Previous case-control studies have suggested that atopic allergic conditions (AACs) are inversely associated with pancreatic cancer, but this relationship has not been supported in many prospective settings. In this study, we investigated the influence of AACs (asthma, hay fever, or allergy) and the treatment of these conditions on pancreatic cancer risk among participants of the Multiethnic Cohort Study (MEC). AACs and antihistamine use were assessed via a baseline questionnaire when participants joined the MEC in 1993-1996. Risk ratios (RRs) and 95% confidence intervals (CIs) for pancreatic cancer incidence by AACs and antihistamines were calculated using Cox regression, adjusting for age, sex, ethnicity, education, smoking status, family history of pancreatic cancer, body mass index, diabetes, and alcohol intake. We further evaluated associations among subgroups defined by age, sex, ethnicity, follow-up time, and known pancreatic cancer risk factors. During an average 16-year follow-up, 1,455 incident cases of pancreatic cancer were identified among 187,226 white, African American, Latino, Japanese American, and Native Hawaiian men and women. AACs (RR 1.00, 95% CI 0.88-1.12) and antihistamines (RR 0.92, 95% CI 0.78-1.07) were not clearly associated with pancreatic cancer incidence. While these associations were also null for most subgroups, we did observe protective associations of AACs (RR 0.74, 95% CI 0.56-0.98) and antihistamines (RR 0.66, 95% CI 0.45-0.96) among the oldest participants (70+). Our results, in agreement with past prospective studies, suggest that AACs are not associated with pancreatic cancer in general, but the observed protective associations among the oldest age group may warrant future investigation.

Objectives

We conducted a prospective analysis of 145,886 participants in the multiethnic cohort to examine the relationship of alcohol drinking and smoking with pancreatitis.

Methods

Pancreatitis cases were categorized as gallstone-related acute pancreatitis (GSAP) (N = 1,065), non-GSAP (N = 1,222), and recurrent acute (RAP)/chronic pancreatitis (CP) (N = 523). We used the baseline questionnaire to identify alcohol intake and smoking history. Associations were estimated by hazard ratios (HRs) and 95% confidence intervals (CIs) using Cox models.

Results

Cigarette smoking was associated with non-GSAP and RAP/CP. Moderate alcohol intake was inversely associated with all types of pancreatitis in women (HRs, 0.66 to 0.81 for <1 drink per day), and with RAP/CP in men (HR, 0.57; 95% CI, 0.41-0.79 for <2 drinks per day). The risk of non-GS pancreatitis associated with current smoking was highest among men who consumed more than 4 drinks per day (HR, 2.06; 95% CI, 1.28-3.30), whereas among never smokers, moderate drinking was associated with a reduced risk (HR, 0.70; 95% CI, 0.51-0.96). In women, drinking less than 2 drinks per day was associated with a reduced risk of GSAP among never smokers (HR, 0.61; 95% CI, 0.46-0.80).

Conclusions

Smoking is a risk factor for non-GS pancreatitis. Moderate alcohol intake is protective against all types of pancreatitis in women and against RAP/CP in men.

Purpose

Prior studies conducted primarily in white populations have suggested that pre-diagnostic cholesterol lowering drugs (CLDs) improved survival among women with breast cancer (BC). However, this association had not been well characterized in diverse racial/ethnic populations. We investigated whether pre-diagnostic CLD use is associated with all-cause and BC-specific mortality among female BC cases of the Multiethnic Cohort (MEC).

Methods

CLD use was ascertained through questionnaires administered in 2003-2008. A total of 1448 incident BC cases were identified by linkage to SEER cancer registries in Hawaii and California from 2003 to 2014. Multivariable Cox regression was conducted to estimate hazard ratios (HR) and 95% confidence intervals (CI) of the associations of pre-diagnostic CLD use with all-cause and BC-specific mortality, adjusting for tumor characteristics, first course of treatment, health behaviors, co-morbidities, and demographics. Subgroup analyses by stage and hormone receptor status were conducted for all-cause mortality.

Results

There were 224 all-cause and 87 BC-specific deaths among the 1448 BC cases during a median follow-up of 4.5 years after diagnosis. Women with BC who ever used CLDs had a 27% lower hazard of all-cause mortality (HR 0.73, 95% CI 0.54-0.98) and 17% lower hazard of BC-specific mortality (HR 0.83, 95% CI 0.49-1.39) compared to never users. CLD use reduced mortality among women with advanced-stage tumors and hormone receptor-positive breast tumors (HR 0.54 95% CI 0.33-0.90; HR 0.69, 95% CI 0.48-0.99, respectively).

Conclusion

These findings demonstrate an improved survival associated with CLD use prior to diagnosis in a multiethnic population of women with BC.

While smoking is the primary cause of lung cancer, only 11-24% of smokers develop the malignancy over their lifetime. The primary addictive agent in tobacco smoke is nicotine and variation in nicotine metabolism may influence the smoking levels of an individual. Therefore, inter-individual variation in lung cancer risk among smokers may be due in part to differences in the activity of enzymes involved in nicotine metabolism. In most smokers, cytochrome P450 2A6 (CYP2A6)-catalyzed C-oxidation accounts for >75% of nicotine metabolism, and the activity of this enzyme has been shown to correlate with the amount of nicotine and carcinogens drawn from cigarettes. We prospectively evaluated the association of urinary biomarkers of nicotine uptake (total nicotine equivalents [TNE]) and CYP2A6 activity (ratio of urinary total trans-3'-hydroxycotinine to cotinine) with lung cancer risk among 2,309 Multiethnic Cohort Study participants who were current smokers at time of urine collection; 92 cases were diagnosed during a mean follow-up of 9.5 years. We found that higher CYP2A6 activity and TNE was associated with increased lung cancer risk after adjusting for age, sex, race/ethnicity, body mass index, smoking duration, and urinary creatinine (p's = 0.002). The association for CYP2A6 activity remained even after adjusting for self-reported cigarettes per day (CPD) (Hazard Ratio [HR] per unit increase in log-CYP2A6 activity = 1.52; p = 0.005) and after adjusting for TNE (HR = 1.46; p = 0.01). In contrast, the association between TNE and lung cancer risk was of borderline statistical significance when adjusted for CPD (HR = 1.53; p = 0.06) and not statistically significant when further adjusted for CYP2A6 activity (HR = 1.30; p = 0.22). These findings suggest that CYP2A6 activity provides information on lung cancer risk that is not captured by smoking history or a (short-term) biomarker of dose. CYP2A6 activity should be further studied as a risk biomarker for smoking-related lung cancer.

Aims

Fish and ω-3 fatty acids are reported to be beneficial in pediatric nonalcoholic fatty liver disease (NAFLD), but no studies have assessed their relation to histological severity. The objectives of this study were to evaluate the dietary intake of fish and ω-3 fatty acids in children with biopsy-proven NAFLD, and examine their association with serological and histological indicators of disease.

Methods

This was a cross-sectional analysis of 223 children (6-18 years) who participated in the Treatment of Nonalcoholic Fatty Liver Disease in Children trial or the NAFLD Database study conducted by the Nonalcoholic Steatohepatitis Clinical Research Network. The distribution of fish and ω-3 fatty acid intake was determined from responses to the Block Brief 2000 Food Frequency Questionnaire, and analyzed for associations with serum alanine aminotransferase, histological features of fatty liver disease, and diagnosis of steatohepatitis after adjusting for demographic, anthropometric, and dietary variables.

Results

The minority of subjects consumed the recommended 8 ounces of fish per week (22/223 [10%]) and 200 mg of long-chain ω-3 fatty acids per day (12/223 [5%]). Lack of fish and long-chain ω-3 fatty acid intake was associated with greater portal (P = 0.03 and P = 0.10, respectively) and lobular inflammation (P = 0.09 and P = 0.004, respectively) after controlling for potential confounders.

Conclusions

Fish and ω-3 fatty acid intake was insufficient in children with NAFLD, which may increase susceptibility to hepatic inflammation. Patients with pediatric NAFLD should be encouraged to consume the recommended amount of fish per week.

While disparity in pancreatic cancer incidence between blacks and whites has been observed, few studies have examined disparity in other ethnic minorities. We evaluated variations in pancreatic cancer incidence and assessed the extent to which known risk factors account for differences in pancreatic cancer risk among African Americans, Native Hawaiians, Japanese Americans, Latino Americans, and European Americans in the Multiethnic Cohort Study. Risk factor data were obtained from the baseline questionnaire. Cox regression was used to estimate the relative risks (RRs) and 95% confidence intervals (CIs) for pancreatic cancer associated with risk factors and ethnicity. During an average 16.9-year follow-up, 1,532 incident pancreatic cancer cases were identified among 184,559 at-risk participants. Family history of pancreatic cancer (RR 1.97, 95% CI 1.50-2.58), diabetes (RR 1.32, 95% CI 1.14-1.54), body mass index ≥30 kg/m² (RR 1.25, 95% CI 1.08-1.46), current smoking (<20 pack-years RR 1.43, 95% CI 1.19-1.73; ≥20 pack-years RR 1.76, 95% CI 1.46-2.12), and red meat intake (RR 1.17, 95% CI 1.00-1.36) were associated with pancreatic cancer. After adjustment for these risk factors, Native Hawaiians (RR 1.60, 95% CI 1.30-1.98), Japanese Americans (RR 1.33, 95% CI 1.15-1.54), and African Americans (RR 1.20, 95% CI 1.01-1.42), but not Latino Americans (RR 0.90, 95% CI 0.76-1.07), had a higher risk of pancreatic cancer compared to European Americans. Interethnic differences in pancreatic cancer risk are not fully explained by differences in the distribution of known risk factors. The greater risks in Native Hawaiians and Japanese Americans are new findings and elucidating the causes of these high rates may improve our understanding and prevention of pancreatic cancer.

Aims

Fish and ω-3 fatty acids are reported to be beneficial in pediatric nonalcoholic fatty liver disease (NAFLD), but no studies have assessed their relation to histological severity. The objectives of this study were to evaluate the dietary intake of fish and ω-3 fatty acids in children with biopsy-proven NAFLD, and examine their association with serological and histological indicators of disease.

Methods

This was a cross-sectional analysis of 223 children (6-18 years) who participated in the Treatment of Nonalcoholic Fatty Liver Disease in Children trial or the NAFLD Database study conducted by the Nonalcoholic Steatohepatitis Clinical Research Network. The distribution of fish and ω-3 fatty acid intake was determined from responses to the Block Brief 2000 Food Frequency Questionnaire, and analyzed for associations with serum alanine aminotransferase, histological features of fatty liver disease, and diagnosis of steatohepatitis after adjusting for demographic, anthropometric, and dietary variables.

Results

The minority of subjects consumed the recommended 8 ounces of fish per week (22/223 [10%]) and 200 mg of long-chain ω-3 fatty acids per day (12/223 [5%]). Lack of fish and long-chain ω-3 fatty acid intake was associated with greater portal (P = 0.03 and P = 0.10, respectively) and lobular inflammation (P = 0.09 and P = 0.004, respectively) after controlling for potential confounders.

Conclusions

Fish and ω-3 fatty acid intake was insufficient in children with NAFLD, which may increase susceptibility to hepatic inflammation. Patients with pediatric NAFLD should be encouraged to consume the recommended amount of fish per week.

Background & aims

Pancreatitis is a source of substantial morbidity and health cost in the United States. Little is known about how diet might contribute to its pathogenesis. To characterize dietary factors that are associated with risk of pancreatitis by disease subtype, we conducted a prospective analysis of 145,886 African Americans, Native Hawaiians, Japanese Americans, Latinos, and whites in the Multiethnic Cohort.

Methods

In the Multiethnic Cohort (age at baseline, 45-75 y), we identified cases of pancreatitis using hospitalization claim files from 1993 through 2012. Patients were categorized as having gallstone-related acute pancreatitis (AP) (n = 1210), AP not related to gallstones (n = 1222), or recurrent AP or suspected chronic pancreatitis (n = 378). Diet information was obtained from a questionnaire administered when the study began. Associations were estimated by hazard ratios and 95% confidence intervals using Cox proportional hazard models adjusted for confounders.

Results

Dietary intakes of saturated fat (P trend = .0011) and cholesterol (P trend = .0008) and their food sources, including red meat (P trend < .0001) and eggs (P trend = .0052), were associated positively with gallstone-related AP. Fiber intake, however, was associated inversely with gallstone-related AP (P trend = .0005) and AP not related to gallstones (P trend = .0035). Vitamin D, mainly from milk, was associated inversely with gallstone-related AP (P trend = .0015), whereas coffee consumption protected against AP not related to gallstones (P trend < .0001). With the exception of red meat, no other dietary factors were associated with recurrent acute or suspected chronic pancreatitis.

Conclusions

Associations between dietary factors and pancreatitis were observed mainly for gallstone-related AP. Interestingly, dietary fiber protected against AP related and unrelated to gallstones. Coffee drinking protected against AP not associated with gallstones. Further studies are warranted to confirm our findings.

Background & aims

Obesity is associated with increased risk for hepatocellular carcinoma (HCC), but the risk associated with obesity may vary by sex or ethnicity. We examined whether the association of body mass index (BMI) with HCC incidence, as well as correlations of BMI with total, visceral, and hepatic adiposity, differs among ethnic groups.

Methods

We collected data from the Multiethnic Cohort Study, a population-based prospective cohort study of more than 215,000 men and women from Hawaii and California that was assembled from 1993 through 1996. After a median follow-up of 16.6 years, 482 incident HCC cases were identified among 168,476 participants. BMI and risk factor data were obtained from a baseline questionnaire. Cox regression analyses were used to calculate hazard ratios (HRs) and confidence intervals (CIs) for HCC associated with BMI. The black subjects in the Southern Community Cohort Study were included as a replication cohort.

Results

BMI was associated with HCC in men (HR per 5 kg/m(2) increase, 1.26; 95% CI, 1.12-1.42) but not in women (HR, 1.06; 95% CI, 0.90-1.25) (P(interaction) = .009). Although BMI was strongly associated with HCC in Japanese, white, and Latino men, there was no association in black men (P(interaction) = .002). Similarly, no association was found in the blacks who participated in the Southern Community Cohort Study. BMI correlated with total fat mass, measured by dual-energy x-ray absorptiometry, in men and women and in all ethnic groups (R ≥ 0.9). However, there was a lower correlation value for BMI and visceral or liver fat measured by abdominal magnetic resonance imaging in black men (R < 0.5) and in women (R < 0.8).

Conclusions

On the basis of an analysis of data from the Multiethnic Cohort Study, the association between BMI and HCC differs between sexes and among ethnicities. The lack of association in black men warrants further investigation. Rather than studying markers of total adiposity, studies of obesity and HCC should move beyond BMI and use a better measure for fat-specific depots.

BACKGROUND: Frailty status has been sparsely studied in some groups including Native Hawaiians and Asian Americans. METHODS: We developed a questionnaire-based deficit accumulation frailty index (FI) in the Multiethnic Cohort (MEC) and examined frailty status (robust, FI 0 to <0.2, prefrail, FI 0.2 to <0.35, and frail FI ≥ 0.35) among 29 026 men and 40 756 women. RESULTS: After adjustment for age, demographic, lifestyle factors, and chronic conditions, relative to White men, odds of being frail was significantly higher (34%-54%) among African American, Native Hawaiian, and other Asian American men, whereas odds was significantly lower (36%) in Japanese American men and did not differ in Latino men. However, among men who had high school or less, none of the groups displayed significantly higher odds of prefrail or frail compared with White men. Relative to White women, odds of being frail were significantly higher (14%-33%) in African American and Latino women, did not differ for other Asian American women and lower (14%-36%) in Native Hawaiian and Japanese American women. These racial and ethnic differences in women were observed irrespective of education. Risk of all-cause mortality was higher in prefrail and frail men than robust men (adjusted hazard ratio [HR] = 1.69, 1.59-1.81; HR = 3.27, 3.03-3.53); results were similar in women. All-cause mortality was significantly positively associated with frailty status and frailty score across all sex, race, and ethnic groups. CONCLUSIONS: Frailty status differed significantly by race and ethnicity and was consistently associated with all-cause mortality. The FI may be a useful tool for aging studies in this multiethnic population.