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Meta-Analysis of Dose-Response Relationships
Published in Christopher H. Schmid, Theo Stijnen, Ian R. White, Handbook of Meta-Analysis, 2020
Nicola Orsini, Donna Spiegelman
We combine the dose-response relation between alcohol intake and colorectal cancer rate arising from eight prospective cohort studies including 489,979 women and men participating in the Pooling Project of Prospective Studies of Diet and Cancer (Cho et al., 2004). A total of 3646 cases and 2,511,424 person-years are included in the analysis (Orsini et al., 2012). Each study categorized alcohol intake into six intervals using the same cutpoints. So, an alternative to dose-response meta-analysis in this specific case could be a multivariate meta-analysis of the estimated contrasts between categories. In general, however, cutpoints are likely to vary across studies. Basic information about cases, person-years, incidence rate ratios, and their confidence intervals is summarized into 6 × 8 = 48 rows of data (I = 8, Ji = 6) (Table 18.4). Rate ratios were adjusted for age, energy intake (kcal/day), multivitamin use, family history of colorectal cancer, current smoking, past smoking, red meat intake, total milk intake, and dietary folate intake. The Hamling method was used to estimate the covariances of multivariable-adjusted rate ratios.
Notes on Cancer
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
Although the role of diet in cancer is much ignored by the oncologist and perhaps the medical profession in general, I do not choose to follow that course here. The evidence is rather overwhelming that those individuals on a high fat diet are much more prone to cancer. A large number of independent laboratory studies have indicated this,103–111 as well as epidemiological studies of human populaces.112–117 Cancer of the colon, one of the four types showing major incidence in the west seems to correlate very well with dietary fat intake.113 Fats appear to act at the promotional stage of carcinogenesis,118 with unsaturated fats showing greater carcinogenic potential than that of saturated ones.119 The role of protein is not well under stood, although high protein diets, especially from red meats, seem to increase cancer incidence,104,120–122 as is also probably true with coronary heart disease.123
The Two-Step Concept of Intestinal Carcinogenesis
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
Norman D. Nigro, Arthur W. Bull
Epidemiological data strongly suggest that a high-fat diet plays an important role in the etiology of cancer of the large bowel in humans.11 This clue induced many investigators to study the effect of dietary fat on intestinal cancer in the animal model. Reddy et al. published one of the first reports of an experiment which showed that the feeding of a high-fat diet enhances cancer formation.12 Rats were fed a 20% fat diet and injected with dimethylhydrazine (DMH). These animals developed twice as many intestinal tumors as rats fed a 5% fat diet. This finding has been confirmed by others including Nigro et al.,13 who reported that rats fed a 35% beef fat diet and injected with azoxymethane (AOM) developed nearly twice as many intestinal cancers as rats fed a 5% fat diet. The cancers in the animals fed the high-fat diet were larger, more anaplastic, and metastasized to a greater degree. As far as we know, a high-fat diet alone has not produced intestinal tumors.
Ovarian Cancer: Lifestyle, Diet and Nutrition
Published in Nutrition and Cancer, 2021
Ahmed El-Sherif, Sherif El-Sherif, Anthony Henry Taylor, Thangesweran Ayakannu
Hypotheses for the effect of diet on cancer risk were derived from studies that examined the association between cancer rates in different populations and the dietary patterns of those study populations. Because diets in developed western countries are rich in animal products, sugar and fat (5) whilst diets in developing countries are characterized by the intake of starchy food, but have low intake of fat, sugar and animal products (12), then the western world diet was considered to a major contributory factor. In populations that migrate from one country to another, cancer rates often change and even can change within countries over time as dietary preferences change. For example, the rates of colorectal cancer among Japanese people who migrate to the USA have increased (13). This is not a cultural change, because westernization of Japanese diets in Japan has led to an increase in rates of colorectal cancer too (13). Consequently, these international variations in diet and cancer rates suggest that diet has a major impact for many common cancers and that many cancers may be partly preventable by having the most beneficial dietary habits.
Chili Consumption and Risk of Gastric Cancer: A Meta-Analysis
Published in Nutrition and Cancer, 2021
Yanbin Du, Yuan Lv, Wenting Zha, Xiuqin Hong, Qinghong Luo
Gastric cancer (GC) is one of the most common digestive tractmalignanttumors, and it is also one of the tumors with a higher mortality in the world. GC is the fourth most frequently occurring malignancy after lung, breast, and colorectal cancer, and the second most common cause of death from cancer worldwide (5). It has been estimated that one million patients are newly diagnosed with GC worldwide each year, with 700,000 patients dying from this disease annually (6). Diet has been found to be an important factor in the development of gastric cancer. A report published in 2007 by the World Cancer Research Fund and the American Institute for Cancer Research on the relationship between diet and cancer suggested that the consumption of certain types of food may be directly associated with the development of this disease (7). So, what is the relationship between the Chili consumption and gastric cancer risk?
Effect of Dietary Insulinemia on All-Cause and Cause-Specific Mortality: Results From a Cohort Study
Published in Journal of the American College of Nutrition, 2020
Mohsen Mazidi, Niki Katsiki, Dimitri P. Mikhailidis, Maciej Banach
We found that the significant and positive association of cancer mortality with the DHI remained (whereas with the DIRI it was lost) in the fully adjusted analysis. Only two other studies investigated the link between DHI and risk of cancer (32,33). In line with our findings, another study (985 women with colorectal cancer, 20 years’ follow-up) found a 29% higher risk of colorectal cancer in the highest quartile of DHI compared with the lowest quartile (HR: 1.29; 95% CI: 1.05–1.58) (33). Similar results were reported for a link between an empirical dietary index for hyperinsulinemia and colorectal cancer risk in both genders (HR: 1.26; 95% CI: 1.12–1.42) (32). Few studies evaluated the association between C-peptide and cancer risk (64–66). For example, Wei et al. reported that women in extreme C-peptide quartiles had a 1.76-fold increased risk (95% CI: 0.85–3.63) for colorectal cancer (64). Ma et al. also found a 150% higher risk (HR: 2.5(67)) of colorectal cancer in men in extreme C-peptide quintiles (56). However, no study has examined the link between the IR potential of diet and cancer risk.