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][33]. 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][33,34].

Dietary caloric intake and total CHO intake have been linked to BC. Simple sugar, sucrose, maltose, and fructose were positively associated with BC ^[3][35]. 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][36].

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][37,38], lean (BMI < 25) ^[7][39], or irrespective of BMI ^[8][40] premenopausal women, as well as in those with low levels of physical activity ^[9][41]. The association of only GI with increased BC risk was found by Sasanfar et al. ^[10][42]. When hormone receptor status was examined, Woo et al. reported this association for the ER+ or PR+ type ^[11][43]. 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][44]. 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][45]. 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][46]. In regard to CHO, higher-quality CHO intake was related to a lower risk of BC in premenopausal women ^[10][15][42,47].

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]}[43,48,49,50,51]. 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][48], while Silvera et al. noted this association mainly in normal-weight women ^[20][52].

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][49], in the ER-BC subtype ^[16][21][48,53], in the ER-/PR-BC subtype ^[22][54], as well as in all subgroups of hormone receptor status ^[11][43]. Evidence also links GL to in situ BC ^[23][55]. 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][50].

Endometrial cancer (EC) ranks as the 15th most frequent cancer overall and the sixth most frequent cancer in women ^[24][78]. 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][79]. 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][29].

The Mediterranean diet has been proven beneficial in several aspects of gynecological health ^[27][80], whereas a diet high in complex CHO causes hormonal imbalance that leads to obesity and many other diseases, including cancer ^[28][81]. Several in vivo and in vitro studies also support that a high GL diet over an extended period causes hyperinsulinemia and IR ^[29][82].

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][83].

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]}[84,85,86,87,88,89]. 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][78]. In addition, several case–control studies found no connection between dietary CHO intake, GI and GL, and EC risk ^{[24][29][37][38][39]}[78,82,90,91,92].

The impact of high GI and GL diets seems to be evident in obese pre- or postmenopausal women, especially under hormone replacement treatment ^[40][93]. 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][87]. 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][84]. The Australian National Endometrial Cancer Study also showed that GI but not GL was linked to an increased risk for EC ^[29][82].

Galeone et al.’s meta-analysis supported an elevated risk for EC with high GL but not GI ^[41][94]. Similar findings were found in studies in non-diabetic and obese women with low levels of physical activity ^[32][33][85,86]. 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][92].

Prostate cancer (PC) is the second most frequent malignancy in men ^[42][95]. 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][96]. Multiple studies have shown that there is a link between obesity, excessive body fat, and PC, especially the aggressive variant ^[44][97].

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][98], finding no significant associations between a high intake of refined CHO and the risk of PC ^[46][99].

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][30]. 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][100]. A higher dietary fat intake is also correlated with higher PC mortality rates ^[49][101].

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][65,102].

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][103]. 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][96,104].

Some clinical studies have demonstrated a direct correlation between dietary GI and GL and the risk of PC ^{[47][51][53][54]}[25,30,102,104]. A positive dose–response relationship between only GI and PC has been identified ^[55][56][57][105,106,107], with GI playing a role in more aggressive diseases ^[57][107]. However, other studies have failed to uncover any meaningful link ^{[47][48][50][58]}[30,65,100,108].

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.

Ovarian cancer (OC) is the fifth most frequent cancer worldwide and one of the most lethal female gynecological malignancies ^[59][109]. 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][110,111].

Although the role of obesity in OC is still unclear ^[62][63][112,113], recent research suggests that body composition, namely high adiposity and sarcopenia, may impact OC outcomes ^[64][114]. 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][115]. Consumption of greater quality macronutrients, such as carbohydrates, fats, and proteins, has also been linked to improved survival in OC patients ^[66][116]. Total consumption of CHO, complex CHO, but mostly sugar, has been linked to OC in obese patients ^[67][117].

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][117] or irrespective of BMI ^[68][118]. 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][119].

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][123]. Among them, obesity affects both screening results and overall survival in CC patients ^[71][124].

Even though both a high-CHO diet ^[72][73][125,126] and plasma glucose levels ^[74][127] 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][128].

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][129]. 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][130]. 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][131,132,133], while diet-associated inflammation is potentially associated with an increased risk for ThC ^[81][134].

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][136]. 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][137].

Testicular cancer (TC) is a relatively uncommon cancer affecting young men ^[84][138]. Current evidence does not support that the pathogenesis of testicular cancer is related to obesity ^[85][139].

Excessive fat consumption and dairy products have been associated with an elevated risk of TC ^[86][140]. 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][141,142]. Overall, the association remains unclear and requires further research.