The epidemiologic literature in the English language regarding intake of tomatoes and tomato-based products and blood lycopene (a compound derived predominantly from tomatoes) level in relation to the risk of various cancers was reviewed. Among 72 studies identified, 57 reported inverse associations between tomato intake or blood lycopene level and the risk of cancer at a defined anatomic site; 35 of these inverse associations were statistically significant. No study indicated that higher tomato consumption or blood lycopene level statistically significantly increased the risk of cancer at any of the investigated sites. About half of the relative risks for comparisons of high with low intakes or levels for tomatoes or lycopene were approximately 0.6 or lower. The evidence for a benefit was strongest for cancers of the prostate, lung, and stomach. Data were also suggestive of a benefit for cancers of the pancreas, colon and rectum, esophagus, oral cavity, breast, and cervix. Because the data are from observational studies, a cause-effect relationship cannot be established definitively. However, the consistency of the results across numerous studies in diverse populations, for case-control and prospective studies, and for dietary-based and blood-based investigations argues against bias or confounding as the explanation for these findings. Lycopene may account for or contribute to these benefits, but this possibility is not yet proven and requires further study. Numerous other potentially beneficial compounds are present in tomatoes, and, conceivably, complex interactions among multiple components may contribute to the anticancer properties of tomatoes. The consistently lower risk of cancer for a variety of anatomic sites that is associated with higher consumption of tomatoes and tomato-based products adds further support for current dietary recommendations to increase fruit and vegetable consumption.

/pdf/tomatoes-tomato-based-products-lycopene-and-cancer-review-of-58ewr3o8rf.pdf

Tomatoes, Tomato-Based Products, Lycopene, and Cancer: Review of the Epidemiologic Literature

Gastric cancer epidemiology and risk factors

It has been estimated by various authorities that about one-third of cancers in Western high-income societies are attributable to factors relating to food, nutrition and physical activity. Identifying with confidence specific associations between dietary patterns, foods, body composition or individual nutrients is not simple because of the long latent period for cancer development, its complex pathogenesis and the challenge of characterising the multidimensional aspects of diet and activity over a lifetime. Reliable conclusions must therefore be drawn not only from randomised controlled trials but from a variety of methodological approaches, judged within a classic framework for inferring causality. Using a newly-developed method with a protocol for standardising the literature search and for analysis and display of the evidence, nine independent academic centres have conducted systematic reviews addressing the causal associations between food, nutrition and physical activity and risk of development of seventeen cancers, as well as of weight gain and obesity. A review has also examined the efficacy of such interventions in subjects with cancer. The reviews have been assessed by an independent Panel of twenty-one international experts who drew conclusions with grades of confidence in the causality of associations and made recommendations. Recommendations are given as public health goals as well as for individuals.

/pdf/the-second-world-cancer-research-fund-american-institute-for-4wjy2ptzze.pdf

The second World Cancer Research Fund/American Institute for Cancer Research expert report. Food, nutrition, physical activity, and the prevention of cancer: a global perspective.

Background Several risk factors have been identified for esophageal adenocarcinoma, gastric cardia adenocarcinoma, esophageal squamous cell carcinoma, and noncardia gastric adenocarcinoma, but no study has comprehensively examined their contributions to the cancer burden in the general population. Herein, we estimate the population attributable risks (PARs) for various risk factors observed in a multicenter population-based case-control study. Methods We calculated PARs by using 293 patients with esophageal adenocarcinoma, 261 with gastric cardia adenocarcinoma, 221 with esophageal squamous cell carcinoma, 368 with noncardia gastric adenocarcinoma, and 695 control subjects. We included smoking for all four tumor types and Helicobacter pylori infection for noncardia gastric adenocarcinoma as established causal risk factors as well as several other factors for which causality is under evaluation. Results Ever smoking, body mass index above the lowest quartile, history of gastroesophageal reflux, and low fruit and vegetable consumption accounted for 39.7% (95% confidence interval [CI] = 25.6% to 55.8%), 41.1% (95% CI = 23.8% to 60.9%), 29.7% (95% CI = 19.5% to 42.3%), and 15.3% (95% CI = 5.8% to 34.6%) of esophageal adenocarcinomas, respectively, with a combined PAR of 78.7% (95% CI = 66.5% to 87.3%). Ever smoking and body mass index above the lowest quartile were responsible for 45.2% (95% CI = 31.3% to 59.9%) and 19.2% (95% CI = 4.9% to 52.0%) of gastric cardia adenocarcinomas, respectively, with a combined PAR of 56.2% (95% CI = 38.1% to 72.8%). Ever smoking, alcohol consumption, and low fruit and vegetable consumption accounted for 56.9% (95% CI = 36.6% to 75.1%), 72.4% (95% CI = 53.3% to 85.8%), and 28.7% (95% CI = 11.1% to 56.5%) of esophageal squamous cell carcinomas, respectively, with a combined PAR of 89.4% (95% CI = 79.1% to 95.0%). Ever smoking, history of gastric ulcers, nitrite intake above the lowest quartile, and H. pylori infection were responsible for 18.3% (95% CI = 6.5% to 41.8%), 9.7% (95% CI = 5.4% to 16.8%), 40.7% (95% CI = 23.4% to 60.7%), and 10.4% (95% CI = 0.3% to 79.6%) of noncardia gastric adenocarcinomas, respectively, with a combined PAR of 59.0% (95% CI = 16.2% to 91.4%). Conclusion In this population, a few known risk factors account for a majority of esophageal and gastric cancers. These results suggest that the incidence of these cancers may be decreased by reducing the prevalence of smoking, gastroesophageal reflux, and being overweight and by increasing the consumption of fruits and vegetables.

/pdf/population-attributable-risks-of-esophageal-and-gastric-1yq3pd9bsi.pdf

Population attributable risks of esophageal and gastric cancers.

Background 
Red meat and processed meat have been associated with carcinogenesis at several anatomic sites, but no prospective study has examined meat intake in relation to a range of malignancies. We investigated whether red or processed meat intake increases cancer risk at a variety of sites.


Methods and Findings 
The National Institutes of Health (NIH)-AARP (formerly the American Association for Retired Persons) Diet and Health Study is a cohort of approximately 500,000 people aged 50–71 y at baseline (1995–1996). Meat intake was estimated from a food frequency questionnaire administered at baseline. Cox proportional hazards regression was used to estimate hazard ratios and 95% confidence intervals within quintiles of red and processed meat intake. During up to 8.2 y of follow-up, 53,396 incident cancers were ascertained. Statistically significant elevated risks (ranging from 20% to 60%) were evident for esophageal, colorectal, liver, and lung cancer, comparing individuals in the highest with those in the lowest quintile of red meat intake. Furthermore, individuals in the highest quintile of processed meat intake had a 20% elevated risk for colorectal and a 16% elevated risk for lung cancer.


Conclusions 
Both red and processed meat intakes were positively associated with cancers of the colorectum and lung; furthermore, red meat intake was associated with an elevated risk for cancers of the esophagus and liver.

/pdf/a-prospective-study-of-red-and-processed-meat-intake-in-4ga8smr0ap.pdf

A prospective study of red and processed meat intake in relation to cancer risk.

A multi-centre case-control study of diet and gastric cancer was carried out in 4 regions of Spain (Aragon, Castile, Catalonia and Galicia). We selected 354 cases of pathologically confirmed gastric adenocarcinoma from 15 hospitals, representative of nearly all those in the study areas. A control for each case, matched by age, sex and area of residence, was selected from the same hospital as the case. Habitual diet was investigated by the dietary history method, and past diet by means of a frequency questionnaire. The results regarding consumption of food items are presented here. With respect to habitual diet, an increase in risk was associated with consumption of preserved fish, cold cuts and oleaginous fruits. A high intake of cooked green vegetables, fresh noncitrus fruit and dried fruit showed an inverse association with the risk of gastric cancer. Simultaneous intake of 2 groups of food which increase or decrease the risk of cancer strengthens the respective individual effect. The intake of protective food items seems to neutralize the effects of food items which increase risk. With reference to past diet, a possible protective effect was observed for daily consumption of fresh fruit and green vegetables.

Dietary factors and stomach cancer in Spain: a multi-centre case-control study.

0.18 (95% CI, 0.06-0.52). Considering the level of consumption in four categories (nonconsumers as the referent category and three categories among consumers), the ORs (and 95% Cl) were 0.31 (0.08-1 .18) for the low level of consumption, 0.15 (0.03-0.72) for moderate consumers, and 0.09 (0.02-0.46) for high consumers, showing a clear dose-response relationship (P for trend, 0.0006). These results are based on 88 case-control pairs of residents of the province of Zaragoza. The consumption of borage was extremely low in two areas of the study (Barcelona and Galicia). In the province of Sonia (72 case-control pairs) 22% of controls were consumers (at least 0.5 times a week); the risk for consumers, ad

https://cebp.aacrjournals.org/content/cebp/2/2/157.full.pdf

Borage consumption as a possible gastric cancer protective factor.

Coronary atherosclerosis is the main pathophysiological mechanism underlying myocardial infarction. The gut microbiota has been implicated in cardiometabolic disease but its relationship with subclinical coronary atherosclerosis is unknown. We identified 73 gut metagenomics species associated with coronary artery calcium score (CACS) in 8,973 SCAPIS participants without previous cardiovascular disease. Streptococcus associations were overrepresented and were validated in an independent case-control study together with eight non-Streptococcus spp. We further found enrichment for bacterial genes linked to amino acid and carbohydrate degradation functions. Gut Streptococcus spp. were associated with circulating biomarkers of inflammation and infection response, bile acids, androgenic steroids and sphingomyelins, and were associated with their homologous species in the oral cavity, which were in turn associated with oral pathologies. This study provides robust evidence of the association of Streptococcus spp., with subclinical atherosclerosis and markers of systemic inflammation and infection, calling for studies re-investigating the infectious hypothesis in atherosclerosis pathogenesis.

Streptococcus species abundance in the gut is linked to subclinical coronary atherosclerosis in 8,973 participants from the SCAPIS cohort

A case-control study on diet and gastric cancer, carried out in selected areas of four regions of Spain (Aragon, Castile, Catalonia, and Galicia) in 1988 and 1989, included 354 cases of histologically confirmed gastric adenocarcinoma and 354 controls matched by age, sex, and area of residence. Cases and controls were selected from 15 hospitals, representing most of the hospital facilities in the study areas. Usual diet was estimated by means of a dietary history questionnaire administered by interview. An increased risk of gastric cancer was observed for high consumption of exogenous nitrosamines (odds ratio = 2.1 for the highest quartile of consumption versus the lowest; p for linear trend = 0.007), nitrites, fat, and cholesterol. However, in a multivariate regression model, the effect of fat and cholesterol disappeared. An inverse association with the risk for gastric cancer was seen for high intake of fiber, vitamin C, folate, carotene, and nitrates. High consumption of vitamin C seemed to neutralize the increased risk related to simultaneous consumption of nitrosamines. For histologic type, the authors found no meaningful differences in the effect of most of the nutrients between intestinal and diffuse cancers. Their findings are consistent with previously reported results about the protective effect of fruit and vegetables and the increased risk associated with foods that are important sources of nitrites and preformed nitrosamines.

Nutritional Factors and Gastric Cancer in Spain

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Dietary factors and stomach cancer in Spain: a multi-centre case-control study.

Borage consumption as a possible gastric cancer protective factor.

Streptococcus species abundance in the gut is linked to subclinical coronary atherosclerosis in 8,973 participants from the SCAPIS cohort

Nutritional Factors and Gastric Cancer in Spain