Dietary glycemic index and glycemic load and risk of colorectal cancer: results from the EPIC‐Italy study

A carbohydrate‐rich diet, resulting in high blood glucose and insulin, has been hypothesized as involved in colorectal cancer etiology. We investigated dietary glycemic index (GI) and glycemic load (GL), in relation to colorectal cancer, in the prospectively recruited EPIC‐Italy cohort. After a median 11.7 years, 421 colorectal cancers were diagnosed among 47,749 recruited adults. GI and GL were estimated from validated food frequency questionnaires. Multivariable Cox modeling estimated hazard ratios (HRs) for associations between colorectal cancer and intakes of total, high GI and low GI carbohydrate and GI and GL. The adjusted HR of colorectal cancer for highest versus lowest GI quartile was 1.35; 95% confidence interval (CI) 1.03–1.78; p trend 0.031. Increasing high GI carbohydrate intake was also significantly associated with increasing colorectal cancer risk (HR 1.45; 95% CI 1.04–2.03; p trend 0.034), whereas increasing low GI carbohydrate was associated with reducing risk (HR 0.73; 95% CI 0.54–0.98; p trend 0.033). High dietary GI and high GI carbohydrate were associated with increased risks of cancer at all colon sites (HR 1.37; 95% CI 1.00–1.88, HR 1.80; 95% CI 1.22–2.65, respectively), whereas high GI carbohydrate and high GL were associated with increased risk of proximal colon cancer (HR 1.94; 95% CI 1.18–3.16, HR 2.01; 95% CI 1.08–3.74, respectively). After stratification for waist‐to‐hip ratio (WHR), cancer was significantly associated with GI, and high GI carbohydrate, in those with high WHR. These findings suggest that high dietary GI and high carbohydrate intake from high GI foods are associated with increased risk of colorectal cancer.     

Dietary glycemic load and colorectal cancer risk

Background:Insulin and insulin-like growth factors can stimulateproliferation of colorectal cells. High intake of refined carbohydrates andmarkers of insulin resistance are associated with colorectal cancer. To testthe insulin/colon cancer hypothesis, we determined whether the dietaryglycemic index and the glycemic load are associated with colorectal cancerrisk. Design:A case-control study on colorectal cancer conducted inItaly. Cases included 1125 men and 828 women with histologically confirmedincident cancer of the colon or rectum. Controls were 2073 men and 2081 womenhospitalized for acute conditions. We calculated average daily dietaryglycemic index and glycemic load, and fiber intake from a validated foodfrequency questionnaire. Results:Direct associations with colorectal cancer risk emergedfor glycemic index (odds ratio (OR) in highest vs. lowest quintile = 1.7;95% confidence interval (CI): 1.4–2.0) and glycemic load (OR =1.8; 95% CI: 1.5–2.2), after allowance for sociodemographicfactors, physical activity, number of daily meals, and intakes of fiber,alcohol and energy. ORs were more elevated for cancer of the colon thanrectum. Overweight and low intake of fiber from vegetables and fruit appearedto amplify the adverse consequences of high glycemic load. Conclusions:The positive associations of glycemic index and loadwith colorectal cancer suggest a detrimental role of refined carbohydrates inthe etiology of the disease.     

Glycemic index, glycemic load, and carbohydrate intake in relation to risk of distal colorectal adenoma in women.

Case-control studies and a cohort study have shown inconsistent associations between a high glycemic index or a high glycemic load and risk of colorectal cancer. These dietary variables have not been examined in relation to risk of colorectal adenoma. We thus examined the associations between dietary glycemic index, glycemic load, and carbohydrate intake with risk of adenoma of the distal colon or rectum among 34,428 US women who were initially free of cancer or polyps, who completed a semi-quantitative food-frequency questionnaire in 1980, and who underwent endoscopy from 1980 through 1998. 1,715 adenoma cases (704 large adenomas, 894 small adenomas, 1,277 distal colon adenomas, and 504 rectal adenomas) were documented during 18 years of follow-up. Dietary glycemic index, glycemic load, and carbohydrate intake were not related to risk of total colorectal adenoma after adjustment for age and established risk factors [relative risk (RR) for extreme quintiles of glycemic index = 1.11, 95% confidence interval (CI) 0.94-1.32, P for trend = 0.66; RR for glycemic load = 0.92, 95% CI 0.76-1.11, P for trend = 0.63; RR for carbohydrate intake = 0.90, 95% CI 0.73-1.11, P for trend = 0.64]. In addition, no significant associations were found for large or small adenoma, distal colon or rectal adenoma, or across strata of body mass index. Our findings do not support the hypothesis that a high glycemic index diet, a high glycemic load diet, or high carbohydrate intake overall are associated with risk of colorectal adenoma.     

Carbohydrate intake, glycemic index and glycemic load in relation to risk of endometrial cancer: A prospective study of Swedish women

The associations of carbohydrate intake, glycemic index and glycemic load with endometrial cancer risk were examined among 61,226 participants of the Swedish Mammography Cohort who were cancer-free at enrollment between 1987 and 1990 and completed a food frequency questionnaire. During a mean follow-up of 15.6 years, through June 2005, 608 incident cases of endometrial adenocarcinoma were diagnosed. We observed no overall association between carbohydrate intake, glycemic index or glycemic load and incidence of endometrial cancer; the rate ratios (RRs) for the highest versus the lowest quintile were 1.12 (95% CI, 0.85-1.47) for carbohydrate intake, 1.00 (95% CI, 0.77-1.30) for glycemic index and 1.15 (95% CI, 0.88-1.51) for glycemic load. However, among obese women (body mass index, BMI > or =30 kg/m2), endometrial cancer incidence was nonsignificantly elevated in the top versus bottom quintiles of carbohydrate intake (RR, 1.68; 95% CI, 0.86-3.29) and glycemic load (RR, 1.57; 95% CI, 0.82-2.99). In a subanalysis of women who completed a follow-up questionnaire in 1997, which collected information on physical activity, carbohydrate intake and glycemic load were positively related to endometrial cancer risk among overweight women (BMI > or =25 kg/m2) with low physical activity. In this subgroup, the multivariate RRs comparing extreme quartiles were 1.90 (95% CI, 0.84-4.31) for carbohydrate intake and 2.99 (95% CI, 1.17-7.67) for glycemic load. Results from this cohort study suggest that a high carbohydrate intake and a high glycemic load may increase the risk of endometrial cancer among overweight women with low physical activity.     

Dietary glycemic load and risk of colorectal cancer in the Women's Health Study

Although diet is believed to influence colorectal cancer risk, the long-term effects of a diet with a high glycemic load are unclear. The growing recognition that colorectal cancer may be promoted by hyperinsulinemia and insulin resistance suggests that a diet inducing high blood glucose levels and an elevated insulin response may contribute to a metabolic environment conducive to tumor growth. We prospectively followed a cohort of 38 451 women for an average of 7.9 years and identified 174 with incident colorectal cancer. We used baseline dietary intake measurements, assessed with a semiquantitative food-frequency questionnaire, to examine the associations of dietary glycemic load, overall dietary glycemic index, carbohydrate, fiber, nonfiber carbohydrate, sucrose, and fructose with the subsequent development of colorectal cancer. Cox proportional hazards models were used to estimate relative risks (RRs). Dietary glycemic load was statistically significantly associated with an increased risk of colorectal cancer (adjusted RR = 2.85, 95% confidence interval [CI] = 1.40 to 5.80, comparing extreme quintiles of dietary glycemic load; P(trend) =.004) and was associated, although not statistically significantly, with overall glycemic index (corresponding RR = 1.71, 95% CI = 0.98 to 2.98; P(trend) =.04). Total carbohydrate (adjusted RR = 2.41, 95% CI = 1.10 to 5.27, comparing extreme quintiles of carbohydrate; P(trend) =.02), nonfiber carbohydrate (corresponding RR = 2.60, 95% CI = 1.22 to 5.54; P(trend) =.02), and fructose (corresponding RR = 2.09, 95% CI = 1.13 to 3.87; P(trend) =.08) were also statistically significantly associated with increased risk. Thus, our data indicate that a diet with a high dietary glycemic load may increase the risk of colorectal cancer in women.     

Glycemic load, glycemic index and carbohydrate intake in relation to risk of stomach cancer: a prospective study

The glycemic effects of diets high in refined grains and starchy foods might increase stomach cancer risk by affecting circulating glucose, insulin and insulin-like growth factor-I levels. No prospective data on the role of high glycemic load and glycemic index diets on stomach cancer risk have been reported. We therefore prospectively investigated dietary glycemic load, overall glycemic index and carbohydrate intake in relation to the incidence of stomach cancer among 61,433 women in the population-based Swedish Mammography Cohort. Diet was assessed at baseline (1987-1990) and again in 1997. During 903,586 person-years of follow-up, a total of 156 incident cases of stomach cancer were ascertained. We observed no material associations of dietary glycemic load, overall glycemic index and total carbohydrate intake with the risk of stomach cancer. The multivariate hazard ratios for the highest versus the lowest quintile were 0.76 (95% CI = 0.46-1.25) for glycemic load, 0.77 (95% CI = 0.46-1.30) for overall glycemic index and 0.85 (95% CI = 0.50-1.43) for carbohydrate intake. The associations did not vary according to body mass index. Lack of information on Helicobacter pylori infection status did not allow stratification by this potential effect modifier. Findings from this population-based prospective cohort of middle-aged and elderly women did not provide evidence of a positive association between glycemic load, glycemic index and carbohydrate intake with risk of stomach cancer.     

Dietary carbohydrate,glycemic index,and glycemic load and the risk of colorectal cancer in the BCDDP cohort

Background There is considerable support for associations between insulin and IGF-I levels and colorectal cancer. Diet may relate to colorectal cancer through this mechanism, for example, diets high in glycemic index, glycemic load and/or carbohydrate are hypothesized to increase insulin load and the risk of insulin resistance, hyperinsulinemia. Case–control studies support this hypothesis, but prospective cohorts have had mixed results. Methods In the Breast Cancer Detection Demonstration Project (BCDDP) follow-up cohort of 45,561 women, we used Cox proportional hazards regression to assess the distribution of 490 incident cases of colorectal cancer ascertained during 8.5 years of follow-up across quintiles of carbohydrate intake, glycemic index, and glycemic load. We also stratified by combined BMI and physical activity levels. Results We found reductions in colorectal cancer risk for diets high in carbohydrate (RR for Q5 vs. Q1 = 0.70, 95% CI: 0.50–0.97) and glycemic index (0.75, 95% CI: 0.56–1.00), and no significant association for glycemic load (0.91, 95% CI: 0.70–1.20). Inverse associations were weakest in normal weight active persons. The inverse association for glycemic index was strongest for the portion from dairy food. Conclusions These results do not support an association between diets high in carbohydrate, glycemic index or glycemic load and colorectal cancer.     

Glycemic index,glycemic load,and pancreatic cancer risk (Canada)

There is some evidence that plasma insulin and postload plasma glucose may be associated with risk of pancreatic cancer. Glycemic index and glycemic load are measures, which allow the carbohydrate content of individual foods to be classified according to their postprandial glycemic effects and hence their effects on circulating insulin levels. Therefore, we examined pancreatic cancer risk in association with glycemic index (GI), glycemic load (GL), and intake of dietary carbohydrate and sugar in a prospective cohort of 49,613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths, with follow-up ending between 1998 and 2000. During a mean 16.5 years of follow-up, we observed 112 incident pancreatic cancer cases. There was no association between overall glycemic index, glycemic load, total carbohydrate and total sugar intake and pancreatic cancer risk. In multivariate adjusted models, the hazard ratio (HR) for the highest versus lowest quartile levels of overall GI and GL were 1.43 (95% confidence interval [CI]=0.56–3.65, P_trend=0.58) and 0.80 (95% CI=0.45–1.41, P_trend=0.41), respectively. Our data suggest that overall glycemic index and glycemic load, as well as total sugar and total carbohydrate intake, are not associated with pancreatic cancer risk. However, given the limited literature regarding the role of diet in the etiology of pancreatic cancer, particularly with respect to glycemic index/load, further investigation is warranted.     

Glycemic index and glycemic load in endometrial cancer

Glycemic index (GI) and glycemic load (GL) are measures of the metabolic effects of dietary carbohydrates. The higher their value, the greater the glucose and insulin responses. Raised insulin levels are associated with endometrial cancer and with its risk factors including obesity, diabetes and hypertension. To study the role of the GI and GL we analyzed the data of two hospital-based case-control studies on endometrial cancer conducted between 1988-98 in Italy and Switzerland, including a total of 410 women with incident, histologically confirmed endometrial cancer and 753 controls admitted for acute, non-neoplastic diseases. A food frequency questionnaire was used to assess the subjects usual diet and to derive estimates of dietary GI and GL. The odds ratios (OR) of endometrial cancer, after adjustment for major risk factors, for the highest versus the lowest quintile of dietary GI and GL were 2.1 (95% confidence interval [CI] = 1.4-3.2) and 2.7 (95% CI = 1.8-4.2), respectively. The associations were stronger in older women, in those with higher body mass index and in hormone replacement therapy users. Our study supports the hypothesis of a direct association between GI and endometrial cancer risk.     

Glycemic load,glycemic index and breast cancer risk in a prospective cohort of Swedish women

High‐glycemic load diets have been hypothesized to increase the risk of breast cancer but epidemiologic studies have yielded inconsistent findings. We examined the associations of carbohydrate intake, glycemic index and glycemic load with risk of overall and hormone receptor‐defined breast cancer in the Swedish Mammography Cohort, a population‐based cohort of 61,433 women who completed a food frequency questionnaire at enrollment in 1987–1990. During a mean follow‐up of 17.4 years, we ascertained 2,952 incident cases of invasive breast cancer. Glycemic load but not carbohydrate intake or glycemic index was weakly positively associated with overall breast cancer risk (p for trend = 0.05). In analyses stratified by estrogen receptor (ER) and progesterone receptor (PR) status of the breast tumors, we observed statistically significant positive associations of carbohydrate intake, glycemic index and glycemic load with risk of ER+/PR? breast cancer; the multivariate relative risks comparing extreme quintiles were 1.34 [95% confidence interval (CI) = 0.93–1.94; p for trend = 0.04] for carbohydrate intake, 1.44 (95% CI = 1.06–1.97; p for trend = 0.01) for glycemic index and 1.81 (95% CI = 1.29–2.53; p for trend = 0.0008) for glycemic load. No associations were observed for ER+/PR+ or ER?/PR? breast tumors. These findings suggest that a high carbohydrate intake and diets with high glycemic index and glycemic load may increase the risk of developing ER+/PR? breast cancer. © 2009 UICC     

Dietary glycemic index, glycemic load and ovarian cancer risk: a case-control study in Italy.

BACKGROUND: Dietary carbohydrates vary in their ability to raise blood glucose and insulin levels, which, in turn, influence levels of sex hormones and insulin-like growth factors. We analyzed the effect of type and amount of carbohydrates on ovarian cancer risk, using the glycemic index (GI) and the glycemic load (GL) measurement in a large case-control study conducted in Italy. MATERIALS AND METHODS: Cases included 1031 women with incident, histologically confirmed epithelial ovarian cancer, from four Italian regions. Controls included 2411 women admitted to the same hospital networks for acute, non-neoplastic conditions. Average daily GI and GL were calculated from a validated food frequency questionnaire. Odds ratios (OR) and the corresponding 95% confidence intervals (CI) were computed using multiple logistic regression. RESULTS: Ovarian cancer was directly associated with dietary GI (OR for highest versus lowest quartile = 1.7, 95% CI 1.3-2.1) and GL (OR = 1.7, 95% CI 1.3-2.1). The associations were observed in pre- and postmenopausal women, and they remained consistent across strata of major covariates identified. CONCLUSIONS: This study supports the hypothesis of a direct association between GI and GL and ovarian cancer risk and, consequently, of a possible role of hyperinsulinemia/insulin resistance in ovarian cancer development.     

Dietary carbohydrates and breast cancer risk: a prospective study of the roles of overall glycemic index and glycemic load

We examined breast cancer risk in association with overall glycemic index (GI), glycemic load (GL), and dietary carbohydrate and sugar intake in a prospective cohort of 49,613 Canadian women enrolled in the National Breast Screening Study who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. During a mean follow-up of 16.6 years, we observed 1,461 incident breast cancer cases. GI, GL, total carbohydrate and total sugar intake were not associated with breast cancer risk in the total cohort. However, there was evidence of effect modification of the association between GI and breast cancer risk by menopausal status (p = 0.01), the hazard ratio for the highest versus the lowest quintile level of GI being 0.78 (95% CI = 0.52-1.16; ptrend = 0.12) in premenopausal women and 1.87 (95% CI = 1.18-2.97; ptrend = 0.01) in postmenopausal women. The associations between GI and GL were not modified by body mass index (BMI) or by vigorous physical activity among pre- or postmenopausal women. Similarly, the associations between GI/GL and risk in postmenopausal women were not modified by BMI, vigorous physical activity, or ever use of hormone replacement therapy (HRT), although the associations were slightly stronger among those who reported no vigorous physical activity (ptrend = 0.02), among those who reported ever using HRT (ptrend = 0.02) and among normal-weight women (BMI < 25 kg/m2; ptrend = 0.03). Our data suggest that consumption of diets with high GI values may be associated with increased risk of breast cancer among postmenopausal women, possibly more so among subgroups defined by participation in vigorous physical activity, ever use of HRT and those who are not overweight.     

Diet activity, and lifestyle associations with p53 mutations in colon tumors.

Inactivation of the p53 tumor suppressor gene is a common event in the development of colon cancer. We use data collected as part of a multicenter case-control study of colon cancer to evaluate associations between p53 mutations and diet and lifestyle factors. p53 mutational status was determined for 1458 incident cases of colon cancer using single-strand conformational polymorphism/sequencing of exons 5-8. We determined associations among those with and without mutations compared with population-based controls (N = 2410) and to cases with p53 mutations compared with cases without p53 mutations. Associations also were examined by location and function of specific types of p53 mutations. p53 mutations were identified in tumors in 47.1% of cases; 81.9% of people with mutations had a missense mutation. Cases with a p53 mutation were more likely to consume a Western-style diet, compared with controls [odds ratio (OR), 2.03; 95% confidence interval (CI), 1.53-2.69], than were cases who were p53 wild type (Wt), compared with controls (OR, 1.57;95% CI, 1.20-2.06). Specific components of the Western-style diet, including diets with a high glycemic load (mutation versus control: OR, 1.48; 95% CI, 1.11-1.98 and Wt versus control: OR, 0.98; 95% CI, 0.75-1.28) and diets high in red meat, fast food, and trans-fatty acid (mutation versus control: OR, 1.92; 95% CI, 1.47-2.50 and Wt versus control: OR, 1.39; 95% CI, 1.08-1.80) appeared to be most strongly associated with p53 mutations. Diets with a high glycemic load (relative to lowest intake) were significantly associated with missense mutations (OR, 1.69; 95% CI, 1.23-2.33 comparing p53+ to controls and OR, 1.72; 95% CI, 1.19-2.50 comparing cases p53+ to cases p53 Wt), as were diets high in red meat, fast food, and trans-fatty acids (OR, 1.92; 95% CI, 1.14-2.56 comparing p53+ to controls and OR, 1.40; 95% CI, 1.00-1.98 comparing cases p53+ to cases p53 Wt). Physical inactivity, large body mass index, cigarette smoking, using aspirin/nonsteroidal anti-inflammatory drugs, and other dietary factors appeared to be comparably associated with colon cancer in those with and without p53 mutations. These data suggest that components of a Western-style diet such as high consumption of red meat and foods that increase glycemic load are associated with a p53 disease pathway.     

Dietary sugar,glycemic load,and pancreatic cancer risk in a prospective study

BACKGROUND: Evidence from both animal and human studies suggests that abnormal glucose metabolism plays an important role in pancreatic carcinogenesis. We investigated whether diets high in foods that increase postprandial glucose levels are associated with an increased risk of pancreatic cancer. METHODS: In a cohort of U.S. women (n = 88 802) participating in the Nurses' Health Study, 180 case subjects with pancreatic cancer were diagnosed during 18 years of follow-up. We used frequency of intake of individual foods as reported on a food-frequency questionnaire in 1980 to calculate sucrose, fructose, and carbohydrate intakes; glycemic index (postprandial blood glucose response as compared with a reference food); and glycemic load (glycemic index multiplied by carbohydrate content). Analyses of relative risk (RR) were performed by using multivariable Cox proportional hazards models to adjust for potential confounders. All statistical tests were two-sided. RESULTS: Carbohydrate and sucrose intake were not associated with overall pancreatic cancer risk in this cohort. A statistically nonsignificant 53% increase in risk of pancreatic cancer (RR = 1.53, 95% confidence interval [CI] = 0.96 to 2.45) was observed among women with a high glycemic load intake, and a similar association was observed for fructose intake (RR = 1.57, 95% CI = 0.95 to 2.57). The associations of glycemic load and fructose intakes with pancreatic cancer risk were most apparent among women with elevated body mass index (>or=25 kg/m(2)) or with low physical activity. Among women who were both overweight and sedentary, a high glycemic load was associated with an RR of 2.67 (95% CI = 1.02 to 6.99; highest versus lowest quartile of intake; P for trend =.03), and high fructose was associated with an RR of 3.17 (95% CI = 1.13 to 8.91; P for trend =.04). CONCLUSION: Our data support other findings that impaired glucose metabolism may play a role in pancreatic cancer etiology. A diet high in glycemic load may increase the risk of pancreatic cancer in women who already have an underlying degree of insulin resistance.     

Dietary glycemic and insulin scores and colorectal cancer survival by tumor molecular biomarkers

Accumulating evidence suggests that post‐diagnostic insulin levels may influence colorectal cancer (CRC) survival. Yet, no previous study has examined CRC survival in relation to a post‐diagnostic diet rich in foods that increase post‐prandial insulin levels. We hypothesized that glycemic and insulin scores (index or load; derived from food frequency questionnaire data) may be associated with survival from specific CRC subtypes sensitive to the insulin signaling pathway. We prospectively followed 1,160 CRC patients from the Nurses' Health Study (1980–2012) and Health Professionals Follow‐Up Study (1986–2012), resulting in 266 CRC deaths in 10,235 person‐years. CRC subtypes were defined by seven tumor biomarkers (KRAS, BRAF, PIK3CA mutations, and IRS1, IRS2, FASN and CTNNB1 expression) implicated in the insulin signaling pathway. For overall CRC and each subtype, hazard ratio (HR) and 95% confidence interval (95% CI) for an increase of one standard deviation in each of glycemic and insulin scores were estimated using time‐dependent Cox proportional hazards model. We found that insulin scores, but not glycemic scores, were positively associated with CRC mortality (HR = 1.19, 95% CI = 1.02–1.38 for index; HR = 1.23, 95% CI = 1.04–1.47 for load). The significant positive associations appeared more pronounced among PIK3CA wild‐type cases and FASN‐negative cases, with HR ranging from 1.36 to 1.60 across insulin scores. However, we did not observe statistically significant interactions of insulin scores with PIK3CA, FASN, or any other tumor marker (p interaction > 0.12). While additional studies are needed for definitive evidence, a high‐insulinogenic diet after CRC diagnosis may contribute to worse CRC survival.     

Incidence of colorectal cancer in relation to glycemic index and load in a cohort of women.

BACKGROUND: Dietary glycemic index (GI) and glycemic load (GL) affect circulating insulin concentrations. Elevated circulating insulin concentrations can increase insulin-like growth factor-1, and both of these hormones may have growth-promoting effects within the colorectum. METHODS: We examined associations of GI and GL with colorectal cancer (CRC) among participants in the Iowa Women's Health Study (n = 35,197; ages 55-69 years at baseline in 1986). Over 15 years of follow-up, we identified 757 cases of colon cancer and 209 cases of rectal cancer (954 CRC cases). RESULTS: Overall, neither GI nor GL were significantly associated with incident CRC. However, among obese women (baseline body mass index >/=30 kg/m(2)) CRC incidence was increased in the highest versus lowest quintiles of GI (relative risk, 1.66; 95% confidence intervals, 1.13-2.43; P for trend = 0.02) and GL (relative risk, 1.79; 95% confidence intervals, 1.19-2.70; P for trend < 0.01). This pattern of increased risk for obese women with high GI or GL tended to hold for both colon cancer and rectal cancer, and for nondiabetic women as well. No statistically significant associations were observed between GI or GL and CRC among subjects whose baseline body mass index was <30 kg/m(2). CONCLUSION: Our findings suggest that high GI or GL are not major CRC risk factors among older women in general, but may increase CRC risk among women who are obese.     

Glycemic index, glycemic load and risk of prostate cancer

Dietary carbohydrates have different glycemic and insulinemic potentials depending on type (glycemic index, GI) and amount (glycemic load, GL) of carbohydrate consumed or both. Insulin in turn has been implicated as a risk factor for several cancers, including that of the prostate. We assessed the relationship of GI and GL with prostate cancer risk in a multicenter case-control study. Cases and controls were recruited between 1991 and 2002 in the network of major teaching and general hospitals in 4 Italian areas. Cases were 1,204 men (age range 46-74 years) admitted for incident, histologically confirmed prostate cancer. Controls were 1,352 men (age range 46-74 years) admitted for acute, nonmalignant conditions unrelated to long-term modifications of diet. ORs of prostate cancer and the corresponding 95% CIs were derived using unconditional multiple logistic regression, including terms for age, study center, education, family history of prostate cancer, smoking, body mass index, physical activity, alcohol consumption, intake of energy, fiber and lycopenes. Compared to the lowest quintile of GI, the ORs were 1.23, 1.24, 1.47 and 1.57 for subsequent levels of GI. The corresponding values for GL were 0.91, 1.00, 1.20 and 1.41. No heterogeneity was found among strata of selected covariates. We found direct relations between dietary GI and GL and prostate cancer risk. Correcting for potential confounding factors did not substantially modify these associations.     

Dietary glycemic index,glycemic load,and endometrial cancer risk: The Japan Public Health Center-based Prospective Study

Evidence supporting the association of glycemic index (GI) and glycemic load (GL) with the risk of endometrial cancer is controversial and reports from Asia were limited. Therefore, we aimed to investigate the association in Japanese women. We evaluated 52 460 women in the Japan Public Health Center-based Prospective Study aged 45-74 years who responded to the 5-year follow-up survey. GI and GL were calculated from a validated food frequency questionnaire, and the participants were divided into three groups by GI and GL. The hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated with the Cox proportional hazard model adjusted for potential confounding factors. As a result, within 15.5 years of follow-up, 166 new cases of endometrial cancer were identified. Compared with the lowest GI and GL tertile groups, the HR of the risk of endometrial cancer in the highest GI tertile group was 0.80 (95% CI, 0.53-1.20; P_trend = .33), and that of the highest GL tertile group was 0.79 (95% CI, 0.52-1.19; P_trend = .82). The results were unchanged after stratification by body mass index, coffee consumption, and history of diabetes. In conclusion, we did not find any significant association between GI and GL with the risk of endometrial cancer. Further research is required to clarify the association.     

Dietary glycemic index, glycemic load, and risk of incident breast cancer in postmenopausal women.

Insulin and insulin-like growth factor-I (IGF-I) are associated with increased risk of breast cancer in several studies. Circulating concentrations of insulin increase with dietary consumption of high glycemic index foods, which, in turn, may influence IGF-I levels or activity, but the relevance of such dietary patterns for breast cancer risk is unclear. We investigated whether consumption of carbohydrates with high dietary glycemic index would predict risk of postmenopausal breast cancer among 63,307 United States women in the Cancer Prevention Study II Nutrition Cohort. From baseline in 1992, participants 40-87 years of age and free from cancer and diabetes, were followed for 5 years; 1442 incident breast cancer cases were documented. Diet was assessed at baseline by a validated 68-item food frequency questionnaire from which we calculated dietary glycemic index and glycemic load. Dietary glycemic index and load were not associated with increased risk of postmenopausal breast cancer (rate ratio = 1.03; 95% confidence interval, 0.87-1.22 and rate ratio = 0.90; 95% confidence interval, 0.76-1.08, respectively) after adjustment for multiple breast cancer risk factors. Associations were not modified by body mass index, physical activity, hormone use, or stage of disease. Future evaluations of glycemic index and breast cancer risk may be strengthened by longer follow-up, more complete dietary information, and measurement of plasma insulin and IGF-I levels.     

Glycemic index, glycemic load and risk of gastric cancer.

BACKGROUND: Dietary carbohydrates have been directly associated with gastric cancer risk and have been considered general indicators of a poor diet. However, elevated levels of glucose and insulin elicited by consumption of high amounts of refined carbohydrates may stimulate mitogenic and cancer-promoting insulin-like growth factors (IGF). Glycemic index (GI) and glycemic load (GL), which represent indirect measures of dietary insulin demand, were analysed to understand further the association between carbohydrates and gastric cancer. PATIENTS AND METHODS: Data were derived from a hospital-based case-control study on gastric cancer, conducted in Italy between 1985 and 1997, including 769 cases with incident, histologically confirmed gastric cancer and 2081 controls admitted to the same hospital network as cases for acute, non-neoplastic diseases. All subjects were interviewed using a reproducible food frequency questionnaire. RESULTS: The multivariate odds ratios (OR) for subsequent quartiles of dietary GL were 1.44 [95% confidence interval (CI) 1.11-1.87], 1.62 (95% CI 1.24-2.12) and 1.94 (95% CI 1.47-2.55). No consistent pattern of risk was seen with GI. The associations were consistent in different strata of age, education and body mass index, and were stronger in women. CONCLUSIONS: This study supports the hypothesis of a direct association between GL and gastric cancer risk, thus providing an innovative interpretation, linked to excess circulating insulin and related IGFs, for the association between carbohydrates and risk of gastric cancer.