scholarly journals Dietary heterocyclic aromatic amine intake and cancer risk: epidemiological evidence from Japanese studies

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Motoki Iwasaki ◽  
Shoichiro Tsugane

AbstractHeterocyclic aromatic amines (HAAs), which are formed from the reaction of creatine or creatinine, amino acids, and sugars in meat and fish cooked at high temperatures, have been shown to be mutagenic in bacterial assays and carcinogenic in animal models. Following advances in the dietary assessment of HAA intake in epidemiological studies - including development of a validated meat-cooking module and a specialized food composition database - a number of epidemiological studies have specifically examined the association of HAA intake and cancer risk, most of which were conducted in Western countries. Given that dietary habits and cooking methods differ across countries, however, epidemiological investigation of dietary HAA intake requires a population-specific assessment method. Here, we developed a practical method for assessing dietary HAA intake among Japanese using a food frequency questionnaire (FFQ) and evaluated its validity for use in epidemiological studies by comparison with 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP) levels in human hair. The Japan Public Health Center-based Prospective Study reported that daily intake of HAAs among Japanese was relatively low, and that more than 50% of total intake in mainland Japan was derived from fish. Only four case-control studies in Japan have been reported so far, for colorectal, stomach and prostate cancer, and colorectal adenoma. A statistically significant positive association was found between 2-amino-3,4-dimethylimidazo [4,5-f] quinoline (MeIQ) and the risk of colorectal adenoma and between individual and total HAAs and the risk of prostate cancer. In contrast, no association was observed for colorectal or stomach cancer, or for colorectal adenoma among men. We also found that the limited and inconsistent findings among epidemiological studies are due to the difficulty in assessing exposure levels of HAAs. In addition to further evidence from prospective cohort studies in Japanese based on dietary HAA intake estimated by FFQs, studies using other methods to assess HAA exposure, such as biomarkers, are highly anticipated.

2007 ◽  
Vol 98 (6) ◽  
pp. 1112-1115 ◽  
Author(s):  
Sabine Rohrmann ◽  
Dorothee Zoller ◽  
Silke Hermann ◽  
Jakob Linseisen

It was the aim of the present study to estimate the intake of heterocyclic aromatic amines (HCA) from meat, which have been associated with cancer risk in several epidemiological studies, of 21 462 subjects who participated in the European Prospective Investigation into Cancer and Nutrition (EPIC) in Heidelberg. This was accomplished by using a detailed dietary questionnaire that assessed meat consumption, cooking methods, and degree of browning of the respective food items. Median total HCA intake from meat was 31 ng/d (mean 69 ng/d), which was lower than results observed in previous studies. 2-Amino-1-methyl-6-phenylimidazo[4,5b]pyridine was the most common HCA in this cohort (median 17; mean 48 ng/d). The present study offers the opportunity of a detailed examination of the associations between meat cooking as well as HCA intake from meat and cancer risk in a prospective way.


2019 ◽  
Vol 122 (11) ◽  
pp. 1295-1302 ◽  
Author(s):  
Takehiro Michikawa ◽  
Shin Yamazaki ◽  
Makiko Sekiyama ◽  
Tatsuo Kuroda ◽  
Shoji F. Nakayama ◽  
...  

AbstractThe pathogenesis of congenital diaphragmatic hernia (CDH) is largely unknown; however, vitamin A seems to play a role in diaphragmatic development. Previous case–control studies reported that maternal dietary vitamin A intake was inversely associated with the risk of CDH. To our knowledge, however, there is no prospective evidence regarding this association. Our aim was to examine whether maternal intake of vitamin A was associated with CDH occurrence. Baseline data, from the Japan nationwide birth cohort study (2011–2014) of 89 658 mothers (mean age at delivery = 31·2 years) who delivered singleton live births, were analysed. We assessed dietary habits using an FFQ focused on the first trimester and estimated the daily intake of total vitamin A (retinol activity equivalents), retinol, provitamin A carotenoids and vegetables. The occurrence of CDH was ascertained from medical records. A total of forty cases of CDH were documented. The adjusted OR of CDH occurrence for the high total vitamin A intake category (median = 468 μg/d) was 0·6 (95 % CI 0·3, 1·2) with reference to the low intake category (230 μg/d). When we restricted to mothers with a prepregnancy BMI of 18·5–24·9 kg/m2, vitamin A intake was inversely associated with the risk of their children being born with CDH (OR 0·5, 95 % CI 0·2, 1·0). Even given the limited number of cases in the study, our findings provide additional evidence to link vitamin A with CDH.


2018 ◽  
Vol 46 (5) ◽  
pp. 1213-1224 ◽  
Author(s):  
Jessica L. Barnes ◽  
Maria Zubair ◽  
Kaarthik John ◽  
Miriam C. Poirier ◽  
Francis L. Martin

Humans are variously and continuously exposed to a wide range of different DNA-damaging agents, some of which are classed as carcinogens. DNA damage can arise from exposure to exogenous agents, but damage from endogenous processes is probably far more prevalent. That said, epidemiological studies of migrant populations from regions of low cancer risk to high cancer risk countries point to a role for environmental and/or lifestyle factors playing a pivotal part in cancer aetiology. One might reasonably surmise from this that carcinogens found in our environment or diet are culpable. Exposure to carcinogens is associated with various forms of DNA damage such as single-stand breaks, double-strand breaks, covalently bound chemical DNA adducts, oxidative-induced lesions and DNA–DNA or DNA–protein cross-links. This review predominantly concentrates on DNA damage induced by the following carcinogens: polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, mycotoxins, ultraviolet light, ionising radiation, aristolochic acid, nitrosamines and particulate matter. Additionally, we allude to some of the cancer types where there is molecular epidemiological evidence that these agents are aetiological risk factors. The complex role that carcinogens play in the pathophysiology of cancer development remains obscure, but DNA damage remains pivotal to this process.


Author(s):  
Mario Rivera-Izquierdo ◽  
Virginia Martínez-Ruiz ◽  
Elena Mercedes Castillo-Ruiz ◽  
Miriam Manzaneda-Navío ◽  
Beatriz Pérez-Gómez ◽  
...  

The International Agency of Research in Cancer (IARC) has recently confirmed shift work as a type 2A carcinogen. The results presented in published epidemiological studies regarding prostate cancer are inconsistent and the association remains controversial. The aims of this study were: (a) to investigate the possible association between shift work and prostate cancer incidence, identifying possible sources of heterogeneity; and (b) to analyze the potential effect of publication bias. A search for cohort and case-control studies published from January 1980 to November 2019 was conducted. The quality of the articles was assessed using the Newcastle–Ottawa Scale. Pooled OR were calculated using random-effects models. Heterogeneity was evaluated using Cochran’s Q test and data were stratified by potential sources of heterogeneity. Publication bias was analyzed. Eighteen studies were included. No association was found between rotating/night-shift work and prostate cancer, pooled OR 1.07 (95%CI 0.99 to 1.15), I2 = 45.7%, p = 0.016. Heterogeneity was eliminated when only cohort studies (pooled OR 1.03; 95%CI 0.96 to 1.10; I2 = 18.9%, p = 0.264) or high-quality studies (pooled OR 0.99; 95%CI 0.89 to 1.08; I2 = 0.0%, p = 0.571) were considered. A publication bias was detected. An association between shift work and prostate cancer cannot be confirmed with the available current data. Future analytical studies assessing more objective homogeneous exposure variables still seem necessary.


PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e46982 ◽  
Author(s):  
Bingbing Wei ◽  
Zhuoqun Xu ◽  
You Zhou ◽  
Jun Ruan ◽  
Huan Cheng ◽  
...  

2008 ◽  
Vol 179 (4S) ◽  
pp. 66-67
Author(s):  
Kazuya Mikami ◽  
Tsuneharu Miki ◽  
Kotaro Ozasa ◽  
Masahiro Nakao ◽  
Kyohei Hayashi ◽  
...  

Gene ◽  
2014 ◽  
Vol 534 (2) ◽  
pp. 286-297 ◽  
Author(s):  
Yang Chen ◽  
Tianyu Li ◽  
Xiaoqiang Yu ◽  
Jianfeng Xu ◽  
Jianling Li ◽  
...  

2015 ◽  
Vol 19 (2) ◽  
pp. 308-317 ◽  
Author(s):  
Manuela Chiavarini ◽  
Liliana Minelli ◽  
Roberto Fabiani

AbstractObjectiveColorectal cancer shows large incidence variations worldwide that have been attributed to different dietary factors. We conducted a meta-analysis on the relationship between garlic consumption and colorectal cancer risk.DesignWe systematically reviewed publications obtained by searching ISI Web of Knowledge, MEDLINE and EMBASE literature databases. We extracted the risk estimate of the highest and the lowest reported categories of intake from each study and conducted meta-analysis using a random-effects model.ResultsThe pooled analysis of all fourteen studies, seven cohort and seven case–control, indicated that garlic consumption was not associated with colorectal cancer risk (OR=0·93; 95 % CI 0·82, 1·06, P=0·281; I2=83·6 %, P≤0·001). Separate analyses on the basis of cancer sites and sex also revealed no statistically significant effects on cancer risk. However, when separately analysed on the basis of study type, we found that garlic was associated with an approximately 37 % reduction in colorectal cancer risk in the case–control studies (combined risk estimate=0·63, 95 % CI 0·48, 0·82, P=0·001; I2=75·6 %, P≤0·001).ConclusionsOur results suggest that consumption of garlic is not associated with a reduced colorectal cancer risk. Further investigations are necessary to clarify the discrepancy between results obtained from different types of epidemiological studies.


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