diet/vitamin-d-fact-sheet.
41. D. Aune, E. Giovannucci, P. Boffetta, et al., “Fruit and vegetable intake and the risk of cardiovascular disease, total cancer and all-cause mortality—a systematic review and dose-response meta-analysis of prospective studies,” International Journal of Epidemiology 46, no. 3 (June 2017): 1029–56.
42. H. R. Harris, W. C. Willett, R. L. Vaidya, K. B. Michels, “An adolescent and early adulthood dietary pattern associated with inflammation and the incidence of breast cancer,” Cancer Research 77, no. 5 (March 2017): 1179–87.
43. R. Estruch, E. Ros, J. Salas-Salvadó, et al., “Primary prevention of cardiovascular disease with a Mediterranean diet,” New England Journal of Medicine 368, no. 14 (April 2013): 1279–90.
44. E. Toledo, F. B. Hu, R. Estruch, et al., “Effect of the Mediterranean diet on blood pressure in the PREDIMED trial: results from a randomized controlled trial,” BMC Medicine 11 (September 2013): 207.
45. R. Estruch, “Anti-inflammatory effects of the Mediterranean diet: the experience of the PREDIMED study,” Proceedings of the Nutrition Society 69, no. 3 (August 2010): 333–40.
46. J. Salas-Salvado, M. Bullo, N. Babio, et al., “Reduction in the incidence of type 2 diabetes with the Mediterranean diet: results of the PREDIMED-Reus nutrition intervention randomized trial,” Diabetes Care 34, no. 1 (January 2011): 14–19.
47. N. Babio, E. Toledo, R. Estruch, et al., “Mediterranean diets and metabolic syndrome status in the PREDIMED randomized trial,” CMAJ : Canadian Medical Association Journal 186, no. 17 (November 2014): E649–57.
48. E. Toledo, J. Salas-Salvado, C. Donat-Vargas, et al., “Mediterranean diet and invasive breast cancer risk among women at high cardiovascular risk in the PREDIMED trial: a randomized clinical trial,” Journal of the American Medical Association Internal Medicine 175, no. 11 (November 2015): 1752–60.
49. More details on the Mediterranean diet: A placebo-controlled trial published in August 2017 of 10,061 patients with previous myocardial infarction and high C-reactive protein levels found that a drug that blocks inflammation, in this case blocking interleukin-1β—a part of our innate immune system—resulted in fewer cardiovascular events that was driven by reductions in CRP and not changes in lipid levels. Planned secondary analyses also found that cancer mortality was lower in the patients who were getting the anti-inflammatory drug, including reduced incidence of lung cancer and lung-cancer-related deaths. The provocative findings from this trial suggest that inflammation may be a common pathway linked to both cardiovascular disease and cancer. However, fatal infections or sepsis were significantly more common in the drug groups than in the placebo group, a side effect you will not have from eating a Mediterranean diet.
50. M. Yang, S. A. Kenfield, E. L. Van Blarigan, et al., “Dietary patterns after prostate cancer diagnosis in relation to disease-specific and total mortality,” Cancer Prevention Research 8, no. 6 (June 2015): 545–51.
51. M. S. Donaldson, “Nutrition and cancer: a review of the evidence for an anti-cancer diet,” Nutrition Journal 3, no. 1 (October 2004): 19.
52. D. Aune, N. Keum, E. Giovannucci, et al., “Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: systematic review and dose-response meta-analysis of prospective studies,” British Medical Journal 353 (June 2016): i2716.
53. G. Zong, A. Gao, F. B. Hu, Q. Sun, “Whole grain intake and mortality from all causes, cardiovascular disease, and cancer: a meta-analysis of prospective cohort studies,” Circulation 133, no. 24 (June 2016): 2370–80.
54. More details on fiber: A meta-analysis published in 2016 that looked at fourteen long-term studies found that people who ate the most whole grains were 10 percent less likely to die of cancer. For every additional serving of whole grains, their cancer risk declined by an additional 5 percent (G. Zong, A. Gao, F. B. Hu, Q. Sun, “Whole grain intake and mortality from all causes, cardiovascular disease, and cancer: a meta-analysis of prospective cohort studies,” Circulation 133, no. 24 [June 2016]: 2370–80).
The growing international concern about gluten sensitivity and intolerance has blossomed in the past ten years. Almost one in three American consumers now say they hope to cut back on the gluten in their diet. The market has responded to this perceived need with gluten-free food sales that topped $15 billion in 2016. Even products that never had gluten, like potato chips and popcorn, are now advertising their products as “gluten free.” But what is the scientific evidence that gluten is the culprit behind concerns about digestive health?
My Florentine-based colleague Francesco Sofi, who works at the Careggie University Hospital in Florence, Italy, did not want to give up his wheat pasta, so he started researching the effects of ancient wheat compared to modern wheat. In one study, he found that organically grown khorasan wheat resulted in not only improved symptoms in those suffering from irritable bowel disease, but also a marked decrease in the inflammatory profile (F. Sofi, A. Whittaker, A. M. Gori, et al., “Effect of Triticum turgidum subsp. turanicum wheat on irritable bowel syndrome: a double-blinded randomised dietary intervention trial,” British Journal of Nutrition 111, no. 11 [June 14, 2014]: 1992–99). Study participants who ate the ancient grain, which has kernels that contain more proteins, lipids, vitamins, minerals, and amino acids than modern wheat, had reductions in circulating levels of pro-inflammatory cytokines (including IL-6, IL-17, interferon-gama), monocyte chemotactic protein-1, and vascular endothelial growth factor, or VEGF. Inflammation and VEGF are both linked with key cancer hallmarks. In fact, inflammation itself has been labeled a cancer hallmark by some because it is increasingly clear that chronic inflammation increases cancer risk.
Francesco and his colleagues have conducted numerous trials comparing the effects of ancient versus modern wheat using randomized, controlled, blinded, cross-over design clinical trials. They have found benefits of ancient wheat and buckwheat for cardiovascular, diabetes, and inflammatory risk markers in both patient populations and healthy individuals (A. Whittaker, F. Sofi, M. L. Luisi, et al., “An organic khorasan wheat-based replacement diet improves risk profile of patients with acute coronary syndrome: a randomized crossover trial,” Nutrients 7, no. 5 [May 11 2015]: 3401–15; A. Whittaker, M. Dinu, F. Cesari, et al., “A khorasan wheat-based replacement diet improves risk profile of patients with type 2 diabetes mellitus [T2DM]: a randomized crossover trial,” European Journal of Nutrition 56, no. 3 [April 2017]: 1191–1200; A. Sereni, F. Cesari, A. M. Gori, et al., “Cardiovascular benefits from ancient grain bread consumption: findings from a double-blinded randomized crossover intervention trial,” International Journal of Food, Science, and Nutrition 68, no. 1 [February 2017]: 97–103). Even comparing semi-whole-wheat ancient grains, which have a lower gluten content and increased bran and germ components, to semi-whole-wheat modern grains revealed substantially better biological profile for those eating the ancient grains. Ancient grains are naturally more nutritious and do not need the fortification that we see is necessary for modern wheat strains. So, for those who do not want to go totally gluten free but want to reduce the gluten content of your flour, try some of these ancient grains. For those going totally gluten free, you need to know that gluten-free grains are not always fortified with vitamins and iron and they often lack the fiber and phytochemicals of whole grains. It is therefore important to ensure you are getting these important nutrients through other parts of your diet.
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106. More details on sugar: Research points to high sugar levels as the reason for the connection between diabetes and increased cancer risk. In 2013, scientists at the university Rey Juan Carlos in Madrid found that high sugar levels increase the activity of a protein that has been connected to two key cancer hallmarks—cell immortality and cell proliferation. When responding to an uptick in sugars, cells in the intestine secrete a hormone that causes the pancreas to release insulin, which helps the body process sugar into energy or store it for future use. Dr. Garcia Jimenez and his colleagues studied this process at a molecular level. They discovered an unexpected side effect: An increase in ß-catenin (A. Chocarro-Calvo, J. M. Garcia-Martinez, S. Ardila-Gonzalez, A. De la Vieja, C. Garcia-Jimenez, “Glucose-induced beta-catenin acetylation enhances Wnt signaling in cancer,” Molecular Cell 49, no. 3 [February 7, 2013]: 474–86). ß-catenin is a protein known to be a major factor in the development of different cancers. It can make normal cells immortal, an important early step in cancer progression. The accumulation of ß-catenin also leads to cell proliferation. This represents clear evidence of a molecular mechanism through which high blood-sugar levels could predispose the body to cancer, encouraging tumor creation and growth.
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132. More details on red meat: The cancer-causing substances released from cooking red meat include heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH). These compounds are formed when meat is cooked at high temperatures or is charred. Unfortunately, they are also formed when meat is cooked at normal temperatures, including pan fried, broiled, or grilled. However, the longer meat is cooked, the higher the levels of HCA and PAH. These compounds are also present at high levels in grilled chicken. Both HCA and PAH have been classified as mutagens—substances that can initiate the cancer process (carcinogens)—and are known to cause DNA damage (a key cancer hallmark). Rodents fed a diet that included HCAs developed tumors in various organs, including the breast, colon, liver lung, and prostate. Rodents fed PAHs developed leukemia and tumors in their lungs and gastrointestinal tract. Red meat is also a high source of saturated fat, albeit at a higher level in some cuts than in others, and this can have an effect on cancer risk and can modulate hormonal function, relevant for cancers such as breast, endometrial, prostate, and ovarian.
Red meat also contains a chemical called heme—part of the red pigment in the blood, hemoglobin—a source of iron that is broken down in our gut to form a family of chemicals called n-nitroso compounds. N-nitroso compounds damage the cells that line the colon, forcing other cells to replicate more often in order to heal the damage. With excess cell replication comes an increased probability of cell mutations. If cell mutations are left unchecked, through changes in different cancer hallmarks, cancer will form and thrive. In addition, processed red meats contain chemicals that generate n-nitroso compounds, such as nitrite preservatives. When combined with HCA and PAH, these compounds create a perfect storm for cancers to form—HCA and PAH being mutagens and carcinogens combined with n-nitroso compounds cause cell damage and excess cell replication in the colon (all key cancer hallmarks).
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136. More details on meat: Researchers at the University of California, San Diego, may have discovered another key culprit linking red meat and cancer (also via inflammation) (A. N. Samraj, O. M. Pearce, H. Laubli, et al., “A red-meat-derived glycan promotes inflammation and cancer progression,” Proceeding of the National Academy of Sciences of the United States of America 112, no. 2 [January 13, 2015]: 542–47). Pork, beef, and lamb contain a type of sugar that our bodies view as a foreign invader, which sparks an immune response and results in inflammation. In a 2014 study, the California scientists genetically engineered mice so they, like humans, did not naturally produce the sugar in question. The idea was that the mice would view the introduction of the sugar as a foreign substance and mount an inflammatory response. When those genetically altered mice were then fed the foreign sugar in red meats, they developed tumors. This could explain why consuming red meat does not cause disease in other carnivores that have the red-meat sugar in their system. For humans, red meat may not be perceived as a nutrient, but as an invasive compound.
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141. More details on hunger hormones: Evidence suggests that not only are the brain reward circuits modified through exposure to these unhealthy foods that are high in salt, sugar, and fat, but they can also modulate key hormones that regulate our feelings of hunger and satiation—in other words, feeling full. The two key hormones important in this process of appetite stimulation are leptin and ghrelin. Leptin is made by fat cells and decreases our appetite. Ghrelin is released from the stomach and increases appetite through signals to the brain. Ghrelin also plays a role in body weight. Levels of leptin are lower when you’re thin and higher when you’re overweight. However, similar to people with diabetes having insulin resistance, many obese people have built up a resistance to the appetite-suppressing effects of leptin. As a result, the normal regulation of appetite through leptin is not registered and excess stores of fat are built up. People with leptin resistance are not getting appropriate feedback from these key regulatory hormones telling our bodies when to eat and when we are full and should stop eating. High-fat meals have been shown to dysregulate the balance of these hormones. But researchers have shown that either a diet rich in “good” carbohydrates (like whole grains) or a diet high in protein suppresses ghrelin more effectively than a diet high in fat. Sleep deprivation, stress, and depression are also linked with dysregulation of ghrelin and leptin levels. This provides further evidence to avoid the dieting pitfalls and ensure you harness the correct Mix of Six for the ideal and sustainable changes you are seeking.
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162. L. Marseglia, S. Manti, G. D’Angelo, et al., “Oxidative stress in obesity: a critical component in human diseases,” International Journal of Molecular Sciences 16, no. 1 (December 2014): 378–400.
163. J. Luo, R. T. Chlebowski, M. Hendryx, et al., “Intentional weight loss and endometrial cancer risk,” Journal of Clinical Oncology 35, no. 11 (April 2017): 1189–93.
164. J. P. Pierce, L. Natarajan, B. J. Caan, et al., “Influence of a diet very high in vegetables, fruit, and fiber and low in fat on prognosis following treatment for breast cancer: the Women’s Healthy Eating and Living (WHEL) randomized trial,” Journal of the American Medical Association 298, no. 3 (July 2007): 289–98.
165. J. P. Pierce, “Diet and breast cancer prognosis: making sense of the WHEL and WINS trials,” Current Opinion in Obstetrics and Gynecology 21, no. 1 (February 2009): 86–91.
166. More details on the WHEL Study: Another large randomized clinical trial, the Women’s Healthy Eating and Living Study reported mixed results when placing breast cancer survivors on diets high in vegetables and fruits. Benefits were found only for women experiencing hot flashes at study entry. However, one limitation with this study was that the women in the control group were already eating the recommended five servings of fruits and vegetables a day. So everyone in the study was eating a healthy diet from the start. In addition, the principal investigator of the study, John Pierce, told me he and the other researchers were focusing on the wrong target in the WHEL study. At the time, they thought the active mechanism they should target in the women was to increase carotenoids, such as beta-carotene, and these would exert an effect through their antioxidant capacity. In hindsight he said they should have prescribed an anti-inflammatory diet. Adding to this limitation, in order to consume the needed fruits and vegetables in the WHEL study, women were provided with juicers. This could have inadvertently increased overall sugar consumption at the cost of the important fiber in these foods. Although carotenoid levels increased in the intervention compared to the control group, and high carotenoid levels were linked with reduced recurrence of disease, anti-inflammatory markers remained unchanged. Yet inflammation was also a predictor of survival. Targeting increases in carotenoid levels and reducing inflammation may together be the best approach.
167. C. A. Thomson, C. L. Rock, P. A. Thompson, et al., “Vegetable intake is associated with reduced breast cancer recurrence in tamoxifen users: a secondary analysis from the Women’s Healthy Eating and Living Study,” Breast Cancer Research and Treatment 125, no. 2 (January 2011): 519–27.
168. J. P. Pierce, M. L. Stefanick, S. W. Flatt, et al., “Greater survival after breast cancer in physically active women with high vegetable-fruit intake regardless of obesity,” Journal of Clinical Oncology 25, no. 17 (June 2007): 2345–51.
169. C. A. Thomson, T. E. Crane, A. Miller, et al., “A randomized trial of diet and physical activity in women treated for stage II–IV ovarian cancer: rationale and design of the Lifestyle Intervention for Ovarian Cancer Enhanced Survival (LIVES): an NRG Oncology/Gynecologic Oncology Group (GOG-225) Study,” Contemporary Clinical Trials 49 (July 2016): 181–89.
170. More details on diet and cancer: Thomson recently coauthored a study that looked at the link between “energy dense foods” and cancer. High DED (dietary energy density) foods are those that demand a lot of metabolic resources to process but deliver low nutrition. She and her team found that there is a 10 percent increase in cancers typically associated with obesity—in postmenopausal women of normal weight. Low DED foods, on the other hand, deliver high-nutrient content with low calorie demands on the body. Thompson, herself a former cancer patient, relates that these finding are “novel and contrary to our hypothesis and this finding suggests that weight management alone may not protect against obesity-related cancer in women who favor a ‘high-energy-density’ diet.” This may explain why there has been an uptake in the onset of certain cancers (such as breast, prostate, and colorectal) among younger people who may not be eating an anticancer diet.
171. C. A. Thomson, T. E. Crane, D. O. Garcia, et al., “Association between dietary energy density and obesity-associated cancer: results from the Women’s Health Initiative,” Journal of the Academy of Nutrition and Dietetics (August 2017).
172. G. D. Potter, D. J. Skene, J. Arendt, et al., “Circadian rhythm and sleep disruption: causes, metabolic consequences, and countermeasures,” Endocrine Reviews 37, no. 6 (December 2016): 584–608.
173. S. Taheri, L. Lin, D. Austin, T. Young, E. Mignot, “Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index,” PLoS Medicine 1, no. 3 (December 2004): e62.
174. R. Leproult, E. Van Cauter, “Role of sleep and sleep loss in hormonal release and metabolism,” Endocrine Development 17 (November 2010): 11–21.
175. F.-P. J. Martin, S. Rezzi, E. Peré-Trepat, et al., “Metabolic effects of dark chocolate consumption on energy, gut microbiota, and stress-related metabolism in free-living subjects,” Journal of Proteome Research 8, no. 12 (December 2009): 5568–79.
176. J. K. Srivastava, E. Shankar, S. Gupta, “Chamomile: A herbal medicine of the past with bright future,” Molecular Medicine Reports 3, no. 6 (November 2010): 895–901.
177. R. S. Thompson, R. Roller, A. Mika, et al., “Dietary prebiotics and bioactive milk fractions improve NREM sleep, enhance REM sleep rebound and attenuate the stress-induced decrease in diurnal temperature and gut microbial alpha diversity,” Frontiers in Behavioral Neuroscience 10 (January 2017).
178. L. Sominsky, S. J. Spencer, “Eating behavior and stress: a pathway to obesity,” Frontiers in Psychology 5 (May 2014): 434.
179. K. Aschbacher, S. Kornfeld, M. Picard, et al., “Chronic stress increases vulnerability to diet-related abdominal fat, oxidative stress, and metabolic risk,” Psychoneuroendocrinology 46 (August 2014): 14–22.
180. J. A. Foster, L. Rinaman, J. F. Cryan, “Stress & the gut-brain axis: regulation by the microbiome,” Neurobiology of Stress (March 2017).
181. M. Zhang, J. Huang, X. Xie, C. D. Holman, “Dietary intakes of mushrooms and green tea combine to reduce the risk of breast cancer in Chinese women,” International Journal of Cancer 124, no. 6 (March 2009): 1404–08.
182. P. Ghadirian, S. Narod, E. Fafard, et al., “Breast cancer risk in relation to the joint effect of BRCA mutations and diet diversity,” Breast Cancer Research and Treatment 117, no. 2 (September 2009): 417–22.
183. P. Maas, M. Barrdahl, A. D. Joshi, et al., “Breast cancer risk from modifiable and nonmodifiable risk factors among white women in the United States,” Journal of the American Medical Association Oncology 2, no. 10 (October 2016): 1295–1302.
184. More details on diet-gene interaction: In a 2009 study of French-Canadian women who had BRCA mutations, researchers found significantly reduced risk of breast cancer in women who ate the greatest variety of vegetables (P. Ghadirian, S. Narod, E. Fafard, et al., “Breast cancer risk in relation to the joint effect of BRCA mutations and diet diversity,” Breast Cancer Research and Treatment 117, no. 2 [September 2009]: 417–22). A 2013 study of Korean women with the BRCA mutation confirmed the association between vegetable variety and lower risk and also found that soy consumption reduced breast cancer risk, regardless of whether women had the genetic mutation (K. P. Ko, S. W. Kim, S. H. Ma, et al., “Dietary intake and breast cancer among carriers and noncarriers of BRCA mutations in the Korean Hereditary Breast Cancer Study,” American Journal of Clinical Nutrition 98, no. 6 [December 2013]: 1493–1501). Meanwhile, a cohort of men who were at a high risk of prostate cancer due to a genetic mutation (five times more likely than the general population) were able to neutralize their genetic risk by consuming fish on a regular basis (M. Hedelin, E. T. Chang, F. Wiklund, et al., “Association of frequent consumption of fatty fish with prostate cancer risk is modified by COX-2 polymorphism,” International Journal of Cancer 120, no. 2 [January 15, 2007]: 398–405). More recently, a paper in the journal of the American Medical Association examined the contribution of both nonmodifiable and modifiable risk factors for breast cancer. The nonmodifiable factors included gene-related mutations as assessed by a polygenic risk score (PRS) and other nonmodifiable risk factors including family history, age at first birth, parity, age at menarche, height, menopausal status, and age at menopause. The modifiable risk factors included body mass index, hormone therapy use, level of alcohol consumption, and smoking status. For women in the highest decile of risk owing to nonmodifiable factors, those who had low BMI, did not drink or smoke, and did not use hormone therapy had a breast cancer risk comparable to an average woman in the general population (Maas, M. Barrdahl, A. D. Joshi, et al., “Breast cancer risk from modifiable and nonmodifiable risk factors among white women in the United States,” Journal of the American Medical Association Oncology 2, no. 10 [October 2016]: 1295–1302). This suggests that nonmodifiable risk factors such as cancer-specific gene mutations and other demographic factors can be modulated through lifestyle factors.
The Anticancer Living Guide to Nutrition
1. The Full Yield Inc., “The Full Yield,” 2017, www.thefullyield.com.
2. Food and Agriculture Organization of the United Nations, “Food-based dietary guidelines—Japan,” 2010, www.fao.org/nutrition/education/food-based-dietary-guidelines/regions/countries/japan/en.
3. G. Zong, A. Gao, F. B. Hu, Q. Sun, “Whole grain intake and mortality from all causes, cardiovascular disease, and cancer: a meta-analysis of prospective cohort studies,” Circulation 133, no. 24 (June 2016): 2370–80.
4. P. Knekt, J. Kumpulainen, R. Jarvinen, et al., “Flavonoid intake and risk of chronic diseases,” American Journal of Clinical Nutrition 76, no. 3 (September 2002): 560–68.
5. E. Moghaddam, J. A. Vogt, T. M. Wolever, “The effects of fat and protein on glycemic responses in nondiabetic humans vary with waist circumference, fasting plasma insulin, and dietary fiber intake,” Journal of Nutrition 136, no. 10 (October 2006): 2506–11.
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8. C. Geisler, C. M. Prado, M. J. Müller, “Inadequacy of body weight-based recommendations for individual protein intake—lessons from body composition analysis,” Nutrients 9, no. 1 (December 2017): 23.
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10. S. Ahmed, N. H. Othman, “The anti-cancer effects of Tualang honey in modulating breast carcinogenesis: an experimental animal study,” BMC Complementary and Alternative Medicine 17, no. 1 (April 2017): 208.
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12. R. J. Johnson, M. S. Segal, Y. Sautin, et al., “Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease,” American Journal of Clinical Nutrition 86, no. 4 (October 2007): 899–906.
13. A. Bordoni, F. Danesi, D. Dardevet, et al., “Dairy products and inflammation: a review of the clinical evidence,” Critical Reviews in Food Science and Nutrition 57, no. 12 (August 2017): 2497–2525.
14. Y. Song, J. E. Chavarro, Y. Cao, et al., “Whole milk intake is associated with prostate-cancer-specific mortality among U.S. male physicians,” Journal of Nutrition 143, no. 2 (February 2013): 189–96.
15. K. L. Watson, L. Stalker, R. A. Jones, R. A. Moorehead, “High levels of dietary soy decrease mammary tumor latency and increase incidence in MTB-IGFIR transgenic mice,” BMC Cancer 15, (February 2015): 37.
16. S. J. Nechuta, B. J. Caan, W. Y. Chen, et al., “Soy food intake after diagnosis of breast cancer and survival: an in-depth analysis of combined evidence from cohort studies of U.S. and Chinese women,” American Journal of Clinical Nutrition 96, no. 1 (July 2012): 123–32.
17. A. Seow, W. T. Poh, M. Teh, et al., “Diet, reproductive factors and lung cancer risk among Chinese women in Singapore: evidence for a protective effect of soy in nonsmokers,” International Journal of Cancer 97, no. 3 (January 2002): 365–71.
18. K. Dechering, C. Boersma, S. Mosselman, “Estrogen receptors alpha and beta: two receptors of a kind?,” Current Medicinal Chemistry 7, no. 5 (May 2000): 561–76.
19. S. Ali, R. C. Coombes, “Estrogen receptor alpha in human breast cancer: occurrence and significance,” Journal of Mammary Gland Biology and Neoplasia 5, no. 3 (July 2000): 271–81.
20. D. M. Harris, E. Besselink, S. M. Henning, V. L. Go, D. Heber, “Phytoestrogens induce differential estrogen receptor alpha- or beta-mediated responses in transfected breast cancer cells,” Experimental Biology and Medicine 230, no. 8 (September 2005): 558–68.
21. S. Ziaei, R. Halaby, “Dietary isoflavones and breast cancer risk,” Medicines 4, no. 2 (April 2017): 18.
22. F. F. Zhang, D. E. Haslam, M. B. Terry, et al., “Dietary isoflavone intake and all-cause mortality in breast cancer survivors: the breast cancer family registry,” Cancer 123, no. 11 (June 2017): 2070–79.
23. S. Simon, “How your diet may affect your risk of breast cancer,” American Cancer Society, October 25, 2017, www.cancer.org/latest-news/how-your-diet-may-affect-your-risk-of-breast-cancer.html.
24. U.S. Department of Health and Human Services, “14th report on carcinogens,” 2016, www.ntp.niehs.nih.gov/pubhealth/roc/index-1.html#toc1.
25. D. E. Nelson, D. W. Jarman, J. Rehm, et al., “Alcohol-attributable cancer deaths and years of potential life lost in the United States,” American Journal of Public Health 103, no. 4 (April 2013): 641–48.
26. N. K. LoConte, A. M. Brewster, J. S. Kaur, J. K. Merrill, A. J. Alberg, “Alcohol and cancer: a statement of the American Society of Clinical Oncology,” Journal of Clinical Oncology (November 2017): JCO2017761155.
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28. B. M. Popkin, K. E. D’Anci, I. H. Rosenberg, “Water, hydration, and health,” Nutrition Reviews 68, no. 8 (August 2010): 439–58.
29. E. T. Perrier, E. C. Johnson, A. L. McKenzie, L. A. Ellis, L. E. Armstrong, “Urine colour change as an indicator of change in daily water intake: a quantitative analysis,” European Journal of Nutrition 55, no. 5 (August 2016): 1943–49.
30. National Cancer Institute, “Tea and cancer prevention,” November 17, 2010, www.cancer.gov/about-cancer/causes-prevention/risk/diet/tea-fact-sheet.
31. About Herbs, “Green tea,” August 16, 2017, www.mskcc.org/cancer-care/integrative-medicine/herbs/green-tea.
32. Men’s Health, “Which bottled green tea packs the most nutritional punch?,” October 5, 2010, www.menshealth.com/nutrition/best-green-tea.
33. S. Caini, S. Cattaruzza, B. Bendinelli, et al., “Coffee, tea and caffeine intake and the risk of non-melanoma skin cancer: a review of the literature and meta-analysis,” European Journal of Nutrition 56, no. 1 (February 2017): 1–12.
34. D. Loomis, K. Z. Guyton, Y. Grosse, et al., “Carcinogenicity of drinking coffee, mate, and very hot beverages,” The Lancet Oncology 17, no. 7 (July 2016): 877–78.
Chapter Twelve: The Environment and the Quest for Health
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4. L. B. McKenzie, N. Ahir, U. Stolz, N. G. Nelson, “Household cleaning product-related injuries treated in U.S. emergency departments in 1990–2006,” Pediatrics 126, no. 3 (September 2010): 509–16.
5. Q. Di, Y. Wang, A. Zanobetti, et al., “Air pollution and mortality in the Medicare population,” New England Journal of Medicine 376, no. 26 (June 2017): 2513–22.
6. Y. Horii, K. Kannan, “Survey of organosilicone compounds, including cyclic and linear siloxanes, in personal care and household products,” Archives of Environmental Contamination and Toxicology 55, no. 4 (November 2008): 701–10.
7. F. A. Caliman, M. Gavrilescu, “Pharmaceuticals, personal care products and endocrine disrupting agents in the environment—a review,” CLEAN–Soil, Air, Water 37, no. 4–5 (April 2009): 277–303.
8. S. I. Korfali, R. Sabra, M. Jurdi, R. I. Taleb, “Assessment of toxic metals and phthalates in children’s toys and clays,” Archives of Environmental Contamination and Toxicology 65, no. 3 (October 2013): 368–81.
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18. Centers for Disease Control and Prevention, “World Trade Center Health Program—Program at a Glance,” Centers for Disease Control and Prevention, 2016d.
19. Ibid., 2017e.
20. P. J. Lioy, C. P. Weisel, J. R. Millette, et al., “Characterization of the dust/smoke aerosol that settled east of the World Trade Center (WTC) in lower Manhattan after the collapse of the WTC 11 September 2001,” Environmental Health Perspectives 110, no. 7 (July 2002): 703–14.
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22. M. Singer, “Down cancer alley: the lived experience of health and environmental suffering in Louisiana’s chemical corridor,” Medical Anthropology Quarterly 25, no. 2 (June 2011): 141–63.
23. L. Suarez, J. Martin, “Primary liver cancer mortality and incidence in Texas Mexican Americans, 1969–80,” American Journal of Public Health 77, no. 5 (May 1987): 631–33.
24. A. Kirpich, E. Leary, “Superfund locations and potential associations with cancer incidence in Florida,” Statistics and Public Policy 4, no. 1 (December 2017): 1–9.
25. Environmental Working Group, “About Us,” 2017, www.ewg.org/about-us-#.Wnir2LynGUK./
26. A. Formuzis, “Chemical reform law falls short in protecting public health, environment,” May 24, 2016, www.ewg.org/release/chemical-reform-law-falls-short-protecting-public-health-environment-.Wg3u0KIiVpu.
27. J. LaDou, B. Castleman, A. Frank, et al., “The case for a global ban on asbestos,” Environmental Health Perspectives 118, no. 7 (July 2010): 897–901.
28. J. A. Swenberg, B. C. Moeller, K. Lu, et al., “Formaldehyde carcinogenicity research: 30 years and counting for mode of action, epidemiology, and cancer risk assessment,” Toxicologic Pathology 41, no. 2 (February 2013): 181–89.
29. F. Suja, B. K. Pramanik, S. M. Zain, “Contamination, bioaccumulation and toxic effects of perfluorinated chemicals (PFCS) in the water environment: a review paper,” Water Science and Technology 60, no. 6 (September 2009): 1533–44.
30. A. Blum, B. N. Ames, “Flame-retardant additives as possible cancer hazards,” Science 195, no. 4273 (January 1977): 17–23.
31. K. Mulder, M. Knot, “PVC plastic: a history of systems development and entrenchment,” Technology in Society 23, no. 2 (April 2001): 265–86.
32. Office of Environmental Health Hazard Assessment, “Bisphenol-A listed as known to the state of California to cause reproductive toxicity,” May 11, 2015, www.oehha.ca.gov/proposition-65/crnr/bisphenol-listed-known-state-california-cause-reproductive-toxicity.
33. A. Miodovnik, S. M. Engel, C. Zhu, et al., “Endocrine disruptors and childhood social impairment,” Neurotoxicology 32, no. 2 (March 2011): 261–67.
34. C. Casals-Casas, B. Desvergne, “Endocrine disruptors: from endocrine to metabolic disruption,” Annual Review of Physiology 73 (November 2011): 135–62.
35. M. I. Cuomo, A World Without Cancer: The Making of a New Cure and the Real Promise of Prevention (New York: Rodale, 2012).
36. E. Swedenborg, J. Ruegg, S. Makela, I. Pongratz, “Endocrine disruptive chemicals: mechanisms of action and involvement in metabolic disorders,” Journal of Molecular Endocrinology 43, no. 1 (July 2009): 1–10.
37. J. M. Gray, S. Rasanayagam, C. Engel, J. Rizzo, “State of the evidence 2017: an update on the connection between breast cancer and the environment,” Environmental Health 16, no. 1 (September 2017): 94.
38. P. D. Darbre, P. W. Harvey, “Parabens can enable hallmarks and characteristics of cancer in human breast epithelial cells: a review of the literature with reference to new exposure data and regulatory status,” Journal of Applied Toxicology 34, no. 9 (September 2014): 925–38.
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40. Environmental Protection Agency, “Endocrine disruption,” November 22, 2017, www.epa.gov/endocrine-disruption.
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42. M. S. Wolff, S. L. Teitelbaum, K. McGovern, et al., “Environmental phenols and pubertal development in girls,” Environment International 84 (November 2015): 174–80.
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44. M. E. Herman-Giddens, J. Steffes, D. Harris, et al., “Secondary sexual characteristics in boys: data from the pediatric research in office settings network,” Pediatrics 130, no. 5 (November 2012): e1058–68.
45. M. E. Herman-Giddens, L. Wang, G. Koch, “Secondary sexual characteristics in boys: estimates from the National Health and Nutrition Examination Survey III, 1988–1994,” Archives of Pediatrics and Adolescent Medicine 155, no. 9 (September 2001): 1022–28.
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48. C. Bonilla, S. J. Lewis, R. M. Martin, et al., “Pubertal development and prostate cancer risk: Mendelian randomization study in a population-based cohort,” BMC Medicine 14 (April 2016): 66.
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52. Environmental Working Group, “Teen girls’ body burden of hormone-altering cosmetics chemicals,” September 24, 2008, www.ewg.org/research/teen-girls-body-burden-hormone-altering-cosmetics-chemicals.Wg33jlUrJQJ.
53. P. J. Lioy, R. Hauser, C. Gennings, et al., “Assessment of phthalates/phthalate alternatives in children’s toys and childcare articles: review of the report including conclusions and recommendation of the Chronic Hazard Advisory Panel of the Consumer Product Safety Commission,” Journal of Exposure Science & Environmental Epidemiology 25, no. 4 (July–August 2015): 343–53.
54. M. T. Dinwiddie, P. D. Terry, J. Chen, “Recent evidence regarding triclosan and cancer risk,” International Journal of Environmental Research and Public Health 11, no. 2 (February 2014): 2209–17.
55. C. O’Neil, “Organic imports continue to rise alongside organic demand, research shows,” October 25, 2017, www.ewg.org/agmag/2017/10/organic-imports-continue-rise-alongside-organic-demand-research-shows-.Wg36zKIiVps.
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58. H. Malcolm, “Subway: ‘Yoga mat’ chemical almost out of bread,” April 11, 2014, www.usatoday.com/story/money/business/2014/04/11/subway-yoga-mat-chemical-almost-out-of-bread/7587787.
59. The Office of Environmental Health Hazard Assessment, “Notice of amendment of text Title 27, California Code of Regulations amendment of Section 25705 Specific Regulatory Levels: no significant risk levels 4-methylimidazole (4-MEI),” February 8, 2012, www.oehha.ca.gov/proposition-65/crnr/notice-amendment-text-title-27-california-code-regulations-amendment-section.
60. S. R. Lara, “Governor Brown signs Cleaning Product Right to Know Act to create first-in-nation label law for consumers,” October 15, 2017, www.sd33.senate.ca.gov/news/2017-10-15-governor-brown-signs-cleaning-product-right-know-act-create-first-nation-label-law.
61. Governor Andrew M. Cuomo, “Governor Cuomo announces new regulations to require disclosure of chemicals in household cleaning products,” April 25, 2017, www.governor.ny.gov/news/governor-cuomo-announces-new-regulations-require-disclosure-chemicals-household-cleaning.
62. SC Johson Press Room, “SC Johnson introduces industry-first 100 percent fragrance transparency with new Glade® Fresh Citrus Blossoms Collection,” February 11, 2016, www.scjohnson.com/en/press-room/press-releases/02-11-2016/sc-johnson-introduces-industry-first-100-percent-fragrance-transparency-with-new-glade-fresh-citrus-blossoms-collection.aspx.
63. Unilever, “What is Smartlabel™?,” 2017, www.unileverusa.com/brands/smartlabel.
64. Procter & Gamble, “What are preservatives,” 2017, www.us.pg.com/our-brands/product-safety/ingredient-safety/preservatives.
65. Campbell’s, “Campbell to remove BPA from packaging by mid-2017,” March 28, 2016, www.campbellsoupcompany.com/newsroom/press-releases/campbell-to-remove-bpa-from-packaging-by-mid-2017.
66. Getting to Know Cancer, “Assessing the carcinogenic potential of low dose exposures to chemical mixtures in the environment,” 2017, www.gettingtoknowcancer.org/taskforce_environment.php.
67. Getting to Know Cancer, “The Halifax Project,” September 20, 2016, www.gettingtoknowcancer.org/.
68. T. B. Hayes, V. Khoury, A. Narayan, et al., “Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis),” Proceedings of the National Academy of Sciences of the United States of America 107, no. 10 (March 2010): 4612–17.
69. C. Cox, “Atrazine: toxicology,” Journal of Pesticide Reform 21, no. 2 (Summer 2001a): 12–20.
70. A. Dorsey, “Toxicological profile for atrazine,” Agency for Toxic Substances and Disease Registry, January 21, 2015, www.atsdr.cdc.gov/toxprofiles/tp.asp?id=338&tid=59.
71. K. Hu, Y. Tian, Y. Du, et al., “Atrazine promotes RM1 prostate cancer cell proliferation by activating STAT3 signaling,” International Journal of Oncology 48, no. 5 (May 2016): 2166–74.
72. Anticancer Lifestyle Program, “Select comments from course participants,” 2017, www.anticancerlifestyle.org/testimonials/page/4.
73. M. Hanna-Attisha, J. LaChance, R. C. Sadler, A. Champney Schnepp, “Elevated blood lead levels in children associated with the Flint drinking water crisis: a spatial analysis of risk and public health response,” American Journal of Public Health 106, no. 2 (February 2016): 283–90.
74. Environmental Working Group, “Hidden carcinogen taints tap water, consumer products nationwide,” September 6, 2017, www.ewg.org/release/hidden-carcinogen-taints-tap-water-consumer-products-nationwide-.Wign501TEdU.
75. J. E. Cooper, E. L. Kendig, S. M. Belcher, “Assessment of bisphenol A released from reusable plastic, aluminium and stainless steel water bottles,” Chemosphere 85, no. 6 (October 2011): 943–47.
76. S. Eladak, T. Grisin, D. Moison, et al., “A new chapter in the bisphenol A story: bisphenol S and bisphenol F are not safe alternatives to this compound,” Fertility and Sterility 103, no. 1 (January 2015): 11–21.
77. R. Vinas, C. S. Watson, “Bisphenol S disrupts estradiol-induced nongenomic signaling in a rat pituitary cell line: effects on cell functions,” Environmental Health Perspectives 121, no. 3 (March 2013): 352–58.
78. A. Vaiserman, “Early-life exposure to endocrine disrupting chemicals and later-life health outcomes: an epigenetic bridge?,” Aging and Disease 5, no. 6 (December 2014): 419–29.
79. L. Trasande, A. J. Spanier, S. Sathyanarayana, T. M. Attina, J. Blustein, “Urinary phthalates and increased insulin resistance in adolescents,” Pediatrics 132, no. 3 (September 2013): e646–55.
80. P. Mirmira, C. Evans-Molina, “Bisphenol A, obesity, and type 2 diabetes mellitus: Genuine concern or unnecessary preoccupation?,” Translational Research: The Journal of Laboratory and Clinical Medicine 164, no. 1 (July 2014): 13–21.
81. F. S. Vom Saal, S. C. Nagel, B. L. Coe, B. M. Angle, J. A. Taylor, “The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity,” Molecular and Cellular Endocrinology 354, no. 1–2 (May 2012): 74–84.
82. F. Grun, B. Blumberg, “Endocrine disrupters as obesogens,” Molecular and Cellular Endocrinology 304, no. 1–2 (May 2009): 19–29.
83. H. A. Beydoun, M. A. Beydoun, H. A. Jeng, A. B. Zonderman, S. M. Eid, “Bisphenol-A and sleep adequacy among adults in the National Health and Nutrition Examination Surveys,” Sleep 39, no. 2 (February 2016): 467–76.
84. S. A. Johnson, M. S. Painter, A. B. Javurek, et al., “Sex-dependent effects of developmental exposure to bisphenol A and ethinyl estradiol on metabolic parameters and voluntary physical activity,” Journal of Developmental Origins of Health and Disease 6, no. 6 (December 2015): 539–52.
The Anticancer Living Guide to Detoxify Your Environment
1. M. Derudi, S. Gelosa, A. Sliepcevich, et al., “Emission of air pollutants from burning candles with different composition in indoor environments,” Environmental Science and Pollution Research International 21, no. 6 (March 2014): 4320–30.
2. Centers for Disease Control and Prevention, “Occupational cancer,” April 24, 2017, www.cdc.gov/niosh/topics/cancer/npotocca.html.
3. X. Zhang, S. K. Brar, S. Yan, R. D. Tyagi, R. Y. Surampalli, “Fate and transport of fragrance materials in principal environmental sinks,” Chemosphere 93, no. 6 (October 2013): 857–69.
4. United States Environmental Protection Agency, “Volatile organic compounds’ impact on indoor air quality,” 2017, www.epa.gov/indoor-air-quality-iaq/volatile-organic-compounds-impact-indoor-air-quality.
5. R. A. Rudel, J. M. Ackerman, K. R. Attfield, J. G. Brody, “New exposure biomarkers as tools for breast cancer epidemiology, biomonitoring, and prevention: a systematic approach based on animal evidence,” Environmental Health Perspectives 122, no. 9 (September 2014): 881–95.
6. Environmental Working Group, “EWG’s healthy home tips: tip 7—filter your tap water,” 2017, www.ewg.org/research/healthy-home-tips/tip-7-filter-your-tap-water-filter.
7. Environmental Working Group, “EWG’s updated water filter buying guide,” 2017, www.ewg.org/tapwater/water-filter-guide.php-.Wg4Ou1UrJQJ.
8. Environmental Working Group, “EWG’s 2017 Shopper’s Guide to Pesticides in Produce™,” 2017, https://www.ewg.org/foodnews/dirty_dozen_list.php-.Wg4PI1UrJQI.
9. International Agency for Research on Cancer, “IARC classifies radiofrequency electromagnetic fields as possibly carcinogenic to humans,” May 31, 2011, www.iarc.fr/en/media-centre/pr/2011/pdfs/pr208_E.pdf.
10. L. Kheifets, M. Repacholi, R. Saunders, E. van Deventer, “The sensitivity of children to electromagnetic fields,” Pediatrics 116, no. 2 (August 2005): e303–13.
11. J. Schüz, “Exposure to electromagnetic fields and cancer: the epidemiological evidence,” General Assembly and Scientific Symposium, 2011 XXXth URSI, 2011.
12. M. Gutierrez, “New records show how state reworked secret cell phone warnings,” San Francisco Chronicle, May 19, 2017, www.sfchronicle.com/health/article/New-records-show-how-state-reworked-secret-cell-11160254.php.
13. California Department of Public Health, “Cell phones and health,” California Department of Public Health, April 2014, www.sfchronicle.com/file/198/6/1986-CellPhones 1-26-15.pdf.
14. N. R. Council, Review of the Environmental Protection Agency’s Draft IRIS Assessment of Tetrachloroethylene (Washington, D.C.: National Academies Press, 2010).
15. E. Hartman, “The messy truth about dry cleaning,” Washington Post, August 10, 2008, www.washingtonpost.com/wp-dyn/content/article/2008/08/07/AR2008080 702759.html.
16. U.S. Environmental Protection Agency, “Reducing air pollution from dry cleaning operations,” September 12, 2005, www.epa.gov/sites/production/files/2017-06/documents/drycleaners_comm_info.pdf.
17. U.S. Environmental Protection Agency, “Surfactant enhancement of liquid C02 for surface cleaning,” May 13, 2003, www.cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryID=56445.
18. R. Gottlieb, L. Bechtel, J. Goodheart, P. Sinsheimer, C. Tranby, “Final report: evaluation and demonstration of wet cleaning alternatives to perchloroethylene-based garment care,” 1997, www.cfpub.epa.gov/ncer_abstracts/index.cfm/fuseaction/display.highlight/abstract/945/report/F.
Concluding Thoughts
1. American Institute for Cancer Research, “Recommendations for cancer prevention,” 2017, www.aicr.org/reduce-your-cancer-risk/recommendations-for-cancer-prevention.
2. B. Arun, T. Austin, G. V. Babiera, et al., “A comprehensive lifestyle randomized clinical trial: design and initial patient experience,” Integrative Cancer Therapies 16, no. 1 (March 2017): 3–20.
Appendix A: The Cancer Hallmarks Explained
1. D. Hanahan, R. A. Weinberg, “The hallmarks of cancer,” Cell 100, no. 1 (January 2000): 57–70.
2. D. Hanahan, R. A. Weinberg, “Hallmarks of cancer: the next generation,” Cell 144, no. 5 (March 2011): 646–74.
Appendix B: Eating by Food Groups—A New Pattern
1. H. L. Nicastro, S. A. Ross, J. A. Milner, “Garlic and onions: their cancer prevention properties,” Cancer Prevention Research 8, no. 3 (March 2015): 181–89.
2. D. Boivin, S. Lamy, S. Lord-Dufour, et al., “Antiproliferative and antioxidant activities of common vegetables: a comparative study,” Food Chemistry 112, no. 2 (January 2009): 374–80.
3. A. Sengupta, S. Ghosh, S. Bhattacharjee, “Allium vegetables in cancer prevention: an overview,” Asian Pacific Journal of Cancer Prevention 5, no. 3 (July–September 2004): 237–45.
4. A. W. Hsing, A. P. Chokkalingam, Y. T. Gao, et al., “Allium vegetables and risk of prostate cancer: a population-based study,” Journal of the National Cancer Institute 94, no. 21 (November 2002): 1648–51.
5. C. A. Thomson, C. L. Rock, B. J. Caan, et al., “Increase in cruciferous vegetable intake in women previously treated for breast cancer participating in a dietary intervention trial,” Nutrition and Cancer 57, no. 1 (May 2007): 11–19.
6. C. A. Thomson, E. Ho, M. B. Strom, “Chemopreventive properties of 3,3’-diindolylmethane in breast cancer: evidence from experimental and human studies,” Nutrition Reviews 74, no. 7 (July 2016): 432–43.
7. M. Lenzi, C. Fimognari, P. Hrelia, “Sulforaphane as a promising molecule for fighting cancer,” Cancer Treatment and Research 159 (October 2014): 207–23.
8. K. L. Kaspar, J. S. Park, C. R. Brown, et al., “Pigmented potato consumption alters oxidative stress and inflammatory damage in men,” Journal of Nutrition 141, no. 1 (January 2011): 108–11.
9. S. Lim, J. Xu, J. Kim, et al., “Role of anthocyanin-enriched purple-fleshed sweet potato p40 in colorectal cancer prevention,” Molecular Nutrition & Food Research 57, no. 11 (November 2013): 1908–17.
10. G. Block, B. Patterson, A. Subar, “Fruit, vegetables, and cancer prevention: a review of the epidemiological evidence,” Nutrition and Cancer 18, no. 1 (January 1992): 1–29.
11. M. Zhang, J. Huang, X. Xie, C. D. Holman, “Dietary intakes of mushrooms and green tea combine to reduce the risk of breast cancer in Chinese women,” International Journal of Cancer 124, no. 6 (March 2009): 1404–8.
12. E. N. Alonso, M. J. Ferronato, N. A. Gandini, et al., “Antitumoral effects of D-Fraction from grifola frondosa (maitake) mushroom in breast cancer,” Nutrition and Cancer 69, no. 1 (January 2017): 29–43.
13. M. E. Balandaykin, I. V. Zmitrovich, “Review on chaga medicinal mushroom, inonotus obliquus (higher basidiomycetes): realm of medicinal applications and approaches on estimating its resource potential,” International Journal of Medicinal Mushrooms 17, no. 2 (March 2015): 95–104.
14. American Institute for Cancer Research, “Berries,” American Institute for Cancer Research, 2017, www.aicr.org/foods-that-fight-cancer/foodsthatfightcancer_berries.html.
15. G. D. Stoner, L.-S. Wang, N. Zikri, et al., “Cancer prevention with freeze-dried berries and berry components,” Seminars in Cancer Biology 17, no. 5 (May 2007): 403–10.
16. A. Basu, M. Rhone, T. J. Lyons, “Berries: emerging impact on cardiovascular health,” Nutrition Reviews 68, no. 3 (March 2010): 168–77.
17. H. N. Luu, W. J. Blot, Y. B. Xiang, et al., “Prospective evaluation of the association of nut/peanut consumption with total and cause-specific mortality,” Journal of the American Medical Association: Internal Medicine 175, no. 5 (May 2015): 755–66.
18. X. Su, R. M. Tamimi, L. C. Collins, et al., “Intake of fiber and nuts during adolescence and incidence of proliferative benign breast disease,” Cancer Causes and Control 21, no. 7 (July 2010): 1033–46.
19. C. Sanchez-Gonzalez, C. J. Ciudad, V. Noe, M. Izquierdo-Pulido, “Health benefits of walnut polyphenols: an exploration beyond their lipid profile,” Critical Reviews in Food Science and Nutrition 57, no. 16 (November 2017): 3373–83.
20. L. R. Jimenez, W. A. Hall, M. S. Rodriquez, et al., “Quantifying residues from postharvest propylene oxide fumigation of almonds and walnuts,” Journal of AOAC International 98, no. 5 (September–October 2015): 1423–27.
21. M. D. Danyluk, T. M. Jones, S. J. Abd, et al., “Prevalence and amounts of salmonella found on raw California almonds,” Journal of Food Protection 70, no. 4 (April 2007): 820–27.
22. L. U. Thompson, J. M. Chen, T. Li, K. Strasser-Weippl, P. E. Goss, “Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer,” Clinical Cancer Research 11, no. 10 (May 2005): 3828–35.
23. A. K. Wiggins, J. K. Mason, L. U. Thompson, “Beneficial influence of diets enriched with flaxseed and flaxseed oil on cancer,” in Cancer Chemoprevention and Treatment by Diet Therapy, ed. William C. S. Cho (Dordrecht, The Netherlands: Springer, 2013), 55–89.
24. J. K. Mason, L. U. Thompson, “Flaxseed and its lignan and oil components: can they play a role in reducing the risk of and improving the treatment of breast cancer?,” Applied Physiology, Nutrition, and Metabolism. Physiologie Appliquée, Nutrition et Métabolisme 39, no. 6 (June 2014): 663–78.
25. T. Huang, M. Xu, A. Lee, S. Cho, L. Qi, “Consumption of whole grains and cereal fiber and total and cause-specific mortality: prospective analysis of 367,442 individuals,” BMC Medicine 13 (March 2015): 59.
26. R. C. Masters, A. D. Liese, S. M. Haffner, L. E. Wagenknecht, A. J. Hanley, “Whole and refined grain intakes are related to inflammatory protein concentrations in human plasma,” Journal of Nutrition 140, no. 3 (March 2010): 587–94.
27. M. Lefevre, S. Jonnalagadda, “Effect of whole grains on markers of subclinical inflammation,” Nutrition Reviews 70, no. 7 (July 2012): 387–96.
28. A. M. Troen, “Folate and vitamin B12: function and importance in cognitive development,” Nestle Nutrition Institute Workshop Series 70 (January 2012): 161–71.
29. American Institute for Cancer Research, “Legumes,” American Institute for Cancer Research, 2017, www.aicr.org/foods-that-fight-cancer/foodsthatfightcancer_berries.html.
30. H. Wang, M. S. Geier, G. S. Howarth, “Prebiotics: a potential treatment strategy for the chemotherapy-damaged gut?,” Critical Reviews in Food Science and Nutrition 56, no. 6 (August 2016): 946–56.
31. B. Petschow, J. Dore, P. Hibberd, et al., “Probiotics, prebiotics, and the host microbiome: the science of translation,” Annals of the New York Academy of Sciences 1306 (December 2013): 1–17.
32. S. J. Bultman, “The microbiome and its potential as a cancer preventive intervention,” Seminars in Oncology 43, no. 1 (September 2016): 97–106.
33. A. Riviere, M. Selak, D. Lantin, F. Leroy, L. De Vuyst, “Bifidobacteria and butyrate-producing colon bacteria: importance and strategies for their stimulation in the human gut,” Frontiers in Microbiology 7 (July 2016): 979.
34. H. M. Chen, Y. N. Yu, J. L. Wang, et al., “Decreased dietary fiber intake and structural alteration of gut microbiota in patients with advanced colorectal adenoma,” The American Journal of Clinical Nutrition 97, no. 5 (May 2013): 1044–52.
35. M. G. Gareau, P. M. Sherman, W. A. Walker, “Probiotics and the gut microbiota in intestinal health and disease,” Nature Reviews Gastroenterology & Hepatology 7, no. 9 (September 2010): 503–14.
36. Human Microbiome Project Consortium, “Structure, function and diversity of the healthy human microbiome,” Nature 486, no. 7402 (June 2012b): 207–14.
37. S. J. Hewlings, D. S. Kalman, “Curcumin: a review of its effects on human health,” Foods 6, no. 10 (October 2017).
38. G. P. Lim, T. Chu, F. Yang, et al., “The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse,” Journal of Neuroscience 21, no. 21 (November 2001): 8370–77.
39. R. Wilken, M. S. Veena, M. B. Wang, E. S. Srivatsan, “Curcumin: a review of anti-cancer properties and therapeutic activity in head and neck squamous cell carcinoma,” Molecular Cancer 10 (February 2011): 12.
40. S. S. Percival, J. P. Vanden Heuvel, C. J. Nieves, et al., “Bioavailability of herbs and spices in humans as determined by ex vivo inflammatory suppression and DNA strand breaks,” Journal of the American College of Nutrition 31, no. 4 (August 2012): 288–94.
41. K. Griffiths, B. B. Aggarwal, R. B. Singh, et al., “Food antioxidants and their anti-inflammatory properties: a potential role in cardiovascular diseases and cancer prevention,” Diseases 4, no. 3 (August 2016).
Appendix C: Environmental Toxin Hit List
1. T. B. Hayes, V. Khoury, A. Narayan, et al., “Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis),” Proceedings of the National Academy of Sciences of the United States of America 107, no. 10 (March 2010): 4612–17.
2. C. Cox, “Herbicide Factsheet Atrazine: Toxicology,” Journal of Pesticide Reform 21, no. 2 (Summer 2001b).
3. M. C. Alavanja, C. Samanic, M. Dosemeci, et al., “Use of agricultural pesticides and prostate cancer risk in the Agricultural Health Study cohort,” American Journal of Epidemiology 157, no. 9 (May 2003): 800–14.
4. K. Hu, Y. Tian, Y. Du, et al., “Atrazine promotes RM1 prostate cancer cell proliferation by activating STAT3 signaling,” International Journal of Oncology 48, no. 5 (May 2016): 2166–74.
5. J. R. Rochester, “Bisphenol A and human health: a review of the literature,” Reproductive Toxicology 42 (December 2013): 132–55.
6. S. Eladak, T. Grisin, D. Moison, et al., “A new chapter in the bisphenol A story: bisphenol S and bisphenol F are not safe alternatives to this compound,” Fertility and Sterility 103, no. 1 (January 2015): 11–21.
7. F. Salazar-Garcia, E. Gallardo-Diaz, P. Ceron-Mireles, D. Loomis, V. H. Borja-Aburto, “Reproductive effects of occupational DDT exposure among male malaria control workers,” Environmental Health Perspectives 112, no. 5 (April 2004): 542–47.
8. N. Shivapurkar, K. L. Hoover, L. A. Poirier, “Effect of methionine and choline on liver tumor promotion by phenobarbital and DDT in diethylnitrosamine-initiated rats,” Carcinogenesis 7, no. 4 (April 1986): 547–50.
9. M. Kogevinas, “Human health effects of dioxins: cancer, reproductive and endocrine system effects,” Human Reproduction Update 7, no. 3 (May–June 2001): 331–39.
10. S. N. Bhupathiraju, F. Grodstein, M. J. Stampfer, et al., “Exogenous hormone use: oral contraceptives, postmenopausal hormone therapy, and health outcomes in the Nurses’ Health Study,” American Journal of Public Health 106, no. 9 (September 2016): 1631–37.
11. M. E. Samson, S. A. Adams, C. M. Mulatya, et al., “Types of oral contraceptives and breast cancer survival among women enrolled in Medicaid: a competing-risk model,” Maturitas 95 (January 2017): 42–49.
12. U.S. Food and Drug Administration, “Fragrances in cosmetics,” November 25, 2017, www.fda.gov/Cosmetics/ProductsIngredients/Ingredients/ucm388821.htm.
13. F. A. Caliman, M. Gavrilescu, “Pharmaceuticals, personal care products and endocrine disrupting agents in the environment—a review,” CLEAN–Soil, Air, Water 37, no. 4–5 (April 2009): 277–303.
14. Environmental Working Group, “Not so sexy: hidden chemicals in perfume and cologne,” May 12, 2010, www.ewg.org/research/not-so-sexy-.Wh3IDFVKsdV.
15. B. Eskenazi, A. Bradman, R. Castorina, “Exposures of children to organophosphate pesticides and their potential adverse health effects,” Environmental Health Perspectives 107, Supplement 3 (June 1999): 409–19.
16. P. D. Darbre, P. W. Harvey, “Parabens can enable hallmarks and characteristics of cancer in human breast epithelial cells: a review of the literature with reference to new exposure data and regulatory status,” Journal of Applied Toxicology 34, no. 9 (September 2014): 925–38.
17. A. M. Leung, E. N. Pearce, L. E. Braverman, “Perchlorate, iodine and the thyroid,” Best Practice & Research: Clinical Endocrinology & Metabolism 24, no. 1 (February 2010): 133–41.
18. K. M. Rappazzo, E. Coffman, E. P. Hines, “Exposure to perfluorinated alkyl substances and health outcomes in children: a systematic review of the epidemiologic literature,” International Journal of Environmental Research and Public Health 14, no. 7 (June 2017): 691.
19. C. Lau, “Perfluorinated compounds: an overview,” in Toxicological Effects of Perfluoroalkyl and Polyfluoroalkyl Substances, ed. Jamie C. DeWitt (Cham, Switzerland: Humana Press, 2015), 1–21.
20. J. D. Meeker, K. K. Ferguson, “Urinary phthalate metabolites are associated with decreased serum testosterone in men, women, and children from NHANES 2011–2012,” Journal of Clinical Endocrinology and Metabolism 99, no. 11 (November 2014): 4346–52.
21. W. J. Cowell, S. A. Lederman, A. Sjödin, et al., “Prenatal exposure to polybrominated diphenyl ethers and child attention problems at 3–7 years,” Neurotoxicology and Teratology 52 (Pt B) (November–December 2015): 143–50.
22. V. Linares, M. Belles, J. L. Domingo, “Human exposure to PBDE and critical evaluation of health hazards,” Archives of Toxicology 89, no. 3 (March 2015): 335–56.
23. K. A. Jarema, D. L. Hunter, R. M. Shaffer, M. Behl, S. Padilla, “Acute and developmental behavioral effects of flame retardants and related chemicals in zebrafish,” Neurotoxicology and Teratology 52 (Pt B) (November–December 2015): 194–209.
24. L. G. Costa, G. Giordano, “Developmental neurotoxicity of polybrominated diphenyl ether (PBDE) flame retardants,” Neurotoxicology 28, no. 6 (November 2007): 1047–67.
25. M.F. Yueh, K. Taniguchi, S. Chen, et al., “The commonly used antimicrobial additive triclosan is a liver tumor promoter,” Proceedings of the National Academy of Sciences of the United States of America 111, no. 48 (November 2014): 17200–17205.
26. National Toxicology Program, “Report on carcinogens, fourteenth edition,” U.S. Department of Health and Human Services, Public Health Service, 2016b.
27. Health and Food Safety Scientific Committee, “Opinion concerning banning of dialkanolamines which are still in the inventory adopted by the plenary session of the SCCNFP on 17 February 1999,” February 17, 1999, www.ec.europa.eu/health/scientific_committees/consumer_safety/opinions/sccnfp_opinions_97_04/sccp_out64_en.htm.
28. J. B. Knaak, H. W. Leung, W. T. Stott, J. Busch, J. Bilsky, “Toxicology of mono-, di-, and triethanolamine,” Reviews of Environmental Contamination and Toxicology 149 (January 1997): 1–86.
29. The Agency for Toxic Substances and Disease Registry (ATSDR), “Toxic substances portal—ethylene oxide,” July 1999, www.atsdr.cdc.gov/toxfaqs/tf.asp?id=733&tid=133.
30. M. M. Peters, T. W. Jones, T. J. Monks, S. S. Lau, “Cytotoxicity and cell proliferation induced by the nephrocarcinogen hydroquinone and its nephrotoxic metabolite 2,3,5-(tris-glutathion-S-yl)hydroquinone,” Carcinogenesis 18, no. 12 (December 1997): 2393–401.
31. G. Bjorklund, M. Dadar, J. Mutter, J. Aaseth, “The toxicology of mercury: current research and emerging trends,” Environmental Research 159 (November 2017): 545–54.
32. P. Boffetta, E. Merler, H. Vainio, “Carcinogenicity of mercury and mercury compounds,” Scandinavian Journal of Work, Environment and Health 19, no. 1 (February 1993): 1–7.
33. IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, ed., “Mineral oils, untreated or mildly treated,” in Chemical Agents and Related Occupations (Lyon, France: WHO International Agency for Research on Cancer, 2014).
34. S. Maipas, P. Nicolopoulou-Stamati, “Sun lotion chemicals as endocrine disruptors,” Hormones 14, no. 1 (January–March 2015): 32–46.
35. S. Heikkinen, J. Pitkaniemi, T. Sarkeala, N. Malila, M. Koskenvuo, “Does hair dye use increase the risk of breast cancer? A population-based case-control study of Finnish women,” PloS One 10, no. 8 (August 2015): e0135190.
36. The Agency for Toxic Substances and Disease Registry (ATSDR), “Toxic substances portal—ethylene oxide,” July 1999, www.atsdr.cdc.gov/toxfaqs/tf.asp?id=733&tid=133.
37. The Agency for Toxic Substances and Disease Registry (ATSDR), “Toxic substances portal1—dioxane,” September 2007, www.atsdr.cdc.gov/toxfaqs/tf.asp?id=954&tid=199.
38. H.J. Jang, C. Y. Shin, K.-B. Kim, “Safety evaluation of polyethylene glycol (PEG) compounds for cosmetic use,” Toxicological Research 31, no. 2 (June 2015): 105–36.
39. L. Montenegro, D. Paolino, G. Puglisi, “Effects of silicone emulsifiers on in vitro skin permeation of sunscreens from cosmetic emulsions,” Journal of Cosmetic Science 55, no. 6 (November–December 2004): 509–18.
40. C. A. Bondi, J. L. Marks, L. B. Wroblewski, et al., “Human and environmental toxicity of sodium lauryl sulfate (SLS): evidence for safe use in household cleaning products,” Environmental Health Insights 9 (November 2015): 27–32.
41. R. Penninkilampi, G. D. Eslick, “Perineal talc use and ovarian cancer: a systematic review and meta-analysis,” Epidemiology (August 2017).
42. C. M. Filley, W. Halliday, B. K. Kleinschmidt-DeMasters, “The effects of toluene on the central nervous system,” Journal of Neuropathology and Experimental Neurology 63, no. 1 (January 2004): 1–12.