Consumption of Yoghurt and Other Dairy Products and Risk of Colorectal Cancer in Iran: The IROPICAN Study

Background: There is evidence of an inverse association between yoghurt intake and risk of colorectal cancer (CRC). We aimed at investigating the association between the intake of yoghurt and other dairy foods consumed in Iran and CRC risk. Methods: Our analysis included 4070 subjects within the IROPICAN (Iran Study of Opium and Cancer) study. Detailed information was collected by the use of validated questionnaires. We estimated adjusted odds ratios (OR) and 95% confidence intervals (CI) for the association between the intake of total dairy products, and, separately, of yoghurt, milk, cheese, kashk, dough, cream, ice cream, and other milk products, and CRC using unconditional logistic regression analyses. The intake was categorized in tertiles. Results: Overall, we analyzed 865 cases and 3205 controls. Total dairy products intake was not associated with CRC. The OR for one tertile increase (OR_T) in yoghurt intake was 0.97 (95% CI 0.87–1.08) for CRC and 0.66 (95% CI 0.52–0.84) for proximal colon cancer. Cream intake was associated with CRC (OR_T3 = 1.33, 95% CI 1.08–1.64), colon (OR_T3 = 1.37, 95% CI 1.03–1.81), and proximal cancer (OR_T3 = 1.29, 95% CI 1.04–1.61). The OR of distal colon cancer for ice cream intake was 0.59 (95% CI 0.43–0.82). Other dairy products were not associated with CRC risk.     

Serum carotenoids, retinol, and tocopherols, and colorectal cancer risk in a Japanese cohort: effect modification by sex for carotenoids

To examine associations of serum carotenoids, retinol, and tocopherols with colorectal cancer risk, we conducted a case-control study nested within the Japan Collaborative Cohort Study. These micronutrients were measured in prediagnostic serum samples from 116 men and women who developed colorectal cancer during an 8-yr follow-up period and from 298 matched controls. In men, the higher level of serum total carotenoids was associated with a decreased risk: The multivariate-adjusted odds ratio (OR) for the highest vs. the lowest tertile was 0.34 (95% confidence interval [CI] = 0.11-1.00; trend P over tertiles = 0.040). In women, the higher levels of alpha- and and total carotenoids were instead related to an increased risk: The corresponding ORs were 4.72 (95% CI = 1.29-17.3), 2.00 (0.70-5.73), and 2.47 (0.73-8.34), respectively (trend P = 0.007, 0.040, and 0.064, respectively). We also found a somewhat decreasing risk with increased serum retinol in all subjects and alpha-tocopherol in men: The ORs (95% CI) for the highest tertiles were 0.29 (0.11-0.78; trend P over tertiles = 0.010) and 0.29 (0.07-1.17; trend P = 0.098), respectively. The effects of some carotenoids on colorectal cancer risk may be modified by sex or by factors associated with sex, including smoking and drinking habits.     

Longitudinal study of the inception of perimenopause in relation to lifetime history of sexual or physical violence

STUDY OBJECTIVE: To investigate of the extent to which violence over the life course accelerates the onset of perimenopause, as measured by menstrual changes. DESIGN: Prospective cohort study. SETTING: Boston, Massachusetts. PARTICIPANTS: 603 premenopausal women aged 36-45 years at baseline who completed a cross sectional survey on childhood and adult violence history. MAIN OUTCOME MEASURE: Time to perimenopause, defined as time in months from baseline interview to a woman's report of (1) an absolute change of at least seven days in menstrual cycle length from baseline or subjective report of menstrual irregularity; (2) a change in menstrual flow amount or duration; or (3) cessation of periods for at least three months, whichever came first. MAIN RESULTS: Experience of abuse was associated with delayed onset of menstrual changes indicative of onset of perimenopause. Women reporting childhood or adolescent abuse entered perimenopause about 35% slower than women who reported no abuse (IRR(adj) = 0.65, 95% CI 0.45 to 0.95) after adjusting for age, age at menarche, ever live birth, ability to maintain living standard, smoking, BMI, and depression. There was a similar association among women who reported first abuse during adulthood (IRR(adj) = 0.72, 95% CI 0.28 to 1.80). These findings persisted when the cohort was restricted to non-depressed women (childhood/adolescent IRR(adj) = 0.57, 95% CI 0.36 to 0.90; adulthood IRR(adj) = 0.63, 95% CI 0.23 to 1.77). CONCLUSIONS: This study is the first longitudinal analysis of the timing of perimenopause to show an association with a history of physical or sexual abuse. Further study of the relation between violence and reproductive aging is needed.     

Marine fatty acid intake is associated with breast cancer prognosis

EPA and DHA, long-chain (n-3) PUFA largely obtained from fish, inhibit the proliferation of breast cancer cells in vitro and reduce the initiation and progression of breast tumors in laboratory animals. Our purpose in this analysis was to examine whether intake of these marine fatty acids (EPA and DHA) were associated with prognosis in a cohort of women who had been diagnosed and treated for early stage breast cancer (n = 3,081). Median follow-up was 7.3 y. Dietary intake was assessed using 24-h recalls (~4 recalls per dietary assessment obtained at 7 time points over 6 y). Survival models with time-dependent covariates were used to examine the association of repeated measures of dietary intake of EPA and DHA from food (i.e., marine sources) and supplements with disease-free survival and overall survival. Women with higher intakes of EPA and DHA from food had an approximate 25% reduced risk of additional breast cancer events [tertile 2: HR = 0.74 (95% CI = 0.58-0.94); tertile 3: HR = 0.72 (95% CI = 0.57-0.90)] compared with the lowest tertile of intake. Women with higher intakes of EPA and DHA from food had a dose-dependent reduced risk of all-cause mortality [tertile 2: HR = 0.75 (95% CI = 0.55-1.04); tertile 3: HR = 0.59 (95% CI = 0.43-0.82)]. EPA and DHA intake from fish oil supplements was not associated with breast cancer outcomes. The investigation indicates that marine fatty acids from food are associated with reduced risk of additional breast cancer events and all-cause mortality.     

Dairy, calcium, and vitamin D intakes and prostate cancer risk in the National Health and Nutrition Examination Epidemiologic Follow-up Study cohort

BACKGROUND: Dairy intake may increase prostate cancer risk, but whether this is due to calcium's suppression of circulating vitamin D remains unclear. Findings on calcium and vitamin D intake and prostate cancer are inconsistent. OBJECTIVE: We examined the association of dairy, calcium, and vitamin D intake with prostate cancer. DESIGN: In a prospective study of 3612 men followed from 1982-1984 to 1992 for the first National Health and Nutrition Examination Epidemiologic Follow-up Study, 131 prostate cancer cases were identified. Dietary intake was estimated from questionnaires completed in 1982-1984. Relative risk (RR) and 95% CIs were estimated by using Cox proportional hazards models adjusted for age, race, and other covariates. RESULTS: Compared with men in the lowest tertile for dairy food intake, men in the highest tertile had a relative risk (RR) of 2.2 (95% CI: 1.2, 3.9; trend P = 0.05). Low-fat milk was associated with increased risk (RR = 1.5; 95% CI: 1.1, 2.2; third compared with first tertile; trend P = 0.02), but whole milk was not (RR = 0.8; 95% CI: 0.5, 1.3; third compared with first tertile; trend P = 0.35). Dietary calcium was also strongly associated with increased risk (RR = 2.2; 95% CI: 1.4, 3.5; third compared with first tertile; trend P = 0.001). After adjustment for calcium intake, neither vitamin D nor phosphorus was clearly associated with risk. CONCLUSIONS: Dairy consumption may increase prostate cancer risk through a calcium-related pathway. Calcium and low-fat milk have been promoted to reduce risk of osteoporosis and colon cancer. Therefore, the mechanisms by which dairy and calcium might increase prostate cancer risk should be clarified and confirmed.     

Dietary Advanced Glycation End-Products and Colorectal Cancer Risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) Study

Dietary advanced glycation end-products (dAGEs) have been hypothesized to be associated with a higher risk of colorectal cancer (CRC) by promoting inflammation, metabolic dysfunction, and oxidative stress in the colonic epithelium. However, evidence from prospective cohort studies is scarce and inconclusive. We evaluated CRC risk associated with the intake of dAGEs in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Dietary intakes of three major dAGEs: N^ε-carboxy-methyllysine (CML), N^ε-carboxyethyllysine (CEL), and N^δ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) were estimated in 450,111 participants (median follow-up = 13 years, with 6162 CRC cases) by matching to a detailed published European food composition database. Hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of dAGEs with CRC were computed using multivariable-adjusted Cox regression models. Inverse CRC risk associations were observed for CML (HR comparing extreme quintiles: HR_Q5vs._Q1 = 0.92, 95% CI = 0.85–1.00) and MG-H1 (HR_Q5vs._Q1 = 0.92, 95% CI = 0.85–1.00), but not for CEL (HR_Q5vs._Q1 = 0.97, 95% CI = 0.89–1.05). The associations did not differ by sex or anatomical location of the tumor. Contrary to the initial hypothesis, our findings suggest an inverse association between dAGEs and CRC risk. More research is required to verify these findings and better differentiate the role of dAGEs from that of endogenously produced AGEs and their precursor compounds in CRC development.     

Post-cancer diagnosis dietary inflammatory potential is associated with survival among women diagnosed with colorectal cancer in the Women’s Health Initiative

Dietary factors may influence colorectal cancer (CRC) survival through effects on inflammation. We examined the association between post-CRC diagnosis inflammatory potential of diet and all-cause and cancer-specific mortality in the Women’s Health Initiative. The study included 463 postmenopausal women who developed CRC during follow-up and completed a food frequency questionnaire (FFQ), on average 1.7 years after diagnosis. Women were followed from CRC diagnosis until death, censoring, or the end of follow-up in October 2014. Energy-adjusted dietary inflammatory index (E-DII)® scores were calculated from the FFQ and dietary supplement inventory. Cox proportional hazards models were fitted to estimate multivariable-adjusted HRs and 95% confidence intervals (CIs) for all-cause, total cancer, and CRC-specific mortality with the most pro-inflammatory E-DII scores (tertile 3) as referent. After a median 11.6 years of follow-up, 162 deaths occurred, including 77 from CRC. Lowest tertile (i.e., most anti-inflammatory) E-DII scores from diet plus supplements were associated with significantly lower all-cause mortality (HRT1vsT3 = 0.49; 95% CI 0.31–0.79) compared to the most pro-inflammatory E-DII tertile. Modest associations with total cancer mortality or CRC-specific mortality were observed, though 95% CIs included 1. Consuming a dietary pattern and supplements with more anti-inflammatory potential after CRC diagnosis may improve overall survival among postmenopausal women.     

Potato Consumption and Risk of Colorectal Cancer in the Norwegian Women and Cancer Cohort

Potatoes are the fourth most plentiful food crop in the world, yet the scientific literature on the health effects of potato consumption is scarce. This study aimed to investigate the association between potato consumption and the risk of colorectal cancer (CRC) among 79,778 women aged 41–70, in the Norwegian Women and Cancer study. Information on diet, lifestyle, and health was collected by questionnaire. CRC cases (n = 912) were identified through registry linkage. Adjusted Cox proportional hazard models were used to estimate the association between potato consumption and the risk of CRC. Results showed that high potato consumption was associated with a higher risk of CRC (hazard ratio [HR]: 1.32, 95% confidence interval [CI]: 1.10, 1.60 for ≥3 potatoes per day versus 0–7 potatoes per week). The same association was found for rectal cancer (HR: 1.68, 95% CI: 1.19, 2.36), and same tendencies were found for colon cancer (HR: 1.20, 95% CI: 0.96, 1.50). When stratified by body mass index (BMI) (<25 and ≥25 kg/m²), significant associations were found with BMI <25 kg/m² for CRC (HR: 1.48, 95% CI: 1.15, 1.89) and rectal cancer (HR: 1.95, 95% CI: 1.25, 3.06). No significant interaction between potato consumption and BMI (P = 0.49) was found.     

Fruits and vegetables intake differentially affects estrogen receptor negative and positive breast cancer incidence rates

Despite intensive research, the evidence for a protective effect of fruits and vegetables on breast cancer risk remains inconclusive. Other risk factors for breast cancer seem to vary with the estrogen receptor status of the breast tumor, and it is thus possible that the inconsistent results regarding a preventive effect of fruits and vegetables are due to lack of controlling for estrogen receptor status. The objective of this study was to investigate the effect of fruit and vegetable intake on postmenopausal breast cancer and explore whether the estrogen receptor status of the tumor modifies this relation. Postmenopausal women (n = 23,798; aged 50-64 y) provided information about diet and established risk factors for breast cancer in the cohort "Diet, Cancer and Health." During follow-up, 425 cases were diagnosed with breast cancer. Associations between intake of fruits and vegetables and the breast cancer rate were analyzed using Cox's regression model. The association for all breast cancers was an incidence rate ratio (IRR) of 1.02 (95% CI, 0.98-1.06) per 100 g/d increment of total intake of fruits, vegetables and juice. For estrogen receptor-positive (ER(+)) breast cancer, a borderline significant increase in the rate was seen, IRR: 1.05 (95% CI, 1.00-1.10), whereas a preventive effect was seen for estrogen receptor-negative (ER(-)) breast cancers, IRR: 0.90 (95% CI, 0.81-0.99). In conclusion, we did not find the overall breast cancer rate to be associated with the intake of fruits and vegetables, but there seemed to be different effects for ER(+) and ER(-) breast cancer.     

Macro- and Micronutrients Consumption and the Risk for Colorectal Cancer among Jordanians

Objective: Diet and lifestyle have been reported to be important risk factors for the development of colorectal cancer (CRC). However, the association between total energy and nutrient intake and the risk of developing CRC has not been clearly explained. The aim of our study is to examine the relationship between total energy intake and other nutrients and the development of CRC in the Jordanian population. Research Methods and Procedures: Dietary data was collected from 169 subjects who were previously diagnosed with CRC, and 248 control subjects (matched by age, gender, occupation and marital status). These control subjects were healthy and disease free. Data was collected between January 2010 and December 2012, using interview-based questionnaires. Logistic regression was used to evaluate the association between quartiles of total energy, macro- and micronutrient intakes with the risk of developing CRC in our study population. Results: Total energy intake was associated with a higher risk of developing CRC (OR = 2.60 for the highest versus lowest quartile of intake; 95% CI: 1.21–5.56, p-trend = 0.03). Intakes of protein (OR = 3.62, 95% CI: 1.63–8.05, p-trend = 0.002), carbohydrates (OR = 1.41, 95% CI: 0.67–2.99, p-trend = 0.043), and percentage of energy from fat (OR = 2.10, 95% CI: 0.38–11.70, p-trend = 0.009) significantly increased the risk for the development of CRC. Saturated fat, dietary cholesterol and sodium intake showed a significant association with the risk of developing CRC (OR = 5.23, 95% CI: 2.33–11.76; OR = 2.48, 95% CI: 1.18–5.21; and OR = 3.42, 95% CI: 1.59–7.38, respectively), while vitamin E and caffeine intake were indicative of a protective effect against the development of CRC, OR = 0.002 (95% CI: 0.0003–0.011) and 0.023 (95%CI: 0.008–0.067), respectively. Conclusion: Our results suggest an increased risk for the development of CRC in subjects with high dietary intake of energy, protein, saturated fat, cholesterol, and sodium, and diets high in vitamin E and caffeine were suggestive of a protective effect against the risk of developing CRC. Impact: This is the first study in Jordan to suggest that it may be possible to reduce CRC risk by adjusting the intake of some macro-and micronutrients.     

Association Between Dietary Inflammation Index and The Risk of Colorectal Cancer: A Meta-Analysis

Objectives: We performed a meta-analysis to assess the association and possible dose–response relationship between dietary inflammation index (DII)? and colorectal cancer (CRC). Methods: A literature search was performed in PubMed, Web of Science and Chinese National Knowledge Infrastructure (CNKI) database for all relevant studies. The pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated by random effects model. Results: A total of eight studies were included in this meta-analysis. The pooled RRs of CRC, colon and rectal cancer for the highest versus lowest DII categories were 1.43 (95% CI 1.25–1.63), 1.37 (95% CI 1.16–1.62) and 1.44 (95% CI 1.23–1.69), respectively. A significant positive association was observed both in cohort studies (RR = 1.26, 95% CI 1.14–1.38) and case–control studies (RR = 1.81, 95% CI 1.48–2.22). Nonlinear associations between DII scores and the risk of CRC, colon and rectal cancer were found in the dose–response analyses, the results showed that the risks of CRC, colon and rectal cancer increased slowly when the DII score was above 1.30, 2.21, and 1.30, respectively. Conclusion: Higher DII scores might increase CRC risk. Thus, people should adopt more anti-inflammatory diets such as those high in vegetables, fruits, whole grains, herbs, and spices.     

Adherence to the Western,Prudent and Mediterranean Dietary Patterns and Colorectal Cancer Risk: Findings from the Spanish Cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Spain)

The aim of this study was to explore the association between three previously identified dietary patterns (Western, Prudent, and Mediterranean) and colorectal cancer (CRC) risk by sex and cancer subtype. The Spanish cohort of the European Prospective Investigation into Cancer and Nutrition study provided dietary and epidemiological information from 15,629 men and 25,808 women recruited between 1992 and 1996. Among them, 568 CRC cases and 3289 deaths were identified during a median follow-up of 16.98 years. The associations between adherence to the three dietary patterns and CRC risk (overall, by sex, and by tumour location: proximal and distal colon and rectum) were investigated by fitting multivariate Cox proportional hazards regression models stratified by study centre and age. Possible heterogeneity of the effects by sex and follow-up time (1–10 vs. ≥10 years) was also explored. While no clear effect of the Prudent dietary pattern on CRC risk was found, a suggestive detrimental effect of the Western dietary pattern was observed, especially during the first 10 years of follow-up (HR_1SD-increase (95% CI): 1.17 (0.99–1.37)), among females (HR_1SD-increase (95% CI): 1.31 (1.06–1.61)), and for rectal cancer (HR_1SD-increase (95% CI): 1.38 (1.03–1.84)). In addition, high adherence to the Mediterranean pattern seemed to protect against CRC, especially when restricting the analyses to the first 10 years of follow-up (HR_1SD-increase (95% CI): 0.84 (0.73–0.98)), among males (HR_1SD-increase (95% CI): 0.80 (0.65–0.98)), and specifically against distal colon cancer (HR_1SD-increase (95% CI): 0.81 (0.63–1.03)). In conclusion, low adherence to the Western diet and high adherence to the Mediterranean dietary pattern could prevent CRC, especially distal colon and rectal cancer.     

Dietary fibre and risk of colorectal cancer in the Breast Cancer Detection Demonstration Project (BCDDP) follow-up cohort

BACKGROUND: The hypothesis that increased intake of dietary fibre lowers the risk of colorectal cancer (CRC) has recently been weakened by results from cohort and intervention studies that did not detect such an association. We investigated the association between dietary fibre intake and risk of CRC in a cohort of women that prospectively answered a food frequency questionnaire (FFQ). METHODS: We studied 45 491 women in the Breast Cancer Detection Demonstration Project (BCDDP) follow-up cohort. A 62-item FFQ was administered from 1987 and 1989 to assess dietary intake. Participants received follow-up questionnaires (in 1992-1995 and 1995-1998) on which they reported incident cancers. Cases were also identified through searches of the National Death Index and state cancer registries. Cox proportional hazard regression was used to generate risk ratios and 95% CI for quintiles of total fibre intake and fibre subtypes. RESULTS: During a mean follow-up time of 8.5 years we identified 487 colorectal cancer cases. The 10th and 90th percentiles of dietary fibre intake were 5.4 g and 18.2 g respectively. For total fibre we observed no association with colorectal cancer (fifth versus first quintile, RR = 0.94, 95% CI: 0.71-1.23). Analyses by subgroup of fibre and by anatomical subsite did not reveal any stronger inverse associations. CONCLUSIONS: Within a cohort of older women characterized by a relatively low fibre intake, there was little evidence that dietary fibre intake lowers the risk of colorectal cancer.     

Dietary risk factors for kidney cancer in Eastern and Central Europe

The authors examined the role of diet in the high-risk population of Central Europe among 1,065 incident kidney cancer cases and 1,509 controls in Russia, Romania, Poland, and the Czech Republic. They observed an increased association with kidney cancer for consumption of milk (odds ratio (OR) = 1.46, 95% confidence interval (CI): 1.15, 1.84) and yogurt (OR = 1.34, 95% CI: 1.07, 1.67), as well as all meat (OR = 1.27, 95% CI: 1.06, 1.51 compared with the lowest tertile). High consumption of all vegetables (OR = 0.64, 95% CI: 0.51, 0.80) and cruciferous vegetables (OR = 0.68, 95% CI: 0.55, 0.84) was inversely associated with kidney cancer. In addition, high consumption of preserved vegetables increased the risk of kidney cancer (OR = 1.66, 95% CI: 1.24, 2.21). Alcohol consumption did not appear to be associated with kidney cancer. This 1999-2003 study provides further evidence that diet may play a role in the development of kidney cancer, with a particularly strong protective association for high vegetable intake. The increased risk associated with dairy products, preserved vegetables, and red meat provides clues to the high rates of kidney cancer in this population.     

Assessment of risk associated with specific fatty acids and colorectal cancer among French-Canadians in Montreal: a case-control study

BACKGROUND: Discrepancies in findings on the association between dietary fats and colorectal cancer (CRC) persist, and it is hypothesized that fatty acids (FA) may modulate CRC risk because of their physiological functions. METHODS: Between 1989 and 1993, a case-control study involving 402 cases and 668 population-based controls was conducted among French-Canadians. Dietary intake was assessed by a food frequency questionnaire. RESULTS: Oleic acid was the major FA consumed by the study population. A significant inverse association was found among females between CRC and butyrate (OR = 0.57; 95% CI: 0.34-0.96; P = 0.006), alpha-linoleic acid (ALA) (OR = 0.78; 95% CI: 0.46-1.32; P = 0.016), and w-3 FA (OR = 0.84; 95% CI: 0.50-1.41; P = 0.028), comparing the upper to the lower quartiles of intake. An increased risk was associated with arachidonic acid (AA) (OR = 2.03; 95% CI: 1.16-3.54; P = 0.001) among males, and with the w6/w3 ratio (OR = 1.47; 95% CI: 0.86-2.50; P = 0.001) among females. Arachidonic acid was linked with up to fivefold increased risk (OR = 5.33; 95% CI: 2.04-13.95; P = 0.0004 for trend) among men with high vitamin C intake. Females with low carotenoids intake were at elevated risk associated with AA (OR = 4.07; 95% CI: 1.84-8.99; P = 0.003); eicosapentaenoic acid (OR = 3.50; 95% CI: 1.59-7.71; P = 0.015), and docosahexaenoic acid (OR = 5.77; 95% CI: 2.50-13.33; P = 0.002), comparing the upper with the lower quartiles of intake. CONCLUSION: The results of this study suggest that independently of total energy intake, substituting AA by butyrate, ALA, or omega-3 FA may reduce CRC risk. The role of interactions between vitamin C, total carotenoids, and polyunsaturated FA requires further investigation.     

Are children with birth defects at higher risk of childhood cancers?

Birth defects may influence the risk of childhood cancer development through a variety of mechanisms. The rarity of both birth defects and childhood cancers makes it challenging to study these associations, particularly for the very rare instances of each. To address this limitation, the authors conducted a record linkage-based cohort study among Texas children born between 1996 and 2005. Birth defects in the cohort were identified through the Texas Birth Defects Registry, and children who developed cancer were identified by using record linkage with Texas Cancer Registry data. Over 3 million birth records were included; 115,686 subjects had birth defects, and there were 2,351 cancer cases. Overall, children with a birth defect had a 3-fold increased risk of developing cancer (incidence rate ratio (IRR) = 3.05, 95% confidence interval (CI): 2.65, 3.50), with germ cell tumors (IRR = 5.19, 95% CI: 2.67, 9.41), retinoblastomas (IRR = 2.34, 95% CI: 1.21, 4.16), soft-tissue sarcomas (IRR = 2.12, 95% CI: 1.09, 3.79), and leukemias (IRR = 1.39, 95% CI: 1.09, 1.75) having statistically significant elevated point estimates. All birth defect groups except for musculoskeletal had increased cancer incidence. Untangling the strong relation between birth defects and childhood cancers could lead to a better understanding of the genetic and environmental factors that affect both conditions.     

Total homocysteine and cognitive decline in a community-based sample of elderly subjects: the Rotterdam Study.

Homocysteine has been associated with an increased risk of cardiovascular disease. Cardiovascular diseases have been related to cognitive decline. The authors investigated the association of homocysteine with concurrent cognitive impairment and subsequent cognitive decline in a random sample of 702 community-dwelling respondents aged 55 years or over to the prospective Rotterdam Study in 1990-1994. Multiple logistic regression was used to calculate odds ratios and 95 percent confidence intervals for the association between total homocysteine levels and cognitive impairment (Mini-Mental State Examination (MMSE) score <26) and cognitive decline (drop in MMSE score of >1 point/year). Mean duration of follow-up was 2.7 years. After adjustment for age, sex, and education, there was no relation between total homocysteine and cognitive impairment (highest vs. lowest tertile: odds ratio (OR) = 1.30, 95% confidence interval (CI): 0.50, 3.38) or cognitive decline (middle vs. lowest tertile: OR = 1.14, 95% CI: 0.67, 1.93; highest vs. lowest tertile: OR = 0.91, 95% CI: 0.52, 1.58). Subjects who were lost to follow-up due to death or nonresponse had slightly higher age-adjusted homocysteine levels and lower MMSE scores at baseline. Sensitivity analyses showed that selective loss to follow-up was not a likely explanation for the absence of an association in the participants. Although a relation between homocysteine and reduced cognitive function is biologically plausible, this study suggests no such association in a community-based sample of the elderly.     

Bowel movement and constipation frequencies and the risk of colorectal cancer among men in the Netherlands Cohort Study on Diet and Cancer

The authors investigated the associations between bowel movement and constipation frequencies and colorectal cancer (CRC) endpoints among men in the Netherlands Cohort Study on Diet and Cancer (n = 58,279) and explored whether dietary fiber intake may modify associations. After 13.3 years (1986-1999), 1,207 CRC cases and 1,753 subcohort members were available for case-cohort analyses. Multivariate analyses showed a significantly increased hazard ratio for CRC overall and rectal cancer in men who reported having a bowel movement 1-2 times per day (second-highest category) as compared with once a day (CRC: hazard ratio (HR) = 1.29, 95% confidence interval (CI): 1.09, 1.53 (P(trend) < 0.001); rectal cancer: HR = 1.50, 95% CI: 1.15, 1.95 (P(trend) = 0.001)). Hazard ratios for CRC overall and rectal cancer were significantly decreased and lowest in men who reported suffering from constipation sometimes or more often versus never (CRC: HR = 0.76, 95% CI: 0.58, 0.98 (P(trend) = 0.02); rectal cancer: HR = 0.57, 95% CI: 0.35, 0.90 (P(trend) = 0.01)). No trends in the associations with proximal or distal colon cancer risk were observed. Interactions with dietary fiber intake were not significant. In this study, frequent bowel movements were associated with an increased risk of rectal cancer in men, and constipation was associated with a decreased risk.     

Cigarette smoking and colorectal cancer: APC mutations, hMLH1 expression, and GSTM1 and GSTT1 polymorphisms

The contribution of cigarette smoking to sporadic colorectal cancer may differ according to molecular aspects of the tumor or according to glutathione S-transferase M1 (GSTM1) or glutathione S-transferase T1 (GSTT1) genotype. In the prospective Netherlands Cohort Study on Diet and Cancer, adjusted incidence rate ratios for 1986-1993 were computed for overall colorectal cancer, tumors with and without adenomatous polyposis coli (APC) mutations, and tumors with and without human mut-L homologue 1 (hMLH1) expression, according to cigarette smoking characteristics (661 cases, 2,948 subcohort members). Case-only analyses were performed to estimate odds ratios for interaction between cigarette smoking and GSTM1 and GSTT1 genotypes. In comparison with never smokers, a high smoking frequency increased the risk of colorectal cancer (for a five-cigarette/day increment, incidence rate ratio (IRR) = 1.07, 95% confidence interval (CI): 1.03, 1.12), and this association was stronger in 371 tumors without a truncating APC mutation (IRR = 1.11, 95% CI: 1.05, 1.17). Long-term smoking was associated with lack of hMLH1 expression in 56 tumors (for a 10-year increment, IRR = 1.17, 95% CI: 1.00, 1.37). No statistically significant interactions between smoking and GSTM1 or GSTT1 genotype were observed. These results indicate that cigarette smoking is associated with risk of colorectal cancer, and this association may depend on molecular characteristics of the tumor as defined by APC mutation and hMLH1 expression status.     

Associations of Red Meat,Fat, and Protein Intake With Distal Colorectal Cancer Risk

Studies have suggested that red and processed meat consumption elevate the risk of colon cancer; however, the relationship between red meat, as well as fat and protein, and distal colorectal cancer (CRC) specifically is not clear. We determined the risk of distal CRC associated with red and processed meat, fat, and protein intakes in Whites and African Americans. There were 945 cases (720 White, 225 African American) of distal CRC and 959 controls (800 White, 159 African American). We assessed dietary intake in the previous 12 mo. Multivariate logistic regression analyses were used to obtain odds ratios (OR) and 95% confidence intervals (95% CI). There was no association between total, saturated, or monounsaturated fat and distal CRC risk. In African Americans, the OR of distal CRC for the highest category of polyunsaturated fat intake was 0.28 (95% CI = 0.08–0.96). The percent of energy from protein was associated with a 47% risk reduction in Whites (Q4 OR = 0.53, 95% CI = 0.37–0.77). Red meat consumption in Whites was associated with a marginally significant risk reduction (Q4 OR = 0.66, 95% CI = 0.43–1.00). Our results do not support the hypotheses that fat, protein, and red meat increase the risk of distal CRC.