Obesity and incidence of lung cancer: A meta‐analysis

To date, the relationship between obesity and the incidence of lung cancer remains unclear and inconclusive. Thus, we conducted a meta‐analysis of published studies to provide a quantitative evaluation of this association. Relevant studies were identified through PubMed and EMBASE databases from 1966 to December 2011, as well as through the reference lists of retrieved articles. A total of 31 articles were included in this meta‐analysis. Overall, excess body weight (body mass index, BMI ≥ 25 kg/m²) was inversely associated with lung cancer incidence (relative risk, RR = 0.79; 95% confidence interval, CI: 0.73–0.85) compared with normal weight (BMI = 18.5‐24.9 kg/m²). The association did not change with stratification by sex, study population, study design, and BMI measurement method. However, when stratified by smoking status, the inverse association between excess body weight and lung cancer incidence in current (RR = 0.63, 95% CI: 0.57–0.70) and former (RR = 0.73, 95% CI: 0.58–0.91) smokers was strengthened. In non‐smokers, the association was also statistically significant (RR = 0.83, 95% CI: 0.70–0.98), although the link was weakened to some extent. The stratified analyses also showed that excess body weight was inversely associated with squamous cell carcinoma (RR = 0.68, 95% CI: 0.58–0.80) and adenocarcinoma (RR = 0.79, 95% CI: 0.65–0.96). No statistically significant link was found between excess body weight and small cell carcinoma (RR = 0.99, 95% CI: 0.66–1.48). The results of this meta‐analysis indicate that overweight and obesity are protective factors against lung cancer, especially in current and former smokers.     

Food groups and risk of colorectal cancer

The aim of this systematic review and meta‐analysis was to summarize the evidence on the relationship between intake of 12 major food groups, including whole grains, refined grains, vegetables, fruit, nuts, legumes, eggs, dairy, fish, red meat, processed meat and sugar‐sweetened beverages with risk of colorectal cancer (CRC). We conducted a systematic search in PubMed and Embase for prospective studies investigating the association between these 12 food groups and risk of CRC until April 2017. Summary risk ratios (RRs) and 95% confidence intervals (95% CI) were estimated using a random effects model for high vs. low intake categories, as well as for linear and nonlinear relationships. An inverse association was observed for whole grains (RR_30g/d: 0.95, 95% CI 0.93, 0.97; n = 9 studies), vegetables (RR_100g/d: 0.97, 95% CI 0.96, 0.98; n = 15), fruit (RR_100g/d: 0.97, 95% CI 0.95, 0.99; n = 16) and dairy (RR_200g/d: 0.93, 95% CI 0.91, 0.94; n = 15), while a positive association for red meat (RR_100g/d: 1.12, 95% CI 1.06, 1.19; n = 21) and processed meat (RR_50g/d: 1.17, 95% CI 1.10, 1.23; n = 16), was seen in the linear dose‐response meta‐analysis. Some evidence for nonlinear relationships was observed between vegetables, fruit and dairy and risk of colorectal cancer. Findings of this meta‐analysis showed that a diet characterized by high intake of whole grains, vegetables, fruit and dairy products and low amounts of red meat and processed meat was associated with lower risk of CRC.     

Association between the dietary inflammatory index and all-cause mortality in colorectal cancer long-term survivors

Pro-inflammatory dietary factors have been shown to be associated with the incidence of a range of cancers. However, there are many fewer studies on the association between the inflammatory potential of diet and survival after cancer diagnosis. We examined the association between post-diagnosis dietary inflammatory index (DII®) scores and all-cause mortality in long-term survivors of colorectal cancer (CRC). DII scores were calculated from dietary data of 1,404 CRC survivors collected at a median of 6 years after CRC diagnosis. Using multivariable-adjusted Cox proportional hazards regression models, hazard ratios (HR) and 95% confidence intervals (CI) were estimated for the association of DII scores, modeled continuous and in quartiles, with all-cause mortality. After a median follow-up time of 7 years (after dietary assessment), 204 study participants had died. Overall, in the fully adjusted model there was a suggestion of a positive association between DII score and all-cause mortality (HR_{DIIquartile4vs1}: 1.36; 95% CI: 0.88–2.09 and HR_{DIIcontinuous}: 1.08; 95% CI: 0.97–1.20). However, in subgroup analyses, we found significant differences in individuals with metastatic disease (HR_{DIIcontinuous}: 1.34; 95% CI: 1.07–1.67) and the absence of stoma (HR_{DIIcontinuous}: 1.15; 95% CI: 1.02–1.29). Overall, the post-diagnosis DII was not statistically significantly associated with all-cause mortality in CRC long-term survivors; however, there was suggestive evidence of an association in select subgroups.     

Dietary inflammatory index and prostate cancer survival

Systemic inflammatory status has been reported to impact survival of prostate cancer (PCa) patients; however, evidence is lacking on whether the inflammatory potential of diet can influence prognosis of PCa patients. To investigate the association between a dietary inflammatory index (DII) and PCa survival, we conducted a retrospective cohort study including 726 men with PCa originally enrolled, between 1995 and 2002, in an Italian case–control study. Information on diet and Gleason score was collected at PCa diagnosis. DII was derived from a food frequency questionnaire using a validated algorithm. Adjusted hazard ratios (HRs) of death with 95% confidence intervals (CIs) were estimated using a Fine‐Gray model. DII scores were not significantly associated with all‐cause mortality of PCa patients (HR highest vs. lowest DII tertile = 1.25; 95% CI: 0.86–1.83). However, considerable heterogeneity emerged according to Gleason score (p < 0.01): no associations emerged among men with Gleason score 2–6 PCa; whereas, among patients with Gleason score 7–10 PCa, DII was directly associated with both all‐cause and PCa‐specific mortality (HR highest vs. lowest DII tertile: 2.78; 95% CI: 1.41–5.48; and 4.01; 95% CI: 1.25–12.86; respectively). Among patients with Gleason score 7–10 PCa, ten‐year all‐cause survival probabilities were 58% (95% CI: 47–67%) for highest and 78% (95% CI: 67–86%) for lowest DII tertile. Study findings support the hypothesis that diet, through its inflammatory potential, may influence the prognosis of patients with more aggressive PCa. Dietary interventions aimed at decreasing inflammation may be considered to improve survival of men with PCa.     

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.     

Body fatness at an early age and risk of colorectal cancer

While there is convincing evidence that excess body fatness in adulthood is positively associated with colorectal cancer risk, the association between body fatness at an early age (≤30 years) and the risk of colorectal cancer has been equivocal. The present meta‐analysis was performed to clarify this association. PubMed and Web of Science databases were searched for relevant studies that investigated this association. The risk estimates from each study were transformed into a continuous variable for each 5 kg/m² increase in body mass index (BMI). A random effects model was used to calculate the summary relative risks (RRs) with 95% confidence intervals (CIs). A total of 15 observational studies (13 cohort studies and two case‐control studies) were included in this meta‐analysis. Each 5 kg/m² increase in BMI was significantly associated with a 13% (RR 1.13, 95% CI 1.08, 1.19), 17% (RR 1.17, 95% CI 1.09, 1.25) and 8% (RR 1.08, 95% CI 1.04, 1.11) higher risk of colorectal cancer overall, in men, and in women, respectively. Substantial heterogeneity was observed across studies. Based on the anatomic subsite, each 5 kg/m² increase in BMI was significantly associated with a 14% (RR 1.14, 95% CI 1.07, 1.22) higher risk of colon cancer, whereas no association (RR 1.03, 95% CI 0.95, 1.13) was observed with rectal cancer. In summary, body fatness at an early age may affect colon cancer risk later in life. Prevention of overweight and obesity in young individuals should be emphasized to prevent early‐onset colon cancer attributed to excess body fatness.     

Adherence to Mediterranean diet and risk of cancer: A systematic review and meta‐analysis of observational studies

The aim of this research study was to meta‐analyze the effects of adherence to Mediterranean diet (MD) on overall cancer risk, and different cancer types. Literature search was performed using the electronic databases MEDLINE, SCOPUS and EMBASE until January 10, 2014. Inclusion criteria were cohort or case–control studies. Study specific risk ratios (RRs) were pooled using a random effect model by the Cochrane software package Review Manager 5.2. Twenty‐one cohort studies including 1,368,736 subjects and 12 case–control studies with 62,725 subjects met the objectives and were enclosed for meta‐analyses. The highest adherence to MD category resulted in a significantly risk reduction for overall cancer mortality/incidence (cohort; RR: 0.90, 95% CI 0.86–0.95, p < 0.0001; I² = 55%), colorectal (cohort/case–control; RR: 0.86, 95% CI 0.80–0.93, p < 0.0001; I² = 62%], prostate (cohort/case–control; RR: 0.96, 95% CI 0.92–0.99, p = 0.03; I² = 0%) and aerodigestive cancer (cohort/case–control; RR: 0.44, 95% CI 0.26–0.77, p = 0.003; I² = 83%). Nonsignificant changes could be observed for breast cancer, gastric cancer and pancreatic cancer. The Egger regression tests provided limited evidence of substantial publication bias. High adherence to a MD is associated with a significant reduction in the risk of overall cancer mortality (10%), colorectal cancer (14%), prostate cancer (4%) and aerodigestive cancer (56%).     

Dietary inflammatory index and risk of epithelial ovarian cancer in African American women

Chronic inflammation has been implicated in the development of epithelial ovarian cancer (EOC); yet the contribution of inflammatory foods and nutrients to EOC risk has been understudied. We investigated the association between the dietary inflammatory index (DII), a novel literature‐derived tool to assess the inflammatory potential of one's diet, and EOC risk in African American (AA) women in the African American Cancer Epidemiology Study, the largest population‐based case–control study of EOC in AA women to date. The energy‐adjusted DII (E‐DII) was computed per 1,000 kilocalories from dietary intake data collected through a food frequency questionnaire, which measured usual dietary intake in the year prior to diagnosis for cases or interview for controls. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated using multivariable logistic regression for the association between the E‐DII and EOC risk. 493 cases and 662 controls were included in the analyses. We observed a 10% increase in EOC risk per a one‐unit change in the E‐DII (OR = 1.10, 95% CI = 1.03–1.17). Similarly, women consuming the most pro‐inflammatory diet had a statistically significant increased EOC risk in comparison to the most anti‐inflammatory diet (OR_{Quartile4/Quartile1} = 1.72; 95% CI = 1.18–2.51). We also observed effect modification by age (p < 0.05), where a strong, significant association between the E‐DII and EOC risk was observed among women older than 60 years, but no association was observed in women aged 60 years or younger. Our findings suggest that a more pro‐inflammatory diet was associated with an increased EOC risk, especially among women older than 60 years.     

Factors associated with incident and fatal pancreatic cancer in a cohort of middle‐aged women

Risk factors for pancreatic cancer, other than smoking and diabetes, are not well‐established, especially for women. In a cohort of 1.3 million middle‐aged women, followed for 9.2 million person‐years for cancer incidence and 11.5 million person‐years for mortality, there were 1,338 incident pancreatic cancer cases and 1,710 deaths from the disease. Using proportional hazards models, we calculated adjusted relative risks (RRs) and 95% confidence intervals (CIs) by smoking, height, body mass index (BMI), alcohol consumption, physical activity and history of diabetes. Pancreatic cancer incidence was greater in current than never smokers (RR 2.39, CI 2.10–2.73), the risk increasing with the number of cigarettes smoked. The incidence of pancreatic cancer also increased with increasing BMI (RR 1.34, CI 1.13–1.57 for BMI ≥ 30 vs. 22.5–25 kg/m²), and with a history of diabetes (RR 1.58, CI 1.22–2.03, with vs. without such a history). These factors were also associated with increased mortality from pancreatic cancer. Height, alcohol consumption and physical activity showed little or no association with pancreatic cancer risk. © 2008 Wiley‐Liss, Inc.     

Inflammatory potential of diet and risk of oral and pharyngeal cancer in a large case‐control study from Italy

Diet and inflammation have been suggested to be important risk factors for oral and pharyngeal cancer. We examined the association between dietary inflammatory index (DII?) and oral and pharyngeal cancer in a large case‐control study conducted between 1992 and 2009 in Italy. This study included 946 cases with incident, histologically confirmed oral and pharyngeal cancer, and 2,492 controls hospitalized for acute non‐neoplastic diseases. The DII was computed based on dietary intake assessed by a valid 78‐item food frequency questionnaire and was adjusted for nonalcohol energy intake using the residual approach (E‐DII?). Logistic regression models were used to estimate odds ratios (ORs), and 95% confidence intervals (CIs), adjusted for age, sex, non‐alcohol energy intake, study center, year of interview, education, body mass index, tobacco smoking, and alcohol drinking. Subjects with higher DII scores (i.e ., with a more pro‐inflammatory diet) had a higher risk of oral and pharyngeal cancer, the OR being 1.80 (95% CI 1.36–2.38) for the highest versus the lowest DII quartile and 1.17 (95% CI 1.10–1.25) for a one‐unit increase (8% of the DII range). When stratified by selected covariates, a stronger association was observed among women (OR_{quartile4 v.1} 3.30, 95% CI 1.95–5.57). We also observed a stronger association for oral cancers and a strong combined effect of higher DII score and tobacco smoking or alcohol consumption on oral and pharyngeal cancer. These results indicate that the pro‐inflammatory potential of the diet, as shown by higher DII scores, is associated with higher odds of oral and pharyngeal cancer.     

Inflammatory potential of diet and risk of pancreatic cancer in the Prostate,Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial

Inflammation plays a central role in pancreatic cancer etiology and can be modulated by diet. We aimed to examine the association between the inflammatory potential of diet, assessed with the Dietary Inflammatory Index (DII®), and pancreatic cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial prospective cohort. Our study included 101,449 participants aged 52–78 years at baseline who completed both baseline questionnaire and a diet history questionnaire. Energy‐adjusted DII (E‐DII) scores were computed based on food and supplement intake. Cox proportional hazards models and time dependent Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with participants in the lowest E‐DII quintile (most anti‐inflammatory scores) as referent. After a median 8.5 years of follow‐up, 328 pancreatic cancer cases were identified. E‐DII scores were not associated with pancreatic cancer risk in the multivariable model (HR_Q5vsQ1 = 0.94; 95% CI = 0.66–1.35; p‐trend = 0.43). Time significantly modified the association (p‐interaction = 0.01). During follow up <4 years, there was suggestive evidence of an inverse association between E‐DII and pancreatic cancer (HR_Q5vsQ1 = 0.60; 95% CI = 0.35–1.02; p‐trend = 0.20) while there was a significant positive trend in the follow up ≥4 years (HR_Q5vsQ1 = 1.31; 95% CI = 0.83–2.08; p‐trend = 0.03). Similar results were observed for E‐DII from food only. Our study does not support an association between inflammatory potential of diet and pancreatic cancer risk; however, heterogeneous results were obtained with different follow‐up times. These divergent associations may result from the influences of undetected disease in the short‐term.     

Analgesic use and the risk of kidney cancer: A meta‐analysis of epidemiologic studies

Analgesics are the most commonly used over‐the‐counter drugs worldwide with certain analgesics having cancer prevention effect. The evidence for an increased risk of developing kidney cancer with analgesic use is mixed. Using a meta‐analysis design of available observational epidemiologic studies, we investigated the association between analgesic use and kidney cancer risk. We searched the MEDLINE and EMBASE databases to identify eligible case–control or cohort studies published in English until June 2012 for three categories of analgesics: acetaminophen, aspirin or other non‐steroidal anti‐inflammatory drugs (NSAIDs). Study‐specific effect estimates were pooled to compute an overall relative risk (RR) and its 95% confidence interval (CI) using a random‐effects model for each category of the analgesics. We identified 20 studies (14 with acetaminophen, 13 with aspirin and five with other NSAIDs) that were performed in six countries, including 8,420 cases of kidney cancer. Use of acetaminophen and non‐aspirin NSAIDs were associated with an increased risk of kidney cancer (pooled RR: 1.28; 95% CI: 1.15–1.44 and 1.25; 95% CI: 1.06–1.46, respectively). For aspirin use, we found no overall increased risk (pooled RR: 1.10; 95% CI: 0.95–1.28), except for non‐US studies (five studies, pooled RR: 1.17; 95% CI: 1.04–1.33). Similar increases in risks were seen with higher analgesic intake. In this largest meta‐analysis to date, we found that acetaminophen and non‐aspirin NSAIDs are associated with a significant risk of developing kidney cancer. Further work is needed to elucidate biologic mechanisms behind these findings.     

Proinflammatory diet is associated with increased risk of squamous cell head and neck cancer

Diets high in fruits and vegetables and low in red meat intake have been associated with decreased risk of head and neck cancer. Additionally, chronic inflammation pathways and their association with cancer have been widely described. We hypothesized a proinflammatory diet, as measured by the dietary inflammatory index (DII^®), is associated with increased risk of head and neck cancer. We used the Carolina Head and Neck Cancer (CHANCE) study, a population‐based case–control study of head and neck squamous cell carcinoma. Cases were recruited from a 46‐county region in central North Carolina. Controls, frequency‐matched on age, race, and sex were identified through the North Carolina Department of Motor Vehicle records. The DII score, adjusted for energy using the density approach (E‐DII), was calculated from a food frequency questionnaire and split into four quartiles based on the distribution among controls. Adjusted odds ratios (ORs) were estimated with unconditional logistic regression. Cases had higher E‐DII scores (i.e., a more proinflammatory diet) compared with controls (mean: ?0.14 vs. ?1.50; p value < 0.001). When compared with the lowest quartile, the OR for the highest quartile was 2.91 (95% confidence interval (CI): 2.16–3.95), followed by 1.93 (95% CI: 1.43–2.62) for the third quartile, and 1.37 (95% CI: 1.00–1.89) for the second quartile. Both alcohol and smoking had a significant additive interaction with E‐DII (smoking relative excess risk due to interaction (RERI): 2.83; 95% CI: 1.36–4.30 and alcohol RERI: 1.75; 95% CI: 0.77–2.75). These results provide additional evidence for the association between proinflammatory diet and head and neck cancer.     

Coffee consumption and risk of colorectal cancer: A systematic review and meta‐analysis of prospective cohort studies

An inverse association between coffee consumption and the risk of colorectal cancer has been found in several case‐control studies, but such an association was not consistent in prospective cohort studies. We conducted a systematic meta‐analysis of prospective cohort studies on coffee consumption and colorectal cancer published up to June 2008. We combined relative risks (RR) for colorectal cancer comparing high vs. low categories of coffee consumption using random‐effects models. We identified 12 eligible cohort studies, which included 646,848 participants and 5,403 cases for colorectal cancer. The summarized result of the meta‐analysis comparing high‐ vs. low‐consumption categories showed no significant effect of coffee consumption on colorectal cancer risk (RR = 0.91; 95% confidence intervals [CI]: 0.81–1.02). The RR was 0.93 (95% CI: 0.71–1.22) when considering 4 studies conducted in the United States of America, 0.91 (95% CI: 0.76–1.10) for 5 studies from Europe, and 0.83 (95% CI: 0.62–1.10) for 3 Japanese studies. No significant differences by sex and cancer‐site were found, but there was a slight suggestion of an inverse association between coffee consumption and colon cancer in women (RR = 0.79; 95% CI: 0.60–1.04), especially Japanese women (RR = 0.62; 95% CI: 0.37–1.05). The suggestive inverse associations were slightly stronger in studies that controlled for smoking and alcohol, and in studies with shorter follow‐up times. Information on coffee type, its serving size, or brewing method may provide a better understanding of this reassuring result and the real role of coffee on colorectal cancer risk. © 2008 Wiley‐Liss, Inc.     

Obstructive sleep apnoea and the incidence and mortality of cancer: a meta‐analysis

As there are conflicting reports regarding the association between obstructive sleep apnoea (OSA) and cancer incidence and mortality, a meta‐analysis was performed to evaluate whether OSA is independently associated with cancer incidence and mortality. Pubmed, EMBASE and Web of Science were searched up until November 2014. Studies that assessed OSA and the future risk of cancer incidence or mortality were included. Pooled hazard ratios (HR) and corresponding 95% confidence intervals (CI) were calculated. Subgroup analysis was conducted based on the polysomnographic variable, apnoea–hypopnoea index. Six studies, which involved 114 105 participants, were pooled in this meta‐analysis. Fixed‐effects analysis showed the pooled adjusted HR of cancer incidence as 0.91 (95% CI, 0.74–1.13; P = 0.408) for mild OSA, 1.07 (95% CI, 0.86–1.33; P = 0.552) for moderate OSA and 1.03 (95% CI, 0.85–1.26; P = 0.743) for severe OSA. Random‐effects analysis demonstrated neither mild OSA (adjusted HR, 0.79; 95% CI, 0.46–1.34; P = 0.381), moderate OSA (adjusted HR, 1.92; 95% CI, 0.63–5.88; P = 0.251) nor severe OSA (adjusted HR, 2.09; 95% CI, 0.45–9.81; P = 0.349) correlated with cancer mortality. This meta‐analysis indicates that OSA is not independently associated with cancer incidence and mortality according to currently available data. Additional experimental and human research is required to determine the exact association between OSA and cancer.     

A prospective study of dietary patterns and cancer mortality among Blacks and Whites in the REGARDS cohort

Marked racial differences exist in dietary patterns and obesity, as well as cancer mortality. This study aims to assess whether dietary patterns are associated with cancer mortality overall and by race. We identified 22,041 participants from the REasons for Geographic and Racial Differences in Stroke (REGARDS) cohort. Dietary patterns were categorized into: Convenience (Chinese and Mexican foods, pasta, pizza), Plant‐based (fruits, vegetables), Southern (added fats, fried foods, sugar‐sweetened beverages), Sweets/Fats (sugary foods) and Alcohol/Salads (alcohol, green‐leafy vegetables, salad dressing). Using Cox regression, we examined the association between quartiles of dietary patterns and cancer mortality, adjusted for potential confounders, overall among all participants and stratified by race. A total of 873 cancer deaths were observed over the 10‐year observation period: 582 (66.7%) in Whites and 291 (33.3%) in Blacks. Greater adherence to the Southern dietary pattern was associated with an increased risk of cancer mortality (4th vs. 1st quartile HR: 1.67; 95% CI: 1.32–2.10) overall, especially among Whites (4th vs. 1st quartile HR: 1.59; 95% CI: 1.22–2.08). The convenience (HR: 0.73; 95% CI: 0.56–0.94) and Plant‐based (HR: 0.72; 95% CI: 0.55–0.93) dietary patterns were associated with up to a 28% reduced risk of cancer mortality, but only among Whites. Greater adherence to the Southern dietary pattern increased the risk of cancer mortality, while greater adherence to the convenience and Plant‐based diets reduced the risk of cancer mortality among Whites. Racial differences were observed in the association between dietary patterns and cancer mortality, but warrant further study.     

Association between height and thyroid cancer risk: A meta‐analysis of prospective cohort studies

While several epidemiological studies have investigated the relationship between height and risk for thyroid cancer, the results were inconsistent. In the present study, a systematic review and meta‐analysis of prospective cohort studies was conducted to assess the impact of height on thyroid cancer risk. Online databases were searched up to December 30, 2014, for prospective cohort studies on the association between height and thyroid cancer risk. Pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated using a random‐effects model of meta‐analysis. In all, 11 articles were included in this meta‐analysis, including 15 prospective cohort studies, containing 6,695,593 participants and 7,062 cases of thyroid cancer. By comparing the highest versus the lowest categories of height, we reported that risk of thyroid cancer was increased with height in both men (summary RR = 1.40, 95%CI 1.09–1.78, p = 0.008) and women (summary RR = 1.54, 95%CI 1.30–1.83, p < 0.001). The summary RR of thyroid cancer per 5‐cm increase in height was 1.16 (95%CI 1.09–1.23, p < 0.001). The results were similar among men (per 5‐cm increase RR = 1.13, 95%CI 1.03–1.23, p = 0.011) and women (per 5‐cm increase RR = 1.18, 95%CI 1.10–1.27, p < 0.001). No obvious risk of publication bias was observed. Our meta‐analysis provides strong evidence for a dose–response relationship between height and risk of thyroid cancer in both men and women.     

Meat subtypes and their association with colorectal cancer: Systematic review and meta‐analysis

Associations between specific red meat subtypes and risk of colorectal cancer (CRC) have been investigated in a number of epidemiological studies. However, no publication to date has summarised the overall epidemiological evidence. We conducted a systematic review and meta‐analysis of prospective studies (cohort, nested case‐control or case‐cohort studies), which reported relative risk (RR) estimates and 95% confidence intervals (CI) for the association between intake of meat subtypes with colorectal, colon or rectal cancer or colorectal adenoma risk. PubMed and ISI Web of Science were searched up until August 1, 2014. Nineteen studies examined meat subtypes (5 beef, 5 pork, 2 lamb, 1 veal and 19 poultry) and associations with colorectal, colon or rectal cancer risk and 4 studies examined associations with adenoma risk (1 beef and 4 poultry). Comparing highest versus lowest intake, beef consumption was associated with an increased risk of CRC (RR = 1.11, 95% CI = 1.01 to 1.22) and colon cancer (RR = 1.24, 95% CI = 1.07 to 1.44), but no association was found with rectal cancer (RR = 0.95, 95% CI = 0.78 to 1.16). Higher consumption of lamb was also associated with increased risk of CRC (RR = 1.24, 95% CI = 1.08 to 1.44). No association was observed for pork (RR = 1.07, 95% CI = 0.90 to 1.27), but some between study heterogeneity was observed. No association was observed for poultry consumption and risk of colorectal adenomas or cancer. This meta‐analysis suggests that red meat subtypes differ in their association with CRC and its sub sites. Further analysis of data from prospective cohort studies is warranted, especially regarding the role of pork.     

Association between metformin use after surgery for colorectal cancer and oncological outcomes: A nationwide register‐based study

Colorectal cancer is one of the most common malignancies in the Western world, and even after surgical removal, there is a high recurrence rate. Metformin treatment has been associated with a reduced risk of developing cancer, but whether metformin influences the risk of recurrence is unknown. The aim of our study was to examine the association between treatment with metformin and recurrence‐free, disease‐free survival and all‐cause mortality after surgery for colorectal cancer. The study was an observational register‐based study and included 25,785 patients, of which 1,116 had medically treated diabetes and 966 started metformin treatment at some point postoperatively. Diabetes was not associated with neither disease‐free (HR_adjusted = 1.09, 95% CI 0.97–1.21, p = 0.15) nor recurrence‐free survival (HR_adjusted = 1.13, 95% CI 0.95–1.35, p = 0.17). The study found no difference in regards to disease‐free or recurrence‐free survival between the metformin treated group (HR_RFS = 1.06, 95% CI 0.87–1.15, p = 0.57, HR_DFS = 1.01, 95% CI 0.89–1.15, p = 0.85) and non‐diabetic patients. Patients with diabetes had increased all‐cause mortality (HR_adjusted = 1.29, 95% CI 1.16–1.45, p < 0.0001). Metformin treatment did not affect all‐cause mortality (HR = 1.07, 95% CI 0.94–1.22, p = 0.33) compared to non‐diabetic patients. In conclusion, our study did not find an association between diabetes or metformin treatment and recurrence‐free or disease‐free survival after surgery for colorectal cancer. However, diagnosis of diabetes is associated with increased all‐cause mortality.     

Association between physical activity and mortality in colorectal cancer: A meta‐analysis of prospective cohort studies

Several prospective cohort studies have examined the association between prediagnosis and/or postdiagnosis physical activity (PA) on colorectal cancer outcomes and reported conflicting results. To quantitatively assess this association, we have conducted a meta‐analysis of prospective studies. Databases and reference lists of relevant studies were searched using MEDLINE and EMBASE up to January 2013. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated using random‐effects models. For this meta‐analysis, a total of seven prospective cohort studies were included. The analysis included 5,299 patients for prediagnosis PA and 6,348 patients for postdiagnosis PA, followed up over a period ranging from 3.8 to 11.9 years. The analyses showed that patients who participated in any amount of PA before diagnosis had a RR of 0.75 (95% CI: 0.65–0.87, p < 0.001) for colorectal cancer‐specific mortality compared to patients who did not participate in any PA. Those who participated in high PA before diagnosis (vs. low PA) had a RR of 0.70 (95% CI: 0.56–0.87, p = 0.002). Similarly, patients who participated in any PA after diagnosis had a RR of 0.74 (95% CI: 0.58–0.95, p = 0.02) for colorectal cancer‐specific mortality compared to patients who did not participate in any PA. Those who participated in high PA after diagnosis (vs. low PA) had a RR of 0.65 (95% CI: 0.47–0.92, p = 0.01). Similar inverse associations of prediagnosis or postdiagnosis PA were found for all‐cause mortality. In conclusion, both prediagnosis and postdiagnosis PA were associated with reduced colorectal cancer‐specific mortality and all‐cause mortality.