Glycemic index, glycemic load and thyroid cancer risk.

BACKGROUND: Risk of thyroid cancer has already been related to refined cereals and starch food, but the association has not been studied in terms of glycemic index (GI) and glycemic load (GL). PATIENTS AND METHODS: We analyzed data from a case-control study conducted in Italy from 1986 to 1992 and including 399 histologically confirmed and incident cases of thyroid cancer and 616 control subjects. Information on dietary habits was derived through a food-frequency questionnaire and multivariate odds ratios (ORs) for GI and GL levels were estimated with adjustment for age, education, sex, area of residence, history of diabetes, body mass index, smoking, alcohol consumption, intake of fruit and vegetables, and noncarbohydrate energy intake. RESULTS: Compared with the lowest tertile, the ORs in subsequent tertiles were 1.68 and 1.73 for GI, and 1.76 and 2.17 for GL. The OR for highest tertile of GI compared with lowest one was 1.70 for papillary and 1.57 for follicular thyroid cancer. The ORs for GL were 2.17 for papillary and 3.33 for follicular thyroid cancer. CONCLUSION: Our study shows that high dietary levels of GI and GL are associated with thyroid cancer risk.     

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.     

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.     

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,glycemic load and renal cell carcinoma risk

BackgroundThe risk of renal cell carcinoma (RCC) has been related to refined cereals and starchy foods, but the association has not been studied in terms of glycemic index (GI) and glycemic load (GL). To provide information on this issue, we analyzed data from an Italian multicentric case–control study.Materials and methodsCases were 767 patients with histologically confirmed, incident RCC. Controls were 1534 subjects admitted to the same hospitals as cases for a wide spectrum of acute, non-neoplastic conditions, unrelated to known risk factors for RCC. Information on dietary habits was derived through a food-frequency questionnaire. Multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for GI and GL intake were adjusted for major relevant covariates.ResultsCompared with the lowest quintile, the ORs for the highest quintile were 1.43 (95% CI 1.05–1.95) for GI and 2.56 (95% CI 1.78–3.70) for GL, with significant trends in risk. Compared with the lowest quintile, the risk of RCC for all subsequent levels of GL was higher in never drinkers than in ever drinkers.ConclusionsWe found direct relations between dietary levels of GI and GL and RCC risk. This can be related to mechanisms linked to insulin resistance and sensitivity.     

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     

Carbohydrate intake,glycemic load,glycemic index,and risk of ovarian cancer

BackgroundOur objective was to determine the relationship between dietary glycemic load (GL), glycemic index (GI), carbohydrate intake, and ovarian cancer risk in a population-based case–control study.Patients and methodsA self-administered questionnaire was used to collect data on demographic and lifestyle factors, and a food frequency questionnaire was used to collect dietary information from 1366 women with ovarian cancer and 1414 population controls.ResultsGL was positively associated with ovarian cancer. The adjusted odds ratio (OR) for the highest versus the lowest quartile of intake was 1.24 [95% confidence interval (CI) 1.00–1.55, P for trend = 0.03]. Fiber intake was inversely associated with risk. The OR comparing women in the highest fiber-intake group with those in the lowest was 0.78 (95% CI 0.62–0.98, P for trend = 0.11). We found no association between GI, carbohydrate intake, and ovarian cancer. In analyses stratified by body mass index, the risk estimates for GL, carbohydrate, and sugar were higher among overweight/obese women; however, the interaction term was only significant for sugar (P for interaction = 0.004).ConclusionsOur results suggest that diets with a high GL may increase the risk of ovarian cancer, particularly among overweight/obese women, and a high intake of fiber may provide modest protection.     

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.     

Glycemic load,glycemic index,and carbohydrate intake in relation to pancreatic cancer risk in a large US cohort

Background Consumption of diets with high glycemic load has been hypothesized to increase pancreatic cancer risk by raising postprandial glucose levels and insulin secretion. Methods The authors analyzed data from the American Cancer Society Cancer Prevention Study II (CPS-II) Nutrition Cohort to examine the association between pancreatic cancer and glycemic load, glycemic index (GI), and intake of carbohydrates. Diet was assessed among 124,907 men and women who were cancer-free and non-diabetic at baseline in 1992 using a validated 68-item food frequency questionnaire (FFQ). During 9 years of follow-up, 401 incident pancreatic cancer cases were identified. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) adjusted for potential confounding factors. Results We found no association between glycemic load, GI, or carbohydrate intake and risk of pancreatic cancer in this population. The hazard rate ratio (RR) was 1.01 (95% CI 0.75–1.37, trend P = 0.80) for glycemic load, 0.92 (95% CI 0.68–1.24) for GI, and 1.10 (95% CI 0.80–1.51) for carbohydrate intake among men and women in the highest quintile compared to the lowest quintile of each measure. We also found no significant association between these measures and pancreatic cancer risk among individuals who show a greater susceptibility towards insulin insensitivity, such as those who are overweight or more sedentary. Conclusion Overall, our data do not support the hypothesis that glycemic load or index, or carbohydrate intake are associated with a substantial increase in pancreatic cancer risk; however, a weak positive association cannot be ruled out.     

Dietary glycemic index and glycemic load, and breast cancer risk: A case-control study

Background:Certain types of carbohydrates increase glucoseand insulin levels to a greater extent than others. In turn, insulin mayraise levels of insulin-like growth factors, which may influence breastcancer risk. We analyzed the effect of type and amount of carbohydrateson breast cancer risk, using the glycemic index and the glycemic loadmeasures in a large case-control study conducted in Italy. Patients and methods:Cases were 2569 women with incident,histologically-confirmed breast cancer interviewed between 1991 and1994. Controls were 2588 women admitted to the same hospital network fora variety of acute, non-neoplastic conditions. Average daily glycemicindex and glycemic load were calculated from a validated 78-item foodfrequency questionnaire. Results:Direct associationswith breast cancer risk emerged for glycemic index (odds ratio, OR forhighest vs. lowest quintile = 1.4; Pfor trend <0.01) andglycemic load (OR = 1.3; P< 0.01). High glycemic indexfoods, such as white bread, increased the risk of breast cancer (OR= 1.3) while the intake of pasta, a medium glycemic index food, seemedto have no influence (OR = 1.0). Findings were consistent acrossdifferent strata of menopausal status, alcohol intake, and physicalactivity level. Conclusions:This study supports thehypothesis of moderate, direct associations between glycemic index orglycemic load and breast cancer risk and, consequently, a possible roleof hyperinsulinemia/insulin resistance in breast cancer development.     

Glycemic index and glycemic load and risk of colorectal cancer: a population-based cohort study (JPHC Study)

Purpose

The aim of this study was for the first time to assess the association between glycemic index (GI), glycemic load (GL), and colorectal cancer using a prospective Japanese population-based cohort.

Methods

In our study participants aged 40–69 at baseline of the Japan Public Health Center-based prospective Study (JPHC Study) in 10 prefectural public health centers (PHC) were included. Subjects responding to the five-year follow-up survey (1995–1999) without previous history of cancer and missing data were included in the current analysis n = 73,501 (men n = 34,560 and women n = 38,941). We reported results as hazard ratios (HR) and 95 % confidence intervals (CI) by Cox proportional hazards modeling.

Results

The average follow-up time was 12.5 years (919,276 person-years). A total of 1,468 colorectal cancer cases were detected. Overall, no significant results were observed; however, GL was inversely nonsignificantly associated with colon cancer in men HR = 0.74 (95 % CI 0.51–1.09) and rectal cancer in women 0.52 (95 % CI 0.24–1.14). The GL tended to be inversely associated with proximal colon cancer among men 0.62 (95 % CI 0.36–1.08), while a positive association with the GI was observed among women 1.37 (95 % CI 0.88–2.14). Sensitivity analyses excluding the first three years of observation showed similar results. Results stratified by diabetes status, BMI, smoking and red meat were nonsignificant.

Conclusions

In conclusion, the prospective JPHC Study suggests that the GI and GL do not have a substantial impact on the risk of colorectal cancer in Japanese adults.

     

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.     

Dietary glycemic index,glycemic load,insulin index,fiber and whole-grain intake in relation to risk of prostate cancer

Objective  

Insulin may play a role in prostate cancer tumorigenesis. Postprandial blood glucose and insulin responses of foods depend importantly on the carbohydrate quality and quantity, represented by glycemic index (GI), glycemic load (GL), fiber and whole-grain content, but are also influenced by intake of protein and other characteristics. The recently developed insulin index (II) quantifies the postprandial insulin secretion, also taking into account these additional characteristics.     

Dietary glycemic index,glycemic load,and risk of breast cancer: meta-analysis of prospective cohort studies

Consumption diets of high glycemic index (GI) and glycemic load (GL) may increase the risk of breast cancer. We aimed to conduct a meta-analysis of prospective cohort studies to evaluate the associations between dietary GI and GL and risk of breast cancer. We searched the PubMed database for relevant studies through November 2010, with no restrictions. We included prospective cohort studies that reported relative risk (RR) with 95% confidence intervals (CIs) for the associations of dietary GI and GL with breast cancer risk. Summary RRs were calculated using both fixed- and random-effects models. We identified 10 prospective cohort studies eligible for analysis, involving 15,839 cases and 577,538 participants. The summary RR of breast cancer for the highest GI intake compared with the lowest was 1.08 (95% CI: 1.02–1.14), with no evidence of heterogeneity (P = 0.72, I ² = 0%). For GL, the summary RR was 1.04 (95% CI: 0.95–1.15), and substantial heterogeneity was observed (P = 0.02, I ² = 55.6%). The GI and GL and breast cancer associations did not significantly modified by geographic region, length of follow-up, number of cases, or menopausal status at baseline. Dose–response analysis was not performed due to limited number of eligible studies. There was no evidence of publication bias. In summary, the present meta-analysis of prospective cohort studies suggests that high dietary GI is associated with a significantly increased risk of breast cancer. However, there is no significant association between dietary GL and breast cancer risk.     

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 glycemic load, glycemic index and colorectal cancer risk: results from the Netherlands Cohort Study

Since hyperinsulinemia is implicated in the development of colorectal cancer, determinants of serum insulin levels, like the glycemic load and the glycemic index of the diet, could influence cancer risk. Our objective was to evaluate whether a diet with a high glycemic load or glycemic index is associated with increased colorectal cancer risk. In the Netherlands Cohort Study, 120,852 subjects completed a food frequency questionnaire in 1986. After 11.3 years of follow-up, 1,225 colon and 418 rectal cancer cases were available for analysis. A case-cohort approach was used to estimate multivariate adjusted rate ratios and 95% confidence intervals for quintiles of energy-adjusted glycemic load and glycemic index. The RR for colorectal cancer comparing the highest versus the lowest quintile levels of glycemic load and glycemic index were 0.83 (95% CI: 0.64-1.08) and 0.81 (95% CI: 0.61-1.08) for men and 1.00 (95% CI: 0.73-1.36) and 1.20 (95% CI: 0.85-1.67) for women. In general, no clear associations with cancer subsites were observed. Glycemic load and glycemic index were borderline significantly associated with an increased risk of proximal colon cancer in women (p-trend = 0.06 and 0.08, respectively), however, these associations were attenuated after exclusion of the first 2 years of follow-up (p-trend = 0.165 and 0.254, respectively). In men, glycemic index was associated with a reduced risk of distal colon cancer (p-trend = 0.03). Overall, our findings do not support the hypothesis that a diet with a high glycemic load or index is associated with a higher risk of colorectal 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 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.