Dietary inflammatory index and incidence of and death from primary liver cancer: A prospective study of 103,902 American adults

Chronic inflammation plays an important role in primary liver cancer (PLC) etiology and can be influenced by dietary habits. No prospective study has investigated the association of dietary inflammatory index (DII) with PLC incidence and mortality. Therefore, we used prospective data from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial to fill this gap. The DII was calculated from a validated 137-item food frequency questionnaire in a cohort of 103,902 individuals. Cox regression was used to estimate hazard ratios (HRs) for PLC incidence, and competing risk regression was used to estimate subdistribution HRs (SHRs) for PLC mortality. Restricted cubic spline regression was employed to identify the potential dose–response pattern. A total of 120 PLC cases and 102 PLC deaths were observed during follow-up. Higher DII scores from food and supplement were found to be associated with higher risks of developing PLC (HR_{Tertile 3 vs. 1} 2.05; 95% confidence interval [CI] 1.23–3.41) and death from this disease (SHR_{Tertile 3 vs. 1} 1.97; 95% CI 1.13–3.41). Similar results were obtained for DII score from food only. A nonlinear dose–response pattern was identified for the aforementioned associations (all p_nonlinearity < 0.05). Overall, a more pro-inflammatory diet, as suggested by higher DII scores, is associated with higher risks of PLC incidence and mortality. These findings indicate that encouraging intake of more anti-inflammatory dietary components and reducing intake of pro-inflammatory components represent an attractive strategy to reduce PLC incidence and mortality.     

Intake of fatty acids and antioxidants and pancreatic cancer in a large population‐based case‐control study in the San Francisco Bay Area

There are no well‐established modifiable risk factors for pancreatic cancer except smoking. Some dietary factors have been associated with pancreatic cancer risk and require further study. We examined the associations among intake of specific fatty acids and antioxidants and risk of pancreatic cancer in a large population‐based case‐control study in the San Francisco Bay Area. Unconditional logistic regression models were used to compute odds ratios (ORs) and 95% confidence intervals (CI) as estimates of relative risk. Positive associations were observed for high levels of the 8 individual saturated fatty acids (4th vs. 1st quartile: ORs ranged from 1.6 to 2.6; all p_trend < 0.01), monounsaturated palmitoleic and oleic fatty acids [OR = 1.6 (95% CI: 1.2–2.1) and 1.4 (95% CI: 1.1–1.9); both p_trend < 0.01], and polyunsaturated linolenic acid [OR = 1.5 (95% CI: 1.1–2.0); p_trend = 0.02]. Inverse associations were observed for high levels of gadolic acid [4th vs. 1st quartile: OR = 0.68 (95% CI: 0.50–0.92); p_trend = 0.007] and omega‐3 fatty acids [≥0.85 g/day vs. 1st quartile: OR = 0.47 (95% CI: 0.25–0.90)]. An inverse association was also observed for high total intake of vitamin C [4th vs. 1st quartile: OR = 0.69 (95% CI: 0.51–0.94); p_trend = 0.004] and of vitamin E [OR = 0.67 (95% CI: 0.49–0.92); p_trend = 0.01]. Although similar decreased risks were also observed for high supplemental intake of these 2 vitamins (both p_trend < 0.01), no association was observed for intake from food alone. These results support the hypotheses that a high intake of saturated and certain monounsaturated fatty acids may increase the risk of pancreatic cancer, whereas greater intake of omega‐3 fatty acids, vitamins C and E may reduce the risk.     

A prospective study of dairy product intake and the risk of hepatocellular carcinoma in U.S. men and women

Although increasing dairy product intake has been associated with risk of several cancers, epidemiological studies on hepatocellular carcinoma are sparse and have yielded inconsistent results. We prospectively assessed the associations of dairy products (total, milk, butter, cheese and yogurt) and their major components (calcium, vitamin D, fats and protein) with the risk of hepatocellular carcinoma development among 51,418 men and 93,427 women in the Health Professionals Follow-Up Study and the Nurses' Health Study. Diets were collected at baseline and updated every 4 years using validated food frequency questionnaires. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards regression model. During up to 32 years of follow-up, a total of 164 hepatocellular carcinoma cases were documented. After adjustment for most known hepatocellular carcinoma risk factors, higher total dairy product intake was associated with an increased risk of hepatocellular carcinoma (highest vs. lowest tertile, HR = 1.85, 95% CI: 1.19–2.88; p_trend = 0.009). For the same comparison, we observed significant positive associations of high-fat dairy (HR = 1.81, 95% CI: 1.19–2.76; p_trend = 0.008) and butter (HR = 1.58, 95% CI: 1.06–2.36; p_trend = 0.04) with hepatocellular carcinoma risk. There was a nonsignificant inverse association between yogurt intake and hepatocellular carcinoma risk (HR = 0.72, 95% CI: 0.49–1.05; p_trend = 0.26). Our data suggest that higher intake of high-fat dairy foods was associated with higher, whereas higher yogurt consumption might be associated with lower risk of developing hepatocellular carcinoma among U.S. men and women.     

Dietary intake of fiber,whole grains and risk of colorectal cancer: An updated analysis according to food sources,tumor location and molecular subtypes in two large US cohorts

Epidemiologic evidence relating fiber intake to colorectal cancer (CRC) remains inconclusive and data are limited on different food sources of fiber and heterogeneity by tumor subsite and molecular profile. We prospectively followed for CRC incidence 90,869 women from the Nurses’ Health Study (1980–2012) and 47,924 men from the Health Professionals Follow-up Study (1986–2012), who completed a validated food frequency questionnaire every 4 years. Cox proportional hazards regression was used to examine the associations with CRC risk for total, cereal, fruit and vegetable fiber and whole grains. We also assessed the associations according to tumor subsites (proximal colon, distal colon and rectum) and molecular markers (microsatellite instability, BRAF mutation, CpG island methylator phenotype and KRAS mutation). We documented 3,178 CRC cases during 3,685,903 person-years of follow-up in the NHS and HPFS. Intake of total dietary fiber was not associated with CRC risk after multivariable adjustment in either women (hazard ratio [HR] comparing extreme deciles, 1.17; 95% CI, 0.92–1.48, p_trend = 0.55) or men (HR, 0.90; 95% CI, 0.67–1.21, p_trend = 0.47). Higher intake of cereal fiber and whole grains was associated with lower CRC risk in men with an HR of 0.75 (95% CI, 0.57–1.00) and 0.72 (95% CI, 0.54–0.96), respectively. No heterogeneity was detected by tumor subsite or molecular markers (p_{heterogeneity} > 0.05). Higher intake of total dietary fiber within the range of a typical American diet is unlikely to substantially reduce CRC risk. The potential benefit of cereal fiber and whole grains in men warrants further confirmation.     

Endogenous sex hormones and colorectal cancer survival among men and women

Although previous studies have suggested a potential role of sex hormones in the etiology of colorectal cancer (CRC), no study has yet examined the associations between circulating sex hormones and survival among CRC patients. We prospectively assessed the associations of prediagnostic plasma concentrations of estrone, estradiol, free estradiol, testosterone, free testosterone and sex hormone-binding globulin (SHBG) with CRC-specific and overall mortality among 609 CRC patients (370 men and 239 postmenopausal women not taking hormone therapy at blood collection) from four U.S. cohorts. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard regression. We identified 174 deaths (83 CRC-specific deaths) in men and 106 deaths (70 CRC-specific deaths) in women. In men, higher circulating level of free testosterone was associated with lower risk of overall (the highest vs. lowest tertiles, HR = 0.66, 95% CI, 0.45–0.99, p_trend = 0.04) and possibly CRC-specific mortality (HR = 0.73, 95% CI, 0.41–1.29, p_trend = 0.27). We generally observed nonsignificant inverse associations for other sex steroids, and a positive association for SHBG with CRC-specific mortality among male patients. In women, however, we found a suggestive positive association of estrone with overall (HR = 1.54, 95% CI, 0.92–2.60, p_trend = 0.11) and CRC-specific mortality (HR = 1.96, 95% CI, 1.01–3.84, p_trend = 0.06). Total estradiol, free estradiol and free testosterone were generally suggestively associated with higher risk of mortality among female patients, although not statistically significant. These findings implicated a potential role of endogenous sex hormones in CRC prognosis, which warrant further investigation.     

Dairy intake after prostate cancer diagnosis in relation to disease‐specific and total mortality

Information regarding postdiagnostic dairy intake and prostate cancer survival is limited. We evaluated intake of total, high‐fat and low‐fat dairy after prostate cancer diagnosis in relation to disease‐specific and total mortality. We included 926 men from the Physicians’ Health Study diagnosed with non‐metastatic prostate cancer between 1982 and 2000 who completed a diet questionnaire a median of 5 years after diagnosis and were followed thereafter for a median of 10 years to assess mortality. Cox proportional hazards regression was used to estimate associations between dairy intake and prostate cancer specific and all‐cause mortality. During 8,903 person‐years of follow‐up, 333 men died, 56 due to prostate cancer. Men consuming ≥3 servings/day of total dairy products had a 76% higher risk of total mortality and a 141% higher risk of prostate cancer‐specific mortality compared to men who consumed less than 1 dairy product/day (hazard ratio (HR) = 1.76, 95% confidence interval (CI): 1.21, 2.55, p_trend < 0.001 for total mortality; HR = 2.41, 95% CI: 0.96, 6.02, p_trend = 0.04 for prostate cancer‐specific mortality). The association between high‐fat dairy and mortality risk appeared to be stronger than that of low‐fat dairy, but the difference between them was not statistically significant (p for difference = 0.57 for prostate cancer‐specific mortality and 0.56 for total mortality). Among men without metastases when diagnosed, higher intake of dairy foods after prostate cancer diagnosis may be associated with increased prostate cancer‐specific and all‐cause mortality.     

Adolescent and mid‐life diet and subsequent risk of thyroid cancer in the NIH‐AARP diet and health study

Although thyroid cancer is suspected to have a nutritional etiology, prospective studies examining the relationship between diet and thyroid cancer are lacking. During 1996–1997, NIH‐AARP Diet and Health Study participants, ages 51–72 years, completed a 37‐item food frequency questionnaire about diet at ages 12–13 years (adolescence) and 10 years before baseline (mid‐life). Over a median 10 years of follow‐up, 325 individuals (143 men and 182 women) were diagnosed with thyroid cancer. Multivariable‐adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for intakes of foods and food groups comparing the highest to the lowest quartiles. Adolescent intakes of chicken/turkey (HR = 1.59, 95% CI: 0.97–2.60; p_trend < 0.01) and sweet baked goods (HR = 1.59, 95% CI: 1.09–2.34; p_trend = 0.04) were positively associated with thyroid cancer risk, while intake of butter/margarine was inversely associated with risk (HR = 0.64, 95% CI: 0.44–0.91; p_trend < 0.02). Similar to adolescent diet, mid‐life intake of sweet baked goods was nonsignificantly associated with an increased risk of thyroid cancer (HR = 1.39, 95% CI: 0.96–2.00; p_trend = 0.11), but intake of butter/margarine was inversely associated with risk (HR = 0.66, 95% CI: 0.46–0.95; p_trend = 0.03). Among men, higher adolescent consumption of canned tuna was positively associated with risk of thyroid cancer (HR = 1.69, 95% CI: 1.01–2.83; p_trend = 0.03), and greater mid‐life intake of broccoli was associated with a twofold increased risk (HR = 2.13, 95% CI: 1.13–3.99; p_trend < 0.01). This large prospective study suggests that several components of the adolescent and mid‐life diet, including iodine‐rich foods and goitrogens, may influence thyroid cancer risk.     

Dietary trace element intake and liver cancer risk: Results from two population‐based cohorts in China

Dietary factors have been hypothesized to affect the risk of liver cancer via various mechanisms, but the influence has been not well studied and the evidence is conflicting. We investigated associations of dietary trace element intake, assessed through a validated food frequency questionnaire, with risk of liver cancer in two prospective cohort studies of 132,765 women (1997–2013) and men (2002–2013) in Shanghai, China. The associations were first evaluated in cohort studies and further assessed in a case–control study nested within these cohorts adjusting for hepatitis B virus infection. For cohort analyses, Cox proportional hazard models were used to estimate hazard ratios and 95% confidence intervals. For nested case–control analyses, conditional logistic regression was used to calculate odds ratios and 95% confidence intervals. After a median follow‐up time of 15.2 years for the Shanghai Women's Health Study and 9.3 years for the Shanghai Men's Health Study, 192 women and 344 men developed liver cancer. Dietary intake of manganese was inversely associated with liver cancer risk (highest vs. lowest quintile, HR = 0.51, 95% CI: 0.35–0.73; p_trend = 0.001). Further adjustment for hepatitis B virus infection in the nested case–control study yielded a similar result (highest vs. lowest quintile, OR = 0.38, 95% CI: 0.21–0.69; p_trend < 0.001). No significant association was found between dietary intake of selenium, iron, zinc, copper and liver cancer risk. The results suggest that higher intake of manganese may be associated with a lower risk of liver cancer in China.     

Isothiocyanates,glutathione S‐transferase M1 and T1 polymorphisms and gastric cancer risk: A prospective study of men in Shanghai,China

Isothiocyanates (ITC) in cruciferous vegetables may be chemopreventive against gastric cancer development. Glutathione S‐transferases (GSTs) may modify the chemopreventive effect of ITC. The relationship between urinary total ITC and risk of gastric cancer was prospectively examined. Between 1986 and 1989, 18,244 middle‐aged men in Shanghai, China were enrolled in a prospective study of diet and cancer and donated baseline urine and blood samples. Urinary ITC was quantified for 307 incident cases of gastric cancer that occurred during the first 16 years of follow‐up, and 911 matched control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression methods. Seropositivity for antibodies to Helicobacter pylori and homozygous deletions of GSTM1 and GSTT1 were determined. Compared to the first tertile, ORs (95% CIs) of gastric cancer for the second and third tertiles of urinary total ITC were 0.83 (0.61–1.15) and 0.66 (0.47–0.94) (p_trend = 0.02). A stronger protective effect of ITC against gastric cancer development was seen among men with homozygous deletion of GSTM1 (third tertile versus first tertile, OR = 0.50, 95% CI = 0.27–0.93) or GSTT1 (third tertile vs. first tertile, OR = 0.47, 95% CI = 0.25–0.88), and particularly with deletions of both GSTM1 and GSTT1 (second and third tertiles vs. first tertile, OR = 0.44, 95% CI = 0.21–0.93). In this cohort of Chinese men at high risk for gastric cancer, isothiocyanates may protect against the development of gastric cancer. The protection may be stronger for individuals genetically deficient in enzymes that metabolize these chemopreventive compounds. © 2009 UICC     

Associations of intakes of magnesium and calcium and survival among women with breast cancer: results from Western New York Exposures and Breast Cancer (WEB) Study

Magnesium (Mg) and calcium (Ca) antagonizes each other in (re) absorption, cell cycle regulation, inflammation, and many other physiologic activities. However, few studies have investigated the association between magnesium and calcium intakes and breast cancer survival, and the interaction between calcium and magnesium intake. In a cohort of 1,170 women with primary, incident, and histologically confirmed breast cancer from Western New York State, we examined the relationship between intakes of these two minerals and survival. Cox regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI). Mean follow-up time was 87.4 months after breast cancer diagnosis; there were 170 deaths identified. After adjustment for known prognostic factors, and intakes of energy, total vitamin D and total calcium, higher dietary intake of magnesium was inversely associated with risk of all-cause mortality (HR = 0.50, 95% CI, 0.28-0.90 for highest vs. lowest tertile; p trend = 0.02). Likewise, a marginal association was found for total Magnesium intake from foods and supplements combined (HR = 0.58, 95% CI, 0.31-1.08; p trend = 0.09). The inverse association of higher total magnesium intake with all-cause mortality was primarily presented among postmenopausal women and was stronger among women who had a high Ca:Mg intake ratio (>2.59). There were no clear associations for prognosis with intake of calcium. We found that magnesium intake alone may improve overall survival following breast cancer, and the association may be stronger among those with high Ca:Mg intake ratio.     

Healthy dietary patterns and incidence of biliary tract and gallbladder cancer in a prospective study of women and men

BackgroundWhether diet influences the risk of biliary tract cancer (BTC) is unknown. We examined the associations of two healthy dietary patterns, including a modified Dietary Approach to Stop Hypertension (mDASH) diet and a modified Mediterranean (mMED) diet, with the incidence of BTC in a population-based prospective study.MethodsThe study population comprised 76,014 Swedish adults who were 45–83 years of age and cancer-free at baseline. The mDASH and mMED diets were calculated from self-reported dietary data collected by a validated food-frequency questionnaire. Cox proportional hazards regression models were used to estimate hazard ratios (HR) with 95% confidence intervals (CI) adjusted for potential confounders.ResultsOver 1,010,777 person-years (mean 13.3 years) of follow-up, 140 extrahepatic BTC cases (including 77 gallbladder cancers) and 23 intrahepatic BTC cases were ascertained by linkage with the Swedish Cancer Register. Adherence to the mDASH and mMED diets was statistically significantly inversely associated with risk of extrahepatic BTC (P_trend ≤ 0.0003) and gallbladder cancer (P_trend ≤ 0.005) but not intrahepatic BTC (P_trend ≥ 0.11). The multivariable HRs (95% CI) for the highest versus lowest tertile of the mDASH diet were 0.41 (0.26–0.64) for extrahepatic BTC and 0.36 (0.20–0.64) for gallbladder cancer. The corresponding HRs (95% CI) for the mMED diet were respectively 0.41 (0.25–0.67) and 0.42 (0.23–0.79).ConclusionAdherence to a healthy diet may play a role in reducing the risk of extrahepatic BTC.     

Higher diet-dependent acid load is associated with risk of breast cancer: Findings from the sister study

Dietary factors that contribute to chronic low-grade metabolic acidosis have been linked to breast cancer risk, but to date no epidemiologic study has examined diet-dependent acid load and breast cancer. We used data from 43,570 Sister Study participants who completed a validated food frequency questionnaire at enrollment (2003–2009) and satisfied eligibility criteria. The Potential Renal Acid Load (PRAL) score was used to estimate diet-dependent acid load. Higher scores reflect greater consumption of protein and phosphorus, and lower consumption of potassium, calcium and magnesium. The association between PRAL and breast cancer was evaluated using multivariable Cox proportional hazards regression. We identified 1,614 invasive breast cancers diagnosed at least 1 year after enrollment (mean follow-up, 7.6 years). The highest PRAL quartile, reflecting greater acid-forming potential, was associated with increased risk of breast cancer (HR_{highest vs. lowest quartile}: 1.21 [95% CI, 1.04–1.41], p_trend = 0.04). The association was more pronounced for estrogen receptor (ER)-negative (HR_{highest vs. lowest quartile}: 1.67 [95% CI, 1.07–2.61], p_trend = 0.03) and triple-negative breast cancer (HR_{highest vs. lowest quartile}: 2.20 [95% CI, 1.23–3.95], p_trend = 0.02). Negative PRAL scores, representing consumption of alkaline diets, were associated with decreased risk of ER-negative and triple-negative breast cancer, compared to a PRAL score of 0 representing neutral pH. Higher diet-dependent acid load may be a risk factor for breast cancer while alkaline diets may be protective. Since PRAL scores are positively correlated with meat consumption and negatively correlated with fruit and vegetable intake, results also suggest that diets high in fruits and vegetables and low in meat may be protective against hormone receptor negative breast cancer.     

Association between meat and saturated fatty acid intake and lung cancer risk: The Japan Public Health Center-based prospective study

Red meat or saturated fatty acid (SFA) intake has been reported to increase lung cancer (LC) risk in several western countries. However, in Asia, studies on the relationship between meat and SFA intake with LC incidence are still relatively insufficient, and their conclusions are inconsistent. We investigated the association of meat and SFA intake with LC incidence in a population-based prospective cohort study in Japan. Cox regression was used to estimate the hazard ratio (HR) and 95% confidence interval (CI) for LC risk according to meat intake and SFA intake. A total of 73 187 participants (32 934 men and 40 253 women) aged 45 to 74 years participated in our study. During the follow-up period of 1 151 839 person-years (median, 16.0 year) from 1995 to 2013 for Cohort I and from 1998 to 2013 for Cohort II, 1315 (901 men and 414 women) newly diagnosed cases of LC were identified. In men, we found an adverse association between total red meat intake (HR and 95% CI: 1.25 [1.02-1.53]; P_trend = .008) and LC risk. Additionally, borderline statistically significant elevated risks of LC were seen with high intake of unprocessed red meat and processed red meat. However, no positive association between total red meat intake and LC risk was observed in women. In contrast, poultry and fish intake were not associated with LC risk in either men or women. We concluded that a high total intake of total red meat was associated with moderately elevated LC risk in men.     

Iron intake,oxidative stress-related genes and breast cancer risk

Iron has been suggested to contribute to breast cancer development through oxidative stress generation. Our study investigated associations between iron intake and breast cancer risk, overall and by menopausal and estrogen receptor/progesterone receptor (ER/PR) status, and modification by oxidative stress-related genetic polymorphisms (MnSOD, GSTM1 and GSTT1). A population-based case–control study (3,030 cases and 3,402 controls) was conducted in Ontario, Canada. Iron intake (total, dietary, supplemental, heme, nonheme) was assessed using a validated food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated from multivariable logistic regression models. Interactions between iron intake and genotypes were assessed among 1,696 cases and 1,761 controls providing DNA. Overall, no associations were observed between iron intake and breast cancer risk. Among premenopausal women, total, dietary and dietary nonheme iron were positively associated with ER–/PR– breast cancer risk (all p_trend < 0.05). Among postmenopausal women, supplemental iron was associated with reduced breast cancer risk (OR_{>18 vs. 0 mg/day} = 0.68, 95% CI: 0.51–0.91), and dietary heme iron was associated with an increased risk, particularly the ER–/PR– subtype (OR_{highest vs. lowest quintile} = 1.69, 95% CI: 1.16–2.47; p_trend = 0.02). Furthermore, GSTT1 and combined GSTM1/GSTT1 polymorphisms modified some of the associations. For example, higher dietary iron was most strongly associated with increased breast cancer risk among women with GSTT1 deletion or GSTM1/GSTT1 double deletions (p_interaction < 0.05). Findings suggest that iron intake may have different effects on breast cancer risk according to menopausal and hormone receptor status, as well as genotypes affecting antioxidant capacity.     

Prediagnostic blood levels of organochlorines and risk of non-Hodgkin lymphoma in three prospective cohorts in China and Singapore

Specific organochlorines (OCs) have been associated with non-Hodgkin lymphoma (NHL) with varying degrees of evidence. These associations have not been evaluated in Asia, where the high exposure and historical environmental contamination of certain OC pesticides (e.g., dichlorodiphenyltrichloroethane [DDT], hexachlorocyclohexane [HCH]) are different from Western populations. We evaluated NHL risk and prediagnostic blood levels of OC pesticides/metabolites and polychlorinated biphenyl congeners in a case–control study of 167 NHL cases and 167 controls nested within three prospective cohorts in Shanghai and Singapore. Conditional logistic regression was used to analyze lipid-adjusted OC levels and NHL risk. Median levels of p,p′-dichlorodiphenyldichloroethylene (p,p′-DDE), the primary DDT metabolite, and β-HCH were up to 12 and 65 times higher, respectively, in samples from the Asian cohorts compared to several cohorts in the United States and Norway. An increased risk of NHL was observed among those with higher β-HCH levels both overall (3rd vs. 1st tertile OR = 1.8, 95%CI = 1.0–3.2; p_trend = 0.049) and after excluding cases diagnosed within 2 years of blood collection (3rd vs. 1st tertile OR = 2.0, 95%CI = 1.1–3.9; p_trend = 0.03), and the association was highly consistent across the three cohorts. No significant associations were observed for other OCs, including p,p′-DDE. Our findings provide support for an association between β-HCH blood levels and NHL risk. This is a concern because substantial quantities of persistent, toxic residues of HCH are present in the environment worldwide. Although there is some evidence that DDT is associated with NHL, our findings for p,p′-DDE do not support an association.     

Intake of trans fatty acids from partially hydrogenated vegetable and fish oils and ruminant fat in relation to cancer risk

Intake of trans fatty acids (TFA) may influence systemic inflammation, insulin resistance and adiposity, but whether TFA intake influences cancer risk is insufficiently studied. We examined the association between TFA intake from partially hydrogenated vegetable oils (PHVO‐TFA), partially hydrogenated fish oils (PHFO‐TFA), and ruminant fat (rTFA) and cancer risk in the Norwegian counties study, a large cohort study with a participation rate >80%. TFA intake was assessed three times in 1974–1988 by questionnaire. A total of 77,568 men and women were followed up through 2007, during which time 12,004 cancer cases occurred. Hazard ratios (HRs) and confidence intervals (CIs) were estimated with Cox regression for cancer sites with ≥150 cases during follow‐up. Significantly increased or decreased risks were found when comparing the highest and lowest intake categories (HRs, 95% CIs) for PHVO‐TFA and pancreatic cancer in men (0.52, 0.31–0.87) and non‐Hodgkin lymphoma (NHL) in both genders (0.70, 0.50–0.98); PHFO‐TFA and rectal cancer (1.43, 1.09–1.88), prostate cancer (0.82, 0.69–0.96), and multiple myeloma (2.02, 1.24–3.28); and rTFA and all cancers (1.09, 1.02–1.16), cancer of the mouth/pharynx (1.59, 1.08–2.35), NHL (1.47, 1.06–2.04) and multiple myeloma (0.45, 0.24–0.84). Furthermore, positive trends were found for PHFO‐TFA and stomach cancer (p_trend = 0.01) and rTFA and postmenopausal breast cancer (p_trend = 0.03). Inverse trends were found for PHVO‐TFA and all cancers (p_trend = 0.006) and cancer of the central nervous system in women (p_trend = 0.005). PHFO‐TFA, but not PHVO‐TFA, seemed to increase cancer risk. The increased risks observed for rTFA may be linked to saturated fat.     

Magnesium intake, plasma C-peptide, and colorectal cancer incidence in US women: a 28-year follow-up study

Background:

Laboratory studies suggest a possible role of magnesium intake in colorectal carcinogenesis but epidemiological evidence is inconclusive.

Method:

We tested magnesium–colorectal cancer hypothesis in the Nurses'' Health Study, in which 85 924 women free of cancer in 1980 were followed until June 2008. Cox proportional hazards regression models were used to estimate multivariable relative risks (MV RRs, 95% confidence intervals).

Results:

In the age-adjusted model, magnesium intake was significantly inversely associated with colorectal cancer risk; the RRs from lowest to highest decile of total magnesium intake were 1.0 (ref), 0.93, 0.81, 0.72, 0.74, 0.77, 0.72, 0.75, 0.80, and 0.67 (P_trend<0.001). However, in the MV model adjusted for known dietary and non-dietary risk factors for colorectal cancer, the association was significantly attenuated; the MV RRs were 1.0 (ref), 0.96, 0.85, 0.78, 0.82, 0.86, 0.84, 0.91, 1.02, and 0.93 (P_trend=0.77). Similarly, magnesium intakes were significantly inversely associated with concentrations of plasma C-peptide in age-adjusted model (P_trend=0.002) but not in multivariate-adjusted model (P_trend=0.61). Results did not differ by subsite or modified by calcium intakes or body mass index.

Conclusion:

These prospective results do not support an independent association of magnesium intake with either colorectal cancer risk or plasma C-peptide levels in women.     

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.     

Ingested nitrate and nitrite,disinfection by‐products,and pancreatic cancer risk in postmenopausal women

Nitrate and nitrite are precursors of N‐nitroso compounds (NOC), probable human carcinogens that cause pancreatic tumors in animals. Disinfection by‐products (DBP) exposures have also been linked with digestive system cancers, but few studies have evaluated relationships with pancreatic cancer. We investigated the association of pancreatic cancer with these drinking water contaminants and dietary nitrate/nitrite in a cohort of postmenopausal women in Iowa (1986–2011). We used historical monitoring and treatment data to estimate levels of long‐term average nitrate and total trihalomethanes (TTHM; the sum of the most prevalent DBP class) and the duration exceeding one‐half the maximum contaminant level (>½ MCL; 5 mg/L nitrate‐nitrogen, 40 µg/L TTHM) among participants on public water supplies (PWS) >10 years. We estimated dietary nitrate and nitrite intakes using a food frequency questionnaire. We computed hazard ratios (HR) and 95% confidence intervals (CI) using Cox regression and evaluated nitrate interactions with smoking and vitamin C intake. We identified 313 cases among 34,242 women, including 152 with >10 years PWS use (N = 15,710). Multivariable models of average nitrate showed no association with pancreatic cancer (HR_{p95 vs. Q1} = 1.16, 95% CI: 0.51–2.64). Associations with average TTHM levels were also null (HR_{Q4 vs. Q1} = 0.70, 95% CI:0.42–1.18). We observed no trend with increasing years of exposure to either contaminant at levels >½ MCL. Positive associations were suggested in the highest dietary nitrite intake from processed meat (HR_{p95 vs. Q1} = 1.66, 95% CI 1.00–2.75;p_trend = 0.05). We found no interactions of nitrate with known modifiers of endogenous NOC formation. Our results suggest that nitrite intake from processed meat may be a risk factor for pancreatic cancer.     

Folate intake and breast cancer mortality in a cohort of Swedish women

Folate may influence breast cancer development and progression through its role in one-carbon metabolism. However, epidemiologic data on the relation between folate and breast cancer survival are limited. We investigated whether dietary folate intake was associated with survival in 3,116 women diagnosed with breast cancer in the population-based Swedish Mammography Cohort. Participants completed a 67-item food frequency questionnaire in 1987. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for death from breast cancer and death from any cause. During 25,716 person-years of follow-up from 1987 to 2008, there were 852 deaths with 381 breast cancer deaths. Dietary folate intake was inversely associated with breast cancer and overall mortality. Women in the highest quartile of folate intake had a multivariable HR (95% CI) of death from breast cancer of 0.78 (0.58–1.03) compared to those in the lowest quartile (P _trend = 0.03). The corresponding HR (95% CI) for death from any cause was 0.79 (0.66–0.96; P _trend = 0.004). The protective association between dietary folate intake and breast cancer death was strongest among those with ER-negative tumors (HR = 0.42; 95% = CI 0.22–0.79; P _trend = 0.01) comparing the highest to lowest quartile. Our findings suggest that folate intake before breast cancer diagnosis may improve breast cancer and overall survival. While these findings need to be confirmed in future studies, they do offer assurance that dietary folate intake at the levels observed in our population does not unfavorably affect survival after breast cancer.