Effects of GI and GL Indexes on HRCs: History
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Hormone-related cancers, namely breast, endometrial, cervical, prostate, testicular, and thyroid, constitute a specific group of cancers dependent on hormone levels that play an essential role in cancer growth. In addition to the traditional risk factors, diet seems to be an important environmental factor that partially explains the steadily increased prevalence of this group of cancer. The composition of food, the dietary patterns, the endocrine-disrupting chemicals, and the way of food processing and preparation related to dietary advanced glycation end-product formation are all related to cancer. 

  • cancer
  • hormone-related cancer
  • carbohydrates
  • nutrition

1. Effects of Dietary GI and GL Indexes on Breast Cancer

Breast cancer (BC) is the second most common cancer in women after skin cancers and the second highest cause of death after lung cancer. BC is the leading cancer type in obese women, and increased awareness of this relationship has led to much effort to prevent obesity as a cause of BC [1]. Healthy dietary patterns and weight loss interventions focusing on abdominal adiposity are related to a lower risk and better prognosis of BC, a lower risk of BC recurrence, and reduced all-cause mortality. Nevertheless, there is currently little information about BC’s underlying mechanisms, the proper dietary manipulation, and the most effective dietary pattern for weight management and cancer development and prognosis [1][2].
Dietary caloric intake and total CHO intake have been linked to BC. Simple sugar, sucrose, maltose, and fructose were positively associated with BC [3]. High total sugar intake, especially added sugar, sucrose, and fructose, as well as CHO from fruit juice after a BC diagnosis, were also associated with poorer prognosis [4].
High GL and GI diets have been extensively studied in relation to the development of BC, with conflicting results due to research on different and heterogeneous populations. However, most research supports that high GI and GL dietary patterns are related to BC development and prognosis. Some studies have identified only GI or GL as better correlates with the BC risk in different subgroups of women.
Premenopausal women: Several studies have shown a significant association of GI and GL indexes with BC risk in overweight [5][6], lean (BMI < 25) [7], or irrespective of BMI [8] premenopausal women, as well as in those with low levels of physical activity [9]. The association of only GI with increased BC risk was found by Sasanfar et al. [10]. When hormone receptor status was examined, Woo et al. reported this association for the ER+ or PR+ type [11]. Amadou et al. found no association of BC risk with GI and GL but a strong correlation with the total CHO intake in overweight premenopausal women [12]. Dietary intervention with increased consumption of low GL diet significantly affected several miRNAs related to various cancer pathways in healthy premenopausal women with a high BC risk [13]. A retrospective study on dietary habits during adolescence discovered that a higher dietary GI was associated with an increased risk of BC later in life [14]. In regard to CHO, higher-quality CHO intake was related to a lower risk of BC in premenopausal women [10][15].
Postmenopausal women: High GI and GL have been associated with an increased risk of BC in postmenopausal women, as well [11][16][17][18][19]. Lajous et al. noted that particularly overweight women and women in the greatest waist circumference subgroup were more prone to BC when following a high GI and GL diet [16], while Silvera et al. noted this association mainly in normal-weight women [20].
Concerning the BC receptor subtype, different studies in postmenopausal women had varying results. The link between GL and GI and BC risk was noted in the ER+/PR- BC subtype [17], in the ER-BC subtype [16][21], in the ER-/PR-BC subtype [22], as well as in all subgroups of hormone receptor status [11]. Evidence also links GL to in situ BC [23]. Among postmenopausal women with vegetable intake below the median (307 g/d), elevated dietary GI was also linked to an increased risk of BC [18].

2. Effects of Dietary GI and GL Indexes on Endometrial Cancer

Endometrial cancer (EC) ranks as the 15th most frequent cancer overall and the sixth most frequent cancer in women [24]. Hormonal imbalances in premenopause and menopause, namely increased estrogens/low progesterone levels, polycystic ovarian syndrome, obesity, hyperinsulinemia, IR, physical inactivity, type 2 diabetes, and hypertension, are all connected to EC [25]. More than half of EC cases are currently attributable to obesity, which is recognized as an independent risk factor. This association follows a dose–response relationship, with the incidence of EC increasing as body mass index (BMI) increases [26].
The Mediterranean diet has been proven beneficial in several aspects of gynecological health [27], whereas a diet high in complex CHO causes hormonal imbalance that leads to obesity and many other diseases, including cancer [28]. Several in vivo and in vitro studies also support that a high GL diet over an extended period causes hyperinsulinemia and IR [29].
The quantity and quality of CHO may contribute to the etiology of EC. Consumption of CHO, specifically total sucrose intake and complex CHO intake, was associated with an increased risk of EC [30].
The positive association between GI and GL with the risk of EC has been shown in studies mainly undertaken in Western countries with a high incidence of high GI and GL diets. This correlation was found to be dependent on menopausal status, body size, or physical activity [31][32][33][34][35][36]. However, a study in Japan, where individuals have different dietary habits and lower BMI, found null associations among GI, GL, and the risk of EC [24]. In addition, several case–control studies found no connection between dietary CHO intake, GI and GL, and EC risk [24][29][37][38][39].
The impact of high GI and GL diets seems to be evident in obese pre- or postmenopausal women, especially under hormone replacement treatment [40]. Xu et al. discovered that consumption of high GL or GI meals, but not just regular CHO, may also raise the risk for EC in lean and normal-weight women [34]. Other studies observed a stronger correlation between GI but not GL and EC in obese or older women with greater BMI and those on hormone replacement treatment [31]. The Australian National Endometrial Cancer Study also showed that GI but not GL was linked to an increased risk for EC [29].
Galeone et al.’s meta-analysis supported an elevated risk for EC with high GL but not GI [41]. Similar findings were found in studies in non-diabetic and obese women with low levels of physical activity [32][33]. In contrast with the above data, Coleman et al. found that high CHO and GL diets are preventative measures against the onset of EC [39].

3. Effects of Dietary GI and GL Indexes on Prostate Cancer

Prostate cancer (PC) is the second most frequent malignancy in men [42]. Age, family history, race, and ethnicity are recognized risk factors for PC. Other less-known factors include IR, obesity, metabolic syndrome, and alcohol use [43]. Multiple studies have shown that there is a link between obesity, excessive body fat, and PC, especially the aggressive variant [44].
Various studies have examined the hypothesis that reducing CHO may slow PC growth by lowering serum insulin or altering the insulin-like growth factor (IGF) that has shown mitogenic and antiapoptotic effects on prostate epithelial cells. Animal studies showed that a no-CHO ketogenic or a low-CHO diet may slow prostate tumor growth. In humans, only one study found a high intake of refined CHO associated with increased PC risk, but others did not confirm this hypothesis [45], finding no significant associations between a high intake of refined CHO and the risk of PC [46].
Macronutrients, such as refined CHO, especially high intake of cake, biscuits, pasta, and rice, as well as processed meat, milk, dairy products, and some micronutrients like calcium, lycopene, selenium, and vitamin E, are all related to PC risk [47]. This is further supported by the observation that immigrants from Asia and Africa to Western nations have higher incidence rates of PC, partially mediated by the changes in dietary habits and a different lifestyle inducing IR [48]. A higher dietary fat intake is also correlated with higher PC mortality rates [49].
There is conflicting epidemiological evidence about the contribution of dietary GI, GL, and total CHO intake to PC risk. Although it can be challenging to pinpoint the causes of inconsistencies, significant variations in dietary practices may play a role, as well as race and genetic factors [50][51].
Experimental studies have shown that a low-fat/low-GL diet and the resulting weight loss are linked to several alterations in gene expression, affecting growth, metabolism, and redox in prostate epithelial cells [52]. Moreover, high-fat/low-GI and extremely low-fat vegan diets showed no impact on tumor biology, as measured by changes in tumor gene expression [43][53].
Some clinical studies have demonstrated a direct correlation between dietary GI and GL and the risk of PC [47][51][53][54]. A positive dose–response relationship between only GI and PC has been identified [55][56][57], with GI playing a role in more aggressive diseases [57]. However, other studies have failed to uncover any meaningful link [47][48][50][58].
More research needs to be performed to clarify the effects of dietary manipulation regarding GI GL and PC risk and give further insight into the underlying mechanisms.

4. Effects of Dietary GI and GL Indexes on Ovarian Cancer

Ovarian cancer (OC) is the fifth most frequent cancer worldwide and one of the most lethal female gynecological malignancies [59]. Chronic hyperinsulinemia can develop from long-term CHO consumption, and it has been claimed that hyperinsulinemia may raise the risk of OC by activating numerous pathways that include insulin-like growth factor 1 (IGF-1) [60][61].
Although the role of obesity in OC is still unclear [62][63], recent research suggests that body composition, namely high adiposity and sarcopenia, may impact OC outcomes [64]. Chronic inflammation has been suggested as an underlying mechanism contributing to ovarian carcinogenesis by stimulating DNA damage and promoting enhanced cell division, which can lead to DNA repair abnormalities, promoting angiogenesis, and facilitating invasion. Long-term use of proinflammatory foods such as saturated fat, CHO, and animal proteins increases the risk of OC [65]. Consumption of greater quality macronutrients, such as carbohydrates, fats, and proteins, has also been linked to improved survival in OC patients [66]. Total consumption of CHO, complex CHO, but mostly sugar, has been linked to OC in obese patients [67].
Few studies have investigated the effect of a high GL/GI diet on OC. Most of them have shown a link between GL and OC, either in overweight/obese women [67] or irrespective of BMI [68]. Silvera et al. found that GL was related to a 72% increase in the risk of OC, with the connection being somewhat stronger in postmenopausal women [69].

5. Effects of Dietary GI and GL Indexes on Cervical Cancer

Cervical cancer (CC) is currently the fourth most frequent cancer type in women worldwide and is associated with several environmental and lifestyle risk factors [70]. Among them, obesity affects both screening results and overall survival in CC patients [71].
Even though both a high-CHO diet [72][73] and plasma glucose levels [74] have been associated with an increased risk of CC, dietary GL was linked to an increased incidence of CIN1 but not of CIN2/3 or CC. This correlation was strongest among women with a BMI < 23, premenopausal, or HPV-positive [75].

6. Effects of Dietary GI and GL Indexes on Thyroid Cancer

Thyroid cancer (ThC) is the most common endocrine malignancy, with a clear upward trend in incidence over the last decades and several acknowledged risk factors [76]. Obesity and high waist circumference have both been associated with an increased risk for ThC, possibly via chronic inflammation and the production of various cytokines and adipokines [77]. A series of case–control and prospective studies have consistently found a link between obesity and thyroid cancer risk. Research on the effect of dietary habits in ThC has revealed a protective effect of a diet rich in fruits and vegetables in different populations [78][79][80], while diet-associated inflammation is potentially associated with an increased risk for ThC [81].
Regarding GL and GI, there is a scarcity of studies examining this relationship. A large prospective cohort study with a mean follow-up of 11 years indicated that excessive starch and GI diet intake increased the risk for differentiated ThC in patients with BMI ≥ 25 [82]. Another case–control study found that high levels of GI and GL are linked to greater ThC risk, with follicular ThC exhibiting a slightly higher risk for high levels of GL compared to papillary ThC [83].

7. Effects of Dietary GI and GL Indexes on Testicular Cancer

Testicular cancer (TC) is a relatively uncommon cancer affecting young men [84]. Current evidence does not support that the pathogenesis of testicular cancer is related to obesity [85].
Excessive fat consumption and dairy products have been associated with an elevated risk of TC [86]. However, according to most recent research, there is no reliable indication to support this assumption, and diet does not seem to influence TC risk [87][88]. Overall, the association remains unclear and requires further research.

This entry is adapted from the peer-reviewed paper 10.3390/nu15173810

References

  1. Cava, E.; Marzullo, P.; Farinelli, D.; Gennari, A.; Saggia, C.; Riso, S.; Prodam, F. Breast Cancer Diet “BCD”: A Review of Healthy Dietary Patterns to Prevent Breast Cancer Recurrence and Reduce Mortality. Nutrients 2022, 14, 476.
  2. Terranova, C.O.; Protani, M.M.; Reeves, M.M. Overall Dietary Intake and Prognosis after Breast Cancer: A Systematic Review. Nutr. Cancer 2018, 70, 153–163.
  3. Pishdad, S.; Joola, P.; Bourbour, F.; Rastgoo, S.; Majidi, N.; Gholamalizadeh, M.; Ebrahimi, K.; Abbas Torki, S.; Akbari, M.E.; Montazeri, F.; et al. Association between Different Types of Dietary Carbohydrate and Breast Cancer. Clin. Nutr. ESPEN 2021, 46, 259–263.
  4. Farvid, M.S.; Barnett, J.B.; Spence, N.D.; Rosner, B.A.; Holmes, M.D. Types of Carbohydrate Intake and Breast Cancer Survival. Eur. J. Nutr. 2021, 60, 4565–4577.
  5. McCann, S.E.; McCann, W.E.; Hong, C.-C.; Marshall, J.R.; Edge, S.B.; Trevisan, M.; Muti, P.; Freudenheim, J.L. Dietary Patterns Related to Glycemic Index and Load and Risk of Premenopausal and Postmenopausal Breast Cancer in the Western New York Exposure and Breast Cancer Study. Am. J. Clin. Nutr. 2007, 86, 465–471.
  6. Cho, E.; Spiegelman, D.; Hunter, D.J.; Chen, W.Y.; Colditz, G.A.; Willett, W.C. Premenopausal Dietary Carbohydrate, Glycemic Index, Glycemic Load, and Fiber in Relation to Risk of Breast Cancer. Cancer Epidemiol. Biomark. Prev. 2003, 12, 1153–1158.
  7. Sieri, S.; Pala, V.; Brighenti, F.; Pellegrini, N.; Muti, P.; Micheli, A.; Evangelista, A.; Grioni, S.; Contiero, P.; Berrino, F.; et al. Dietary Glycemic Index, Glycemic Load, and the Risk of Breast Cancer in an Italian Prospective Cohort Study. Am. J. Clin. Nutr. 2007, 86, 1160–1166.
  8. Wen, W.; Shu, X.O.; Li, H.; Yang, G.; Ji, B.-T.; Cai, H.; Gao, Y.-T.; Zheng, W. Dietary Carbohydrates, Fiber, and Breast Cancer Risk in Chinese Women. Am. J. Clin. Nutr. 2009, 89, 283–289.
  9. Higginbotham, S.; Zhang, Z.-F.; Lee, I.-M.; Cook, N.R.; Buring, J.E.; Liu, S. Dietary Glycemic Load and Breast Cancer Risk in the Women’s Health Study. Cancer Epidemiol. Biomark. Prev. 2004, 13, 65–70.
  10. Sasanfar, B.; Toorang, F.; Mohebbi, E.; Zendehdel, K.; Azadbakht, L. Dietary Carbohydrate Quality and Risk of Breast Cancer among Women. Nutr. J. 2021, 20, 93.
  11. Woo, H.D.; Park, K.-S.; Shin, A.; Ro, J.; Kim, J. Glycemic Index and Glycemic Load Dietary Patterns and the Associated Risk of Breast Cancer: A Case-Control Study. Asian Pac. J. Cancer Prev. 2013, 14, 5193–5198.
  12. Amadou, A.; Degoul, J.; Hainaut, P.; Chajes, V.; Biessy, C.; Torres Mejia, G.; Huybrechts, I.; Moreno Macia, H.; Ortega, C.; Angeles-Llerenas, A.; et al. Dietary Carbohydrate, Glycemic Index, Glycemic Load, and Breast Cancer Risk Among Mexican Women. Epidemiology 2015, 26, 917–924.
  13. McCann, S.E.; Liu, S.; Wang, D.; Shen, J.; Hu, Q.; Hong, C.-C.; Newman, V.A.; Zhao, H. Reduction of Dietary Glycaemic Load Modifies the Expression of MicroRNA Potentially Associated with Energy Balance and Cancer Pathways in Pre-Menopausal Women. Br. J. Nutr. 2013, 109, 585–592.
  14. Frazier, A.L.; Li, L.; Cho, E.; Willett, W.C.; Colditz, G.A. Adolescent Diet and Risk of Breast Cancer. Cancer Causes Control. 2004, 15, 73–82.
  15. Romanos-Nanclares, A.; Gea, A.; Martínez-González, M.Á.; Zazpe, I.; Gardeazabal, I.; Fernandez-Lazaro, C.I.; Toledo, E. Carbohydrate Quality Index and Breast Cancer Risk in a Mediterranean Cohort: The SUN Project. Clin. Nutr. 2021, 40, 137–145.
  16. Lajous, M.; Boutron-Ruault, M.-C.; Fabre, A.; Clavel-Chapelon, F.; Romieu, I. Carbohydrate Intake, Glycemic Index, Glycemic Load, and Risk of Postmenopausal Breast Cancer in a Prospective Study of French Women. Am. J. Clin. Nutr. 2008, 87, 1384–1391.
  17. Larsson, S.C.; Bergkvist, L.; Wolk, A. Glycemic Load, Glycemic Index and Breast Cancer Risk in a Prospective Cohort of Swedish Women. Int. J. Cancer 2009, 125, 153–157.
  18. Alboghobeish, Z.; Hekmatdoost, A.; Jalali, S.; Ahmadi, M.; Rashidkhani, B. Carbohydrate Intake, Glycemic Index, and Glycemic Load and the Risk of Breast Cancer among Iranian Women. Nutr. Cancer 2021, 73, 785–793.
  19. Debras, C.; Chazelas, E.; Srour, B.; Julia, C.; Kesse-Guyot, E.; Zelek, L.; Agaësse, C.; Druesne-Pecollo, N.; Andreeva, V.A.; Galan, P.; et al. Glycaemic Index, Glycaemic Load and Cancer Risk: Results from the Prospective NutriNet-Santé Cohort. Int. J. Epidemiol. 2022, 51, 250–264.
  20. Silvera, S.A.N.; Jain, M.; Howe, G.R.; Miller, A.B.; Rohan, T.E. Dietary Carbohydrates and Breast Cancer Risk: A Prospective Study of the Roles of Overall Glycemic Index and Glycemic Load. Int. J. Cancer 2005, 114, 653–658.
  21. Nielsen, T.G.; Olsen, A.; Christensen, J.; Overvad, K.; Tjønneland, A. Dietary Carbohydrate Intake Is Not Associated with the Breast Cancer Incidence Rate Ratio in Postmenopausal Danish Women. J. Nutr. 2005, 135, 124–128.
  22. Romieu, I.; Ferrari, P.; Rinaldi, S.; Slimani, N.; Jenab, M.; Olsen, A.; Tjonneland, A.; Overvad, K.; Boutron-Ruault, M.-C.; Lajous, M.; et al. Dietary Glycemic Index and Glycemic Load and Breast Cancer Risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Am. J. Clin. Nutr. 2012, 96, 345–355.
  23. Shikany, J.M.; Redden, D.T.; Neuhouser, M.L.; Chlebowski, R.T.; Rohan, T.E.; Simon, M.S.; Liu, S.; Lane, D.S.; Tinker, L. Dietary Glycemic Load, Glycemic Index, and Carbohydrate and Risk of Breast Cancer in the Women’s Health Initiative. Nutr. Cancer 2011, 63, 899–907.
  24. Watanabe, Y.; Katagiri, R.; Goto, A.; Shimazu, T.; Yamaji, T.; Sawada, N.; Iwasaki, M.; Inoue, M.; Tsugane, S. Dietary Glycemic Index, Glycemic Load, and Endometrial Cancer Risk: The Japan Public Health Center-based Prospective Study. Cancer Sci. 2021, 112, 3682–3690.
  25. Friedenreich, C.M.; Biel, R.K.; Lau, D.C.W.; Csizmadi, I.; Courneya, K.S.; Magliocco, A.M.; Yasui, Y.; Cook, L.S. Case–Control Study of the Metabolic Syndrome and Metabolic Risk Factors for Endometrial Cancer. Cancer Epidemiol. Biomark. Prev. 2011, 20, 2384–2395.
  26. Onstad, M.A.; Schmandt, R.E.; Lu, K.H. Addressing the Role of Obesity in Endometrial Cancer Risk, Prevention, and Treatment. J. Clin. Oncol. 2016, 34, 4225–4230.
  27. Ciebiera, M.; Esfandyari, S.; Siblini, H.; Prince, L.; Elkafas, H.; Wojtyła, C.; Al-Hendy, A.; Ali, M. Nutrition in Gynecological Diseases: Current Perspectives. Nutrients 2021, 13, 1178.
  28. Tan, B.L.; Norhaizan, M.E.; Liew, W.-P.-P. Nutrients and Oxidative Stress: Friend or Foe? Oxid. Med. Cell. Longev. 2018, 2018, 9719584.
  29. Nagle, C.M.; Olsen, C.M.; Ibiebele, T.I.; Spurdle, A.B.; Webb, P.M. Glycemic Index, Glycemic Load and Endometrial Cancer Risk: Results from the Australian National Endometrial Cancer Study and an Updated Systematic Review and Meta-Analysis. Eur. J. Nutr. 2013, 52, 705–715.
  30. Friberg, E.; Wallin, A.; Wolk, A. Sucrose, High-Sugar Foods, and Risk of Endometrial Cancer—A Population-Based Cohort Study. Cancer Epidemiol. Biomark. Prev. 2011, 20, 1831–1837.
  31. Augustin, L.S.A.; Gallus, S.; Bosetti, C.; Levi, F.; Negri, E.; Franceschi, S.; Dal Maso, L.; Jenkins, D.J.A.; Kendall, C.W.C.; La Vecchia, C. Glycemic Index and Glycemic Load in Endometrial Cancer. Int. J. Cancer 2003, 105, 404–407.
  32. Larsson, S.C.; Friberg, E.; Wolk, A. Carbohydrate Intake, Glycemic Index and Glycemic Load in Relation to Risk of Endometrial Cancer: A Prospective Study of Swedish Women. Int. J. Cancer 2006, 120, 1103–1107.
  33. Folsom, A.R.; Demissie, Z.; Harnack, L. Glycemic Index, Glycemic Load, and Incidence of Endometrial Cancer: The Iowa Women’s Health Study. Nutr. Cancer 2003, 46, 119–124.
  34. Xu, W.H.; Xiang, Y.-B.; Zhang, X.; Ruan, Z.; Cai, H.; Zheng, W.; Shu, X.-O. Association of Dietary Glycemic Index and Glycemic Load with Endometrial Cancer Risk Among Chinese Women. Nutr. Cancer 2015, 67, 89–97.
  35. Haynes, R.B.; Wilczynski, N.; McKibbon, K.A.; Walker, C.J.; Sinclair, J.C. Developing Optimal Search Strategies for Detecting Clinically Sound Studies in MEDLINE. J. Am. Med. Inform. Assoc. 1994, 1, 447–458.
  36. Gnagnarella, P.; Gandini, S.; La Vecchia, C.; Maisonneuve, P. Glycemic Index, Glycemic Load, and Cancer Risk: A Meta-Analysis. Am. J. Clin. Nutr. 2008, 87, 1793–1801.
  37. Hartman, T.J.; McCullough, M.L.; Hodge, J.M.; Gaudet, M.M.; Wang, Y.; Gapstur, S.M. Dietary Energy Density, Glycemic Load, Glycemic Index, and Risk for Endometrial Cancer in the CPS-II Nutrition Cohort. Cancer Epidemiol. Biomark. Prev. 2018, 27, 113–115.
  38. Brenner, D.R.; Speidel, T.; Csizmadi, I.; Biel, R.K.; Cook, L.S.; Courneya, K.S.; Friedenreich, C.M. Glycemic Load and Endometrial Cancer Risk in a Case-Control Study of Canadian Women. Cancer Epidemiol. 2015, 39, 170–173.
  39. Coleman, H.G.; Kitahara, C.M.; Murray, L.J.; Dodd, K.W.; Black, A.; Stolzenberg-Solomon, R.Z.; Cantwell, M.M. Dietary Carbohydrate Intake, Glycemic Index, and Glycemic Load and Endometrial Cancer Risk: A Prospective Cohort Study. Am. J. Epidemiol. 2014, 179, 75–84.
  40. Silvera, S.A.; Rohan, T.E.; Jain, M.; Terry, P.D.; Howe, G.R.; Miller, A.B. Glycaemic Index, Glycaemic Load and Risk of Endometrial Cancer: A Prospective Cohort Study. Public Health Nutr. 2005, 8, 912–919.
  41. Galeone, C.; Augustin, L.S.A.; Filomeno, M.; Malerba, S.; Zucchetto, A.; Pelucchi, C.; Montella, M.; Talamini, R.; Franceschi, S.; La Vecchia, C. Dietary Glycemic Index, Glycemic Load, and the Risk of Endometrial Cancer. Eur. J. Cancer Prev. 2013, 22, 38–45.
  42. Ferlay, J.; Colombet, M.; Soerjomataram, I.; Parkin, D.M.; Piñeros, M.; Znaor, A.; Bray, F. Cancer Statistics for the Year 2020: An Overview. Int. J. Cancer 2021, 149, 778–789.
  43. Freedland, S.J.; Aronson, W.J. Dietary Intervention Strategies to Modulate Prostate Cancer Risk and Prognosis. Curr. Opin. Urol. 2009, 19, 263–267.
  44. Allott, E.H.; Masko, E.M.; Freedland, S.J. Obesity and Prostate Cancer: Weighing the Evidence. Eur. Urol. 2013, 63, 800–809.
  45. Lin, P.-H.; Aronson, W.; Freedland, S.J. An Update of Research Evidence on Nutrition and Prostate Cancer. Urol. Oncol. Semin. Orig. Investig. 2019, 37, 387–401.
  46. Drake, I.; Sonestedt, E.; Gullberg, B.; Ahlgren, G.; Bjartell, A.; Wallström, P.; Wirfält, E. Dietary Intakes of Carbohydrates in Relation to Prostate Cancer Risk: A Prospective Study in the Malmö Diet and Cancer Cohort. Am. J. Clin. Nutr. 2012, 96, 1409–1418.
  47. Alboghobeish, Z.; Hosseini Balam, F.; Askari, F.; Rashidkhani, B. Dietary Carbohydrate Intake Glycemic Index and Glycemic Load and the Risk of Prostate Cancer among Iranian Men: A Case-Control Study. Nutr. Cancer 2022, 74, 882–888.
  48. Nimptsch, K.; Kenfield, S.; Jensen, M.K.; Stampfer, M.J.; Franz, M.; Sampson, L.; Brand-Miller, J.C.; Willett, W.C.; Giovannucci, E. Dietary Glycemic Index, Glycemic Load, Insulin Index, Fiber and Whole-Grain Intake in Relation to Risk of Prostate Cancer. Cancer Causes Control 2011, 22, 51–61.
  49. Ferro, M.; Terracciano, D.; Buonerba, C.; Lucarelli, G.; Bottero, D.; Perdonà, S.; Autorino, R.; Serino, A.; Cantiello, F.; Damiano, R.; et al. The Emerging Role of Obesity, Diet and Lipid Metabolism in Prostate Cancer. Future Oncol. 2017, 13, 285–293.
  50. Makarem, N.; Bandera, E.V.; Lin, Y.; Jacques, P.F.; Hayes, R.B.; Parekh, N. Carbohydrate Nutrition and Risk of Adiposity-Related Cancers: Results from the Framingham Offspring Cohort (1991–2013). Br. J. Nutr. 2017, 117, 1603–1614.
  51. Vidal, A.C.; Williams, C.D.; Allott, E.H.; Howard, L.E.; Grant, D.J.; McPhail, M.; Sourbeer, K.N.; Hwa, L.P.; Boffetta, P.; Hoyo, C.; et al. Carbohydrate Intake, Glycemic Index and Prostate Cancer Risk. Prostate 2015, 75, 430–439.
  52. Lin, D.W.; Neuhouser, M.L.; Schenk, J.M.; Coleman, I.M.; Hawley, S.; Gifford, D.; Hung, H.; Knudsen, B.S.; Nelson, P.S.; Kristal, A.R. Low-Fat, Low-Glycemic Load Diet and Gene Expression in Human Prostate Epithelium: A Feasibility Study of Using CDNA Microarrays to Assess the Response to Dietary Intervention in Target Tissues. Cancer Epidemiol. Biomark. Prev. 2007, 16, 2150–2154.
  53. Kobayashi, N.; Barnard, R.J.; Said, J.; Hong-Gonzalez, J.; Corman, D.M.; Ku, M.; Doan, N.B.; Gui, D.; Elashoff, D.; Cohen, P.; et al. Effect of Low-Fat Diet on Development of Prostate Cancer and Akt Phosphorylation in the Hi-Myc Transgenic Mouse Model. Cancer Res. 2008, 68, 3066–3073.
  54. George, S.M.; Mayne, S.T.; Leitzmann, M.F.; Park, Y.; Schatzkin, A.; Flood, A.; Hollenbeck, A.; Subar, A.F. Dietary Glycemic Index, Glycemic Load, and Risk of Cancer: A Prospective Cohort Study. Am. J. Epidemiol. 2008, 169, 462–472.
  55. Hu, J.; La Vecchia, C.; Augustin, L.S.; Negri, E.; de Groh, M.; Morrison, H.; Mery, L. Glycemic Index, Glycemic Load and Cancer Risk. Ann. Oncol. 2013, 24, 245–251.
  56. Sadeghi, A.; Sadeghi, O.; Khodadost, M.; Pirouzi, A.; Hosseini, B.; Saedisomeolia, A. Dietary Glycemic Index and Glycemic Load and the Risk of Prostate Cancer: An Updated Systematic Review and Dose–Response Meta-Analysis. Nutr. Cancer 2020, 72, 5–14.
  57. Hardin, J.; Cheng, I.; Witte, J.S. Impact of Consumption of Vegetable, Fruit, Grain, and High Glycemic Index Foods on Aggressive Prostate Cancer Risk. Nutr. Cancer 2011, 63, 860–872.
  58. Shikany, J.M.; Flood, A.P.; Kitahara, C.M.; Hsing, A.W.; Meyer, T.E.; Willcox, B.J.; Redden, D.T.; Ziegler, R.G. Dietary Carbohydrate, Glycemic Index, Glycemic Load, and Risk of Prostate Cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) Cohort. Cancer Causes Control 2011, 22, 995–1002.
  59. Siegel, R.L.; Miller, K.D.; Fuchs, H.E.; Jemal, A. Cancer Statistics, 2022. CA Cancer J. Clin. 2022, 72, 7–33.
  60. Kalli, K.R. The Insulin-like Growth Factor Insulin System in Epithelial Ovarian Cancer. Front. Biosci. 2003, 8, 1034.
  61. Lukanova, A.; Kaaks, R. Endogenous Hormones and Ovarian Cancer: Epidemiology and Current Hypotheses. Cancer Epidemiol. Biomark. Prev. 2005, 14, 98–107.
  62. Cheng, E.; Kirley, J.; Cespedes Feliciano, E.M.; Caan, B.J. Adiposity and Cancer Survival: A Systematic Review and Meta-Analysis. Cancer Causes Control 2022, 33, 1219–1246.
  63. Gaitskell, K.; Hermon, C.; Barnes, I.; Pirie, K.; Floud, S.; Green, J.; Beral, V.; Reeves, G.K. Ovarian Cancer Survival by Stage, Histotype, and Pre-Diagnostic Lifestyle Factors, in the Prospective UK Million Women Study. Cancer Epidemiol. 2022, 76, 102074.
  64. Cuello, M.A.; Gómez, F.; Wichmann, I.; Suárez, F.; Kato, S.; Orlandini, E.; Brañes, J.; Ibañez, C. Body Composition and Metabolic Dysfunction Really Matter for the Achievement of Better Outcomes in High-Grade Serous Ovarian Cancer. Cancers 2023, 15, 1156.
  65. Koshiyama, M. The Effects of the Dietary and Nutrient Intake on Gynecologic Cancers. Healthcare 2019, 7, 88.
  66. Zheng, G.; Gong, T.-T.; Ma, Q.-P.; Wei, Y.-F.; Du, Z.-D.; Zhao, J.-Q.; Zou, B.-J.; Yan, S.; Liu, F.-H.; Sun, M.-L.; et al. The association of macronutrient quality and its interactions with energy intake with survival among patients with ovarian cancer: Results from a prospective cohort study. Am. J. Clin. Nutr. 2023, 117, 1362–1371.
  67. Nagle, C.M.; Kolahdooz, F.; Ibiebele, T.I.; Olsen, C.M.; Lahmann, P.H.; Green, A.C.; Webb, P.M. Carbohydrate Intake, Glycemic Load, Glycemic Index, and Risk of Ovarian Cancer. Ann. Oncol. 2011, 22, 1332–1338.
  68. Qin, B.; Moorman, P.G.; Alberg, A.J.; Barnholtz-Sloan, J.S.; Bondy, M.; Cote, M.L.; Funkhouser, E.; Peters, E.S.; Schwartz, A.G.; Terry, P.; et al. Dietary Carbohydrate Intake, Glycaemic Load, Glycaemic Index and Ovarian Cancer Risk in African-American Women. Br. J. Nutr. 2016, 115, 694–702.
  69. Silvera, S.A.; Jain, M.; Howe, G.R.; Miller, A.B.; Rohan, T.E. Glycaemic Index, Glycaemic Load and Ovarian Cancer Risk: A Prospective Cohort Study. Public Health Nutr. 2007, 10, 1076–1081.
  70. Johnson, C.A.; James, D.; Marzan, A.; Armaos, M. Cervical Cancer: An Overview of Pathophysiology and Management. Semin. Oncol. Nurs. 2019, 35, 166–174.
  71. Gnade, C.M.; Hill, E.K.; Botkin, H.E.; Hefel, A.R.; Hansen, H.E.; Sheets, K.A.; Mott, S.L.; Hardy-Fairbanks, A.J.; Stockdale, C.K. Effect of Obesity on Cervical Cancer Screening and Outcomes. J. Low Genit. Tract Dis. 2020, 24, 358–362.
  72. Barchitta, M.; Maugeri, A.; Quattrocchi, A.; Agrifoglio, O.; Scalisi, A.; Agodi, A. The Association of Dietary Patterns with High-Risk Human Papillomavirus Infection and Cervical Cancer: A Cross-Sectional Study in Italy. Nutrients 2018, 10, 469.
  73. Madigan, M.; Karhu, E. The Role of Plant-Based Nutrition in Cancer Prevention. J. Unexplored Med. Data 2018, 3, 9.
  74. Nomelini, R.S.; Neto, A.S.L.; Capuci, K.A.; Murta, B.M.T.; Murta, E.F.C. Relationship between Plasma Glucose Levels and Malignant Uterine Cervical Neoplasias. Clin. Med. Insights Oncol. 2011, 5, CMO.S6916.
  75. Sreeja, S.R.; Seo, S.S.; Kim, M.K. Associations of Dietary Glycemic Index, Glycemic Load and Carbohydrate with the Risk of Cervical Intraepithelial Neoplasia and Cervical Cancer: A Case-Control Study. Nutrients 2020, 12, 3742.
  76. Knudsen, N.; Brix, T.H. Genetic and Non-Iodine-Related Factors in the Aetiology of Nodular Goitre. Best Pract. Res. Clin. Endocrinol. Metab. 2014, 28, 495–506.
  77. Franchini, F.; Palatucci, G.; Colao, A.; Ungaro, P.; Macchia, P.E.; Nettore, I.C. Obesity and Thyroid Cancer Risk: An Update. Int. J. Env. Res. Public Health 2022, 19, 1116.
  78. Liang, J.; Zhao, N.; Zhu, C.; Ni, X.; Ko, J.; Huang, H.; Ma, S.; Udelsman, R.; Zhang, Y. Dietary Patterns and Thyroid Cancer Risk: A Population-Based Case-Control Study. Am. J. Transl. Res. 2020, 12, 180–190.
  79. Markaki, I.; Linos, D.; Linos, A. The Influence of Dietary Patterns on the Development of Thyroid Cancer. Eur. J. Cancer 2003, 39, 1912–1919.
  80. Przybylik-Mazurek, E.; Hubalewska-Dydejczyk, A.; Kuźniarz-Rymarz, S.; Kieć-Klimczak, M.; Skalniak, A.; Sowa-Staszczak, A.; Gołkowski, F.; Kostecka-Matyja, M.; Pach, D. Dietary Patterns as Risk Factors of Differentiated Thyroid Carcinoma. Postep. Hig. Med. Dosw. 2012, 66, 11–15.
  81. Lécuyer, L.; Laouali, N.; Dossus, L.; Shivappa, N.; Hébert, J.R.; Agudo, A.; Tjonneland, A.; Halkjaer, J.; Overvad, K.; Katzke, V.A.; et al. Inflammatory Potential of the Diet and Association with Risk of Differentiated Thyroid Cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) Cohort. Eur. J. Nutr. 2022, 61, 3625–3635.
  82. Zamora-Ros, R.; Rinaldi, S.; Tsilidis, K.K.; Weiderpass, E.; Boutron-Ruault, M.-C.; Rostgaard-Hansen, A.L.; Tjønneland, A.; Clavel-Chapelon, F.; Mesrine, S.; Katzke, V.A.; et al. Energy and Macronutrient Intake and Risk of Differentiated Thyroid Carcinoma in the European Prospective Investigation into Cancer and Nutrition Study. Int. J. Cancer 2016, 138, 65–73.
  83. Randi, G.; Ferraroni, M.; Talamini, R.; Garavello, W.; Deandrea, S.; Decarli, A.; Franceschi, S.; La Vecchia, C. Glycemic Index, Glycemic Load and Thyroid Cancer Risk. Ann. Oncol. 2008, 19, 380–383.
  84. Albers, P.; Albrecht, W.; Algaba, F.; Bokemeyer, C.; Cohn-Cedermark, G.; Fizazi, K.; Horwich, A.; Laguna, M.P. EAU Guidelines on Testicular Cancer: 2011 Update. Eur. Urol. 2011, 60, 304–319.
  85. Papavasileiou, G.; Tsilingiris, D.; Spyrou, N.; Vallianou, N.G.; Karampela, I.; Magkos, F.; Dalamaga, M. Obesity and Main Urologic Cancers: Current Systematic Evidence, Novel Biological Mechanisms, Perspectives and Challenges. Semin. Cancer Biol. 2023, 91, 70–98.
  86. Manecksha, R.P.; Fitzpatrick, J.M. Epidemiology of Testicular Cancer. BJU Int. 2009, 104, 1329–1333.
  87. Signal, V.; Huang, S.; Sarfati, D.; Stanley, J.; McGlynn, K.A.; Gurney, J.K. Dairy Consumption and Risk of Testicular Cancer: A Systematic Review. Nutr. Cancer 2018, 70, 710–736.
  88. McGlynn, K.A.; Trabert, B. Adolescent and Adult Risk Factors for Testicular Cancer. Nat. Rev. Urol. 2012, 9, 339–349.
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