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Biomedical subjects

I-Min Lee

Publications and source records attributed to I-Min Lee.

At least 19 recordsLinked to original sources
PubMed2007

Oral contraceptives, reproductive factors, and risk of colorectal cancer among women in a prospective cohort study.

Previous findings on the associations between oral contraceptive (OC) use and reproductive factors and risk of colorectal cancer have been inconclusive. The authors evaluated associations of OC use and reproductive factors (including parity, age at first birth, age at menarche, and age at menopause) with risk of colorectal cancer among women in a large-scale prospective cohort study. The analysis included 39,680 participants in the Women's Health Study who had usable information on ever use of OCs and potential risk factors for colorectal cancer. Relative risks and 95% confidence intervals were estimated from Cox proportional hazards regression models. All p values were two-sided. During an average of 11 years of follow-up (1992-2004), 267 incident cases of colorectal cancer were documented. Ever use of OCs was associated with a lower risk of colorectal cancer (relative risk = 0.67, 95% confidence interval: 0.50, 0.89). Women who had used OCs for 6 months-<3 years had a relative risk of 0.61 (95% confidence interval: 0.40, 0.94) relative to never users, with little additional decreased risk being seen with longer duration of use (p for multivariate trend = 0.09). No significant association was observed between reproductive factors and colorectal cancer risk. These findings provide some support for a potential role of OCs in reducing risk of colorectal cancer.

Age Factors↗
PubMed2007

Alcohol consumption and breast cancer risk in the Women's Health Study.

The authors assessed the association between moderate alcohol consumption and breast cancer risk in the Women's Health Study (United States, 1992-2004). During an average of 10 years of follow-up, 1,484 cases of total breast cancer (1,190 invasive and 294 in situ) were documented among 38,454 women who, at baseline, were free of cancer and cardiovascular disease and provided detailed dietary information, including alcohol consumption, for the preceding 12 months. Higher alcohol consumption was associated with a modest increase in breast cancer risk; the multivariable relative risks for > or =30 g/day of alcohol vs. none were 1.32 (95% confidence interval (CI): 0.96, 1.82) for total breast cancer and 1.43 (95% CI: 1.02, 2.02) for invasive breast cancer. An increased risk was limited to estrogen receptor (ER)- and progesterone receptor (PR)-positive tumors; the multivariable relative risks for an increment of 10 g/day of alcohol were 1.11 (95% CI: 1.03, 1.20) for ER+PR+ tumors (804 cases), 1.00 (95% CI: 0.81, 1.24) for ER+PR- tumors (125 cases), and 0.99 (95% CI: 0.82, 1.20) for ER-PR- tumors (167 cases). The association also seemed strongest among those taking postmenopausal hormones currently, but the test for interaction was not significant. The findings from this prospective study suggest that moderate alcohol consumption increases breast cancer risk.

Alcohol Drinking↗
PubMed2006

Use of oral conjugated estrogen alone and risk of breast cancer.

The authors conducted a prospective cohort analysis in the Women's Health Study (1992-2004), a completed randomized trial assessing aspirin and vitamin E in the primary prevention of cancer and cardiovascular disease, to evaluate use of oral conjugated estrogen alone (0.625 mg/day) and breast cancer risk in a time-varying fashion. Over an average of 10 years of follow-up, 305 incident cases of breast cancer (258 invasive and 47 in situ cancers) were documented among 12,718 women aged 45 years or more who were either consistent current users of oral conjugated estrogen alone (0.625 mg/day) or never users of any type of postmenopausal hormones at baseline and during follow-up. The multivariable hazard ratios comparing "consistent current users" with "never users" were 1.11 (95% confidence interval: 0.79, 1.56) for total breast cancer and 1.13 (95% confidence interval: 0.77, 1.64) for invasive cases. No significant associations were observed for use of less than 8 and 8 years or more. Restricting the analyses to women with prior hysterectomy somewhat strengthened the associations, albeit still not significantly. These data, like those from the Women's Health Initiative, show no significant increase in breast cancer risk with use of oral conjugated estrogen alone (0.625 mg/day), but a small increase or decrease in risk cannot be excluded.

Administration, Oral↗
PubMed2006

Association of adiponectin gene variations with risk of incident myocardial infarction and ischemic stroke: a nested case-control study.

BACKGROUND: Adiponectin (ADIPOQ) gene variations are associated with risk of cardiovascular disease in patients with diabetes. No prospective data are available, however, on the risk of atherothrombotic disorders in persons with ADIPOQ variations who do not have diabetes. METHODS: From a group of DNA samples collected at baseline in a prospective cohort of 14 916 initially healthy American men, we assessed the presence of 5 ADIPOQ genetic variants (rs266729, rs182052, rs822396, rs2241766, and rs1501299) in samples from 600 Caucasian men who subsequently suffered an atherothrombotic event (incident myocardial infarction or ischemic stroke) and from 600 age- and smoking-matched Caucasian men who remained free of reported vascular disease during follow-up (controls). RESULTS: Genotype distributions for the variations tested were in Hardy-Weinberg equilibrium. Marker-by-marker conditional logistic regression analysis, adjusted for potential risk factors, showed an association of rs266729 [recessive: odds ratio (OR), 0.26; 95% confidence interval (CI), 0.10-0.64; P=0.004] and rs182052 (recessive: OR, 0.40; 95% CI, 0.21-0.76; P=0.006) with decreased risk of ischemic stroke. These findings remained significant after Bonferroni correction. Haplotype-based (constituted by rs266729, rs182052, and rs822396) conditional logistic regression analysis, adjusted for the same potential risk factors, showed an association of haplotype G-A-G (OR, 0.28; 95% CI, 0.09-0.87; P=0.03) with decreased risk of ischemic stroke. Prespecified analysis limited to participants without baseline diabetes showed similar significant findings. CONCLUSIONS: The present prospective investigation provides further evidence for a protective role of adiponectin gene variation in the risk of ischemic stroke that was independent of the presence of diabetes.

Adiponectin↗
PubMed2006

Association of physical activity and body mass index with novel and traditional cardiovascular biomarkers in women.

CONTEXT: There are few data directly comparing the effects of physical activity and body weight on cardiovascular biomarkers. OBJECTIVE: To examine the association of physical activity and body mass index (BMI, defined as weight in kilograms divided by the square of height in meters) alone and in combination with cardiovascular biomarkers. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional analysis of 27,158 apparently healthy US women (mean age, 54.7 years) at the time of enrollment (1992-1995) in the Women's Health Study, a randomized, double-blind, placebo-controlled trial of low-dose aspirin and vitamin E in the primary prevention of cardiovascular disease and cancer. MAIN OUTCOME MEASURES: The association of physical activity and BMI with high-sensitivity C-reactive protein (CRP), fibrinogen, soluble intracellular adhesion molecule 1 (ICAM-1), homocysteine, low- and high-density lipoprotein (LDL and HDL) cholesterol, total cholesterol, apolipoprotein A-1 and B100, lipoprotein(a), and creatinine. RESULTS: Lower levels of physical activity and higher levels of BMI were independently associated (P for trend <.001) with adverse levels of nearly all lipid and inflammatory biomarkers. High BMI showed stronger associations with these biomarkers than physical inactivity. For example, using the reference group of physically active, normal weight women (energy expenditure > or =1000 kcal/week; BMI, 18.5-24.9) and adjusting for age, race, smoking, blood pressure, diabetes, menopausal status, and hormone use, the odds ratios (95% confidence intervals [CIs]) for having CRP >3 mg/L were: for inactive, normal weight women 1.26 (1.15-1.37); active, overweight 2.68 (2.41-2.98); inactive, overweight 3.11 (2.84-3.41); active, obese 8.25 (7.15-9.51); and inactive, obese 9.86 (8.84-10.99). In similar analyses, the odds ratios (95% CIs) for having HDL cholesterol <50 mg/dL were 1.20 (1.11-1.30); 2.25 (2.04-2.49); 2.62 (2.41-2.85); 4.21 (3.68-4.81); and 5.27 (4.77-5.84), respectively, and for having apolipoprotein B100 >120 mg/dL they were 1.21 (1.11-1.33); 1.86 (1.66-2.08); 2.06 (1.88-2.67); 2.35 (2.04-2.70); and 2.33 (2.09-2.59). Fibrinogen, ICAM-1, apolipoprotein A1, total cholesterol, and LDL cholesterol showed similar associations. By contrast, homocysteine, lipoprotein (a), and creatinine showed weak or nonsignificant associations. CONCLUSIONS: High BMI was more strongly related to adverse cardiovascular biomarker levels than physical inactivity. However, within BMI categories, physical activity was generally associated with more favorable cardiovascular biomarker levels than inactivity.

Biomarkers↗
PubMed2006

Androgen receptor polymorphisms and endometrial cancer risk.

The androgen receptor (AR) gene is a transcription factor responsible for mediating the physiological effects of androgens. Evidence suggests that androgens and the androgen receptor are involved in uterine cell proliferation. A polymorphic CAG repeat in exon 1 of the AR gene encodes a polyglutamine tract that is inversely correlated with the transcriptional activity of this gene. We assessed the association between the functional CAG repeat polymorphism and AR haplotypes and the risk of endometrial cancer in two nested case-control studies within the Nurses' Health Study (n = 222 cases, 666 controls) and the Women's Health Study (n = 137 cases, 411 controls) using conditional and unconditional logistic regression. Associations between AR CAG repeat polymorphism and endometrial cancer risk were similar in the 2 case-control studies. In the pooled analysis, women with an average repeat allele > or =22 repeats compared to <22 repeats were at a statistically significant decreased risk of endometrial cancer (odds ratio (OR) = 0.76; 95% confidence interval (CI), 0.59-0.98). Women with one or two long alleles (> or =27 repeats) compared to both alleles <22 repeats were also at a statistically significant decreased risk (OR = 0.60; 95% CI, 0.36-0.99). We observed a modest yet statistically significant association for each one unit increase in the average repeat length and endometrial cancer risk (OR = 0.94; 95% CI, 0.88-1.00). Associations for the AR CAG average repeat length and endometrial cancer risk differed by menopausal status (p = 0.02). No significant associations between the AR haplotypes and endometrial cancer risk were observed. Our findings suggest that an increasing number of functional CAG repeats may be associated with endometrial carcinogenesis because of AR's reduced ability to recruit coregulators and other transcriptional components. (supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020-7136/suppmat/index.html).

Adult↗
PubMed2006

A prospective study of hemoglobin A1c concentrations and risk of breast cancer in women.

Impaired glucose metabolism and hyperinsulinemia have been hypothesized to increase breast cancer risk. However, findings from observational studies relating blood concentrations of hyperinsulinemia markers to breast cancer risk have been inconsistent. We prospectively evaluated whether hemoglobin A1c (HbA1c) concentrations predict breast cancer risk in a large female cohort. We included 27,110 female participants of the Women's Health Study who were, at baseline, free of cancer and had usable blood specimens as well as sufficient information on potential risk factors for breast cancer. Relative risks (RR) and 95% confidence intervals (95% CI) were estimated from Cox proportional hazards regression models. All Ps were two sided. During an average of 10 years of follow-up, 790 incident cases of invasive breast cancer were confirmed. Higher baseline HbA1c levels were not associated with an increased risk of breast cancer. The multivariate RR for the highest relative to the lowest quintile of HbA1c levels was 0.87 (95% CI, 0.69-1.10; P(trend) = 0.22). Higher HbA1c levels were also not associated with an increased risk of breast cancer according to alternative clinical cutoff points for HbA1c or in the analyses stratified by body mass index or according to certain tumor characteristics. However, a weakly inverse association was noted among postmenopausal women, especially among those who had never used hormone therapy. There was also a weakly inverse association between HbA1c levels and estrogen receptor-negative breast tumors. These data suggest that higher HbA1c concentrations do not seem to increase risk of breast cancer among apparently healthy women.

Adult↗
PubMed2006

Colorectal cancer after start of nonsteroidal anti-inflammatory drug use.

PURPOSE: Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, have been consistently shown to reduce the risk of colorectal cancer (CRC) in non-experimental studies, but little is known of the factors associated with starting and continuing regular NSAID use and their effect on the NSAID and CRC association. SUBJECTS AND METHODS: We performed a prospective cohort study of 22,071 healthy male physicians aged 40 to 84 years without indications or contraindications to regular NSAID use at baseline. Annual questionnaires assessed quantity of NSAID use, occurrence of cancer, and risk factors for CRC. Propensity for regular NSAID use (>60 days/year) was estimated using generalized estimating equations. We used a time-varying Cox proportional hazards model to estimate the association between duration since initiation of regular NSAID use and risk for CRC. RESULTS: Regular non-aspirin and any NSAID use increased from 0% to 12% and 1% to 56% over time, respectively and was predicted by age, body mass index, alcohol consumption, medication use, coronary artery disease, gastrointestinal diseases, arthritis, hypertension, and headaches. Over a median follow-up of 18 years, 495 physicians were diagnosed with CRC. There was no trend of CRC risk with increased duration of regular NSAID use. Five or more years of regular use of any NSAID were associated with a relative risk for CRC of 1.0 (95% confidence interval: 0.7-1.5), after adjustment for predictors of regular NSAID use. CONCLUSION: Regular NSAID use was not associated with a substantial risk reduction of CRC after controlling for time-varying predictors of both NSAID use and CRC.

Adult↗
PubMed2006

Perceived exertion in physical activity and risk of gestational diabetes mellitus.

BACKGROUND: Physical activity has been associated with decreased risk of gestational diabetes mellitus. Expanding on 2 previously published analyses of absolute exertion measures (time spent and energy expended), we assessed the relation between perceived exertion during usual prepregnancy recreational physical activity and gestational diabetes. METHODS: We analyzed data from a Washington State 1998-2002 case-control study (216 cases, 472 controls) and a 1996-2002 prospective cohort study (897 participants) separately. We used logistic regression models to derive odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Among case-control participants, risk of gestational diabetes was markedly lower for women who reported very strenuous to maximal exertion in usual activity during the year before pregnancy versus those who reported negligible or minimal exertion (adjusted OR = 0.19; CI = 0.15-0.50). There was a direct inverse relation between perceived exertion and risk of gestational diabetes. This relation was also evident among the subset of participants who did not meet physical activity guidelines in the year before pregnancy. Similarly, the OR among cohort participants reporting very strenuous to maximal exertion was 0.57 (0.24-1.37) versus those reporting negligible to moderate exertion. CONCLUSIONS: These results suggest that risk of gestational diabetes is inversely related to the exertion perceived during recreational physical activity in the year before pregnancy. Perceived exertion may be a valuable addition to behavior and fitness measures in assessing relations between physical activity and pregnancy-related health outcomes.

Adult↗
PubMed2006

Metabolic abnormalities and risk for colorectal cancer in the physicians' health study.

BACKGROUND: Obesity and diabetes are established risk factors for colorectal cancer but have mainly been assessed independently. There are few data about whether the metabolic syndrome, which refers to a clustering of cardiovascular disease risk factors thought to be related to insulin resistance, including obesity, type 2 diabetes, hyperlipidemia, and hypertension, is associated with colorectal cancer risk. METHODS: During and after the randomized trial of aspirin and beta-carotene, 22,071 healthy male physicians, initially ages 40 to 84 years, reported overweight (body mass index, >or=27 kg/m2), diabetes, elevated blood pressure (>or=130/85 mmHg or use of antihypertensive medication), hypercholesterolemia (>or=240 mg/dL or use of lipid-lowering medication), and occurrence of cancer on annual questionnaires. Adjusted relative risks (RR) and 95% confidence intervals (95% CI) for time-varying metabolic abnormalities and colorectal cancer were estimated using a multivariable proportional hazards model. RESULTS: During 369,966 person-years of follow-up (median, 19 years), 494 physicians developed colorectal cancer. With aging of the cohort, the prevalence of having two or more abnormalities increased from 13% to 35%. Overweight (RR, 1.4; 95% CI, 1.1-1.7) and diabetes (RR, 1.5; 95% CI, 1.1-2.0) were associated with increased risk for colorectal cancer, whereas elevated blood pressure (RR, 1.1; 95% CI, 0.9-1.3) and hypercholesterolemia (RR, 0.9; 95% CI, 0.7-1.1) were not. This model assessing metabolic abnormalities independently was more predictive for colorectal cancer than a model based on the number of abnormalities (each additional abnormality RR, 1.16; 95% CI, 1.05-1.29). CONCLUSIONS: Out of the markers of the metabolic syndrome assessed, overweight and diabetes are risk factors for colorectal cancer, whereas, in contrast to their role in cardiovascular disease, elevated blood pressure and hypercholesterolemia are not.

Adult↗
PubMed2006

Vitamin E and risk of type 2 diabetes in the women's health study randomized controlled trial.

We directly assessed the efficacy of vitamin E supplements for primary prevention of type 2 diabetes among apparently healthy women in the Women's Health Study randomized trial. Between 1992 and 2004, 38,716 apparently healthy U.S. women aged >or=45 years and free of diabetes, cancer, and cardiovascular disease were in two randomly assigned intervention groups and received 600 IU of vitamin E (alpha-tocopherol, n = 19,347) or placebo (n = 19,369) on alternate days. During a median 10-year follow-up, there were 827 cases of incident type 2 diabetes in the vitamin E group and 869 in the placebo group, a nonsignificant 5% risk reduction (relative risk [RR] 0.95 [95% CI 0.87-1.05], P = 0.31). There was no evidence that diabetes risk factors including age, BMI, postmenopausal hormone use, multivitamin use, physical activity, alcohol intake, and smoking status modified the effect of vitamin E on the risk of type 2 diabetes. In a sensitivity analysis taking compliance into account, women in the vitamin E group had an RR of 0.93 (95% CI 0.83-1.04) (P = 0.21) compared with those randomized to placebo. In this large trial with 10-year follow-up, alternate-day doses of 600 IU vitamin E provided no significant benefit for type 2 diabetes in initially healthy women.

Aged↗
PubMed2005

Folate, vitamin B6, multivitamin supplements, and colorectal cancer risk in women.

The authors evaluated associations between intakes of folate and vitamin B(6) and colorectal cancer risk among women enrolled in a randomized trial on aspirin and vitamin E in disease prevention. At baseline (1992-1995), 37,916 US women aged >or=45 years who were free of cancer and cardiovascular disease provided dietary information. During an average of 10.1 years of follow-up (through February 20, 2004), 220 colorectal adenocarcinoma cases were documented. Total folate and vitamin B(6) intakes were not significantly associated with the risk of colorectal cancer. However, dietary intakes of folate and vitamin B(6) were significantly inversely associated with colorectal cancer risk among women who were not taking supplements containing folate and vitamin B(6). Multivariable relative risks among women in the highest quintiles of intake versus the lowest were 1.16 (95% confidence interval (CI): 0.76, 1.79) for total folate, 1.14 (95% CI: 0.77, 1.69) for total vitamin B(6), 0.46 (95% CI: 0.26, 0.81) for dietary folate, and 0.69 (95% CI: 0.41, 1.15) for dietary vitamin B(6). The use of multivitamin supplements was not related to colorectal cancer risk. These findings suggest that higher dietary intakes of folate and vitamin B(6) may reduce the risk of colorectal cancer in women. An alternative explanation is that other factors related to dietary intakes of folate and vitamin B(6) account for the inverse associations.

Colorectal Neoplasms↗
PubMed2005

Low-dose aspirin in the primary prevention of cancer: the Women's Health Study: a randomized controlled trial.

CONTEXT: Basic research and observational evidence as well as results from trials of colon polyp recurrence suggest a role for aspirin in the chemoprevention of cancer. OBJECTIVE: To examine the effect of aspirin on the risk of cancer among healthy women. DESIGN, SETTING, AND PARTICIPANTS: In the Women's Health Study, a randomized 2 x 2 factorial trial of aspirin and vitamin E conducted between September 1992 and March 2004, 39 876 US women aged at least 45 years and initially without previous history of cancer, cardiovascular disease, or other major chronic illness were randomly assigned to receive either aspirin or aspirin placebo and followed up for an average of 10.1 years. INTERVENTION: A dose of 100 mg of aspirin (n=19 934) or aspirin placebo (n=19 942) administered every other day. MAIN OUTCOME MEASURES: Confirmed newly diagnosed invasive cancer at any site, except for nonmelanoma skin cancer. Incidence of breast, colorectal, and lung cancer were secondary end points. RESULTS: No effect of aspirin was observed on total cancer (n = 2865; relative risk [RR], 1.01; 95% confidence interval [CI], 0.94-1.08; P = .87), breast cancer (n = 1230; RR, 0.98; 95% CI, 0.87-1.09; P = .68), colorectal cancer (n = 269; RR, 0.97; 95% CI, 0.77-1.24; P = .83), or cancer of any other site, with the exception of lung cancer for which there was a trend toward reduction in risk (n = 205; RR, 0.78; 95% CI, 0.59-1.03; P = .08). There was also no reduction in cancer mortality either overall (n = 583; RR, 0.95; 95% CI, 0.81-1.11; P = .51) or by site, except for lung cancer mortality (n = 140; RR, 0.70; 95% CI, 0.50-0.99; P = .04). No evidence of differential effects of aspirin by follow-up time or interaction with vitamin E was found. CONCLUSIONS: Results from this large-scale, long-term trial suggest that alternate day use of low-dose aspirin (100 mg) for an average 10 years of treatment does not lower risk of total, breast, colorectal, or other site-specific cancers. A protective effect on lung cancer or a benefit of higher doses of aspirin cannot be ruled out.

Aspirin↗
PubMed2005

Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women's Health Study: a randomized controlled trial.

CONTEXT: Basic research provides plausible mechanisms and observational studies suggest that apparently healthy persons, who self-select for high intakes of vitamin E through diet or supplements, have decreased risks of cardiovascular disease and cancer. Randomized trials do not generally support benefits of vitamin E, but there are few trials of long duration among initially healthy persons. OBJECTIVE: To test whether vitamin E supplementation decreases risks of cardiovascular disease and cancer among healthy women. DESIGN, SETTING, AND PARTICIPANTS: In the Women's Health Study conducted between 1992 and 2004, 39 876 apparently healthy US women aged at least 45 years were randomly assigned to receive vitamin E or placebo and aspirin or placebo, using a 2 x 2 factorial design, and were followed up for an average of 10.1 years. INTERVENTION: Administration of 600 IU of natural-source vitamin E on alternate days. MAIN OUTCOME MEASURES: Primary outcomes were a composite end point of first major cardiovascular event (nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death) and total invasive cancer. RESULTS: During follow-up, there were 482 major cardiovascular events in the vitamin E group and 517 in the placebo group, a nonsignificant 7% risk reduction (relative risk [RR], 0.93; 95% confidence interval [CI], 0.82-1.05; P = .26). There were no significant effects on the incidences of myocardial infarction (RR, 1.01; 95% CI, 0.82-1.23; P = .96) or stroke (RR, 0.98; 95% CI, 0.82-1.17; P = .82), as well as ischemic or hemorrhagic stroke. For cardiovascular death, there was a significant 24% reduction (RR, 0.76; 95% CI, 0.59-0.98; P = .03). There was no significant effect on the incidences of total cancer (1437 cases in the vitamin E group and 1428 in the placebo group; RR, 1.01; 95% CI, 0.94-1.08; P = .87) or breast (RR, 1.00; 95% CI, 0.90-1.12; P = .95), lung (RR, 1.09; 95% CI, 0.83-1.44; P = .52), or colon cancers (RR, 1.00; 95% CI, 0.77-1.31; P = .99). Cancer deaths also did not differ significantly between groups. There was no significant effect of vitamin E on total mortality (636 in the vitamin E group and 615 in the placebo group; RR, 1.04; 95% CI, 0.93-1.16; P = .53). CONCLUSIONS: The data from this large trial indicated that 600 IU of natural-source vitamin E taken every other day provided no overall benefit for major cardiovascular events or cancer, did not affect total mortality, and decreased cardiovascular mortality in healthy women. These data do not support recommending vitamin E supplementation for cardiovascular disease or cancer prevention among healthy women.

Aged↗
PubMed2005

Intakes of calcium and vitamin D and risk of colorectal cancer in women.

In vivo and in vitro studies have suggested a protective role of calcium and vitamin D in the development of colorectal cancer. However, epidemiologic data have been inconclusive. The authors prospectively assessed intakes of calcium and vitamin D in relation to risk of colorectal cancer in a large, prospective, female cohort from the US Women's Health Study. In 1993, 39,876 women aged > or = 45 years and free of cardiovascular disease and cancer were enrolled in the study. During an average follow-up of 10 years, 223 of 36,976 women eligible for the present study developed colorectal cancer. Intakes of calcium and vitamin D from dietary sources and supplements were assessed with a baseline food frequency questionnaire. Cox proportional hazards regression was used to estimate relative risks and 95% confidence intervals. Intakes of total calcium and vitamin D were not associated with risk of colorectal cancer; multivariate relative risks comparing the highest with the lowest quintile were 1.20 (95% confidence interval: 0.79, 1.85; p for trend = 0.21) for total calcium and 1.34 (95% confidence interval: 0.84, 2.13; p for trend = 0.08) for total vitamin D. Intakes of both nutrients from specific types of sources, including diet and supplements, were also not significantly associated with colorectal cancer risk. Data provide little support for an association of calcium and vitamin D intake with colorectal cancer risk.

Calcium, Dietary↗
PubMed2005

C-reactive protein levels are not associated with increased risk for colorectal cancer in women.

BACKGROUND: Observations that risk for colorectal cancer is elevated in patients with inflammatory bowel disease and that long-term use of anti-inflammatory drugs may reduce colorectal cancer risk have raised the possibility that inflammation may play a role in the development of colorectal cancer. While a recent prospective study observed a positive association between C-reactive protein (CRP), a marker of inflammation, and risk for colon cancer, data testing this hypothesis are sparse. OBJECTIVE: To evaluate whether plasma CRP levels predict colorectal cancer risk in women. DESIGN: Prospective cohort study, with 97% morbidity follow-up and 100% mortality follow-up within the past 2 years. SETTING: Women's Health Study. PARTICIPANTS: 27,913 apparently healthy women age 45 years or older who had CRP measured at entry into a trial of low-dose aspirin and vitamin E. Maximum length of intervention and follow-up was 10.8 years. MEASUREMENTS: Self-reported incident colorectal adenocarcinoma confirmed by medical record review. RESULTS: 169 women developed colorectal adenocarcinomas during follow-up. Baseline CRP levels were not significantly associated with colorectal cancer risk. The multivariate hazard ratios according to cutoff points for CRP proposed in clinical guidelines were 0.79 (95% CI, 0.53 to 1.17) for the category of 1 to 3 mg/L and 0.66 (CI, 0.43 to 1.03) for the category of greater than 3 mg/L (P for trend = 0.09), as compared with the category of less than 1 mg/L. High CRP levels were also not associated with increased risk in analyses done according to tumor location and stage at diagnosis, according to alternative cutoff points for CRP, or in any of the subgroups evaluated. LIMITATIONS: Despite multivariate analysis, residual confounding might still be present. Although this study was prospective, we cannot completely exclude undetected cancer at baseline. Measurements for CRP were available for only 71% of women in the cohort; however, the women who did and those who did not provide blood were mostly similar. CONCLUSIONS: Plasma CRP levels do not appear to predict an increased risk for developing colorectal cancer in apparently healthy women. Low-grade inflammation may not play an important role in increasing the risk for colorectal cancer.

Adenocarcinoma↗