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Dietary habits and breast cancer incidence among seventh‐day adventists
Abstract
Breast cancer incidence was monitored in a cohort of 20,341 California Seventh-day Adventist women who completed a detailed lifestyle questionnaire in 1976, and who were followed for 6 years. There were 215 histologically confirmed primary breast cancer detected among some 115,000 person-years of follow-up. Mean age at diagnosis was 66 years, indicating a primarily postmenopausal case series. Established risk factors for breast cancer showed strong relationships to risk in these data. Age at first live birth, maternal history of breast cancer, age at menopause, educational attainment, and obesity were all significantly related to risk. However, increasing consumption of high fat animal products was not associated with increased risk of breast cancer in a consistent fashion. Nor were childhood and early teenage dietary habits (vegetarian versus nonvegetarian) related to subsequent, adult risk of developing breast cancer. Also, a derived index of percent of calories from animal fat in the adult years was not significantly related to risk. These results persisted after simultaneously controlling for other, potentially confounding variables, utilizing Cox proportional hazard regression models.
This umbrella review aims to provide a systematic and comprehensive overview of current evidence from prospective studies on the diverse health effects of cheese consumption. We searched PubMed, Embase, and Cochrane Library to identify meta-analyses/pooled analyses of prospective studies examining the associations between cheese consumption and major health outcomes from inception to August 31, 2022. We reanalyzed and updated previous meta-analyses and performed de novo meta-analyses with recently published prospective studies, where appropriate. We calculated the summary effect size, 95% prediction confidence intervals, between-study heterogeneity, small-study effects, and excess significance bias for each health outcome. We identified 54 eligible articles of meta-analyses/pooled analyses. After adding newly published original articles, we performed 35 updated meta-analyses and 4 de novo meta-analyses. Together with eight previous meta-analyses, we finally included 47 unique health outcomes. Cheese consumption was inversely associated with all-cause mortality (highest vs. lowest category: RR=0.95, 95%CI: 0.92, 0.99), cardiovascular mortality (RR=0.93, 95%CI: 0.88, 0.99), incident cardiovascular disease (CVD) (RR=0.92, 95%CI: 0.89, 0.96), coronary heart disease (CHD) (RR=0.92, 95%CI: 0.86, 0.98), stroke (RR=0.93, 95%CI: 0.89, 0.98), estrogen receptor-negative (ER-) breast cancer (RR=0.89, 95%CI: 0.82, 0.97), type 2 diabetes (RR=0.93, 95%CI: 0.88, 0.98), total fracture (RR=0.90, 95%CI: 0.86, 0.95), and dementia (RR=0.81, 95%CI: 0.66, 0.99). Null associations were found for other outcomes. According to the NutriGrade scoring system, moderate quality of evidence was observed for inverse associations of cheese consumption with all-cause and cardiovascular mortality, incident CVD, CHD, and stroke, and for null associations with cancer mortality, incident hypertension, and prostate cancer. Our findings suggest that cheese consumption has neutral to moderate benefits for human health.
Characterizing the potential health effects of exposure to risk factors such as red meat consumption is essential to inform health policy and practice. Previous meta-analyses evaluating the effects of red meat intake have generated mixed findings and do not formally assess evidence strength. Here, we conducted a systematic review and implemented a meta-regression—relaxing conventional log-linearity assumptions and incorporating between-study heterogeneity—to evaluate the relationships between unprocessed red meat consumption and six potential health outcomes. We found weak evidence of association between unprocessed red meat consumption and colorectal cancer, breast cancer, type 2 diabetes and ischemic heart disease. Moreover, we found no evidence of an association between unprocessed red meat and ischemic stroke or hemorrhagic stroke. We also found that while risk for the six outcomes in our analysis combined was minimized at 0 g unprocessed red meat intake per day, the 95% uncertainty interval that incorporated between-study heterogeneity was very wide: from 0–200 g d⁻¹. While there is some evidence that eating unprocessed red meat is associated with increased risk of disease incidence and mortality, it is weak and insufficient to make stronger or more conclusive recommendations. More rigorous, well-powered research is needed to better understand and quantify the relationship between consumption of unprocessed red meat and chronic disease.
Red meat and processed meat consumption has been hypothesized to increase risk of cancer, but the evidence is inconsistent. We performed a systematic review and meta-analysis of prospective studies to summarize the evidence of associations between consumption of red meat (unprocessed), processed meat, and total red and processed meat with the incidence of various cancer types. We searched in MEDLINE and EMBASE databases through December 2020. Using a random-effect meta-analysis, we calculated the pooled relative risk (RR) and 95% confidence intervals (CI) of the highest versus the lowest category of red meat, processed meat, and total red and processed meat consumption in relation to incidence of various cancers. We identified 148 published articles. Red meat consumption was significantly associated with greater risk of breast cancer (RR = 1.09; 95% CI = 1.03–1.15), endometrial cancer (RR = 1.25; 95% CI = 1.01-1.56), colorectal cancer (RR = 1.10; 95% CI = 1.03–1.17), colon cancer (RR = 1.17; 95% CI = 1.09-1.25), rectal cancer (RR = 1.22; 95% CI = 1.01-1.46), lung cancer (RR = 1.26; 95% CI = 1.09–1.44), and hepatocellular carcinoma (RR = 1.22; 95% CI = 1.01-1.46). Processed meat consumption was significantly associated with a 6% greater breast cancer risk, an 18% greater colorectal cancer risk, a 21% greater colon cancer risk, a 22% greater rectal cancer risk, and a 12% greater lung cancer risk. Total red and processed meat consumption was significantly associated with greater risk of colorectal cancer (RR = 1.17; 95% CI = 1.08–1.26), colon cancer (RR = 1.21; 95% CI = 1.09–1.34), rectal cancer (RR = 1.26; 95% CI = 1.09–1.45), lung cancer (RR = 1.20; 95% CI = 1.09-1.33), and renal cell cancer (RR = 1.19; 95% CI = 1.04–1.37). This comprehensive systematic review and meta-analysis study showed that high red meat intake was positively associated with risk of breast cancer, endometrial cancer, colorectal cancer, colon cancer, rectal cancer, lung cancer, and hepatocellular carcinoma, and high processed meat intake was positively associated with risk of breast, colorectal, colon, rectal, and lung cancers. Higher risk of colorectal, colon, rectal, lung, and renal cell cancers were also observed with high total red and processed meat consumption.
Despite increasing evidence for the association of food-based dietary patterns with breast cancer risk, knowledge about the shape of the relationship and the quality of meta-evidence are insufficient. We aimed to summarize the associations between food groups and risks of breast cancer. We performed a systematic literature search of the PubMed and Embase databases up to March 2020. We included cohort, case-cohort, nested case-control studies, and follow-up studies of randomized controlled trials that investigated the relationship between breast cancer risk and at least 1 of the following food groups: red meat, processed meat, fish, poultry, egg, vegetables, fruit, dairy product (overall, milk, yogurt, and cheese), grains/cereals, nuts, legumes, soy, and sugar-sweetened beverages. Summary risk ratios (RRs) and 95% CIs were estimated using a random-effects model for linear and nonlinear relationships. Inverse linear associations were observed for vegetables (RR per 100 g/d, 0.97; 95% CI, 0.95–0.99), fruit (RR per 100 g/d, 0.97; 95% CI, 0.95–0.99), cheese (RR per 30 g/d, 0.95; 95% CI, 0.91–1.00), and soy (RR per 30 g/d, 0.96; 95% CI, 0.94–0.99), while positive associations were observed for red (RR per 100 g/d, 1.10; 95% CI, 1.03–1.18) and processed meat (RR per 50 g/d, 1.18; 95% CI, 1.04–1.33). None of the other food groups were significantly associated with breast cancer risk. A nonlinear association was observed only for milk, such that the intake of >450 g/d increased the risk, while no association was observed for lower intake amounts. High intakes of vegetables, fruit, cheese, and soy products and low intakes of red and processed meat were associated with lower risks of breast cancer. However, causality cannot be inferred from these statistical correlations.
In this review, the influence of dietary fat on the development of cancer is discussed. In epidemiological studies, a relationship between dietary fat and breast cancer has been found in correlational studies, but prospective studies do not support a role for dietary fat. Prospective epidemiological studies examining the role of dietary fat in the development of colon, pancreatic, and prostate cancers have produced conflicting results. The Women’s Health Initiative intervention studies did not show any statistically significant effects of dietary fat on the development of either colon or breast cancer in women. In experimental studies, dietary fat generally enhances chemically-induced skin, liver, pancreatic, and mammary carcinogenesis, whereas conflicting results have been observed in colon carcinogenesis. Dietary fat appears to act primarily during the promotional stage of carcinogenesis in all of these models except the liver, where the effect of dietary fat is primarily on initiation.
Over the past few decades, the number of women adopting vegetarian diets¹⁻³ has increased significantly.1,2 Professionals in the health care industry are seeking knowledge on vegetarian dietary practices to better counsel their expanding vegetarian clientele.² Parallel to this trend, there has been an increase in published scientific literature on the various aspects of vegetarian diets.³ In the broadest context, a vegetarian diet is one that contains no meat, poultry or fish, but in practice, there are several variations of this. The American Dietetic Association issued a position statement saying that appropriately planned vegetarian diets are healthful, nutritionally adequate and provide health benefits in the prevention and treatment of certain diseases.⁴ However, because of the different vegetarian dietary practices that exist, the nutritional adequacy and the potential risks and benefits may vary. This chapter will focus primarily on the adequacy of a vegetarian diet for women through different stages of the life-cycle, discuss the role of plant foods in the prevention of chronic diseases in women and present some practical guidelines for planning an optimal vegetarian diet.
Prior studies on red and processed meat consumption with breast cancer risk have generated inconsistent results. We performed a systematic review and meta‐analysis of prospective studies to summarize the evidence regarding the relation of red meat and processed meat consumption with breast cancer incidence. We searched in MEDLINE and EMBASE databases through January 2018 for prospective studies that reported the association between red meat and processed meat consumption with incident breast cancer. The multivariable‐adjusted relative risk (RR) was combined comparing the highest with the lowest category of red meat (unprocessed) and processed meat consumption using a random‐effect meta‐analysis. We identified 13 cohort, 3 nested case‐control, and 2 clinical trial studies. Comparing the highest to the lowest category, red meat (unprocessed) consumption was associated with a 6% higher breast cancer risk (pooled RR,1.06; 95% confidence intervals (95%CI):0.99‐1.14; I²=56.3%), and processed meat consumption was associated with a 9% higher breast cancer risk (pooled RR, 1.09; 95%CI, 1.03‐1.16; I²=44.4%). In addition, we identified two nested case‐control studies evaluating the association between red meat and breast cancer stratified by N‐acetyltransferase 2 acetylator genotype. We did not observe any association among those with either fast (per 25 gram/day pooled odds ratio (OR), 1.18; 95%CI, 0.93‐1.50) or slow N‐acetyltransferase 2 acetylators (per 25 gram/day pooled OR, 0.99; 95%CI, 0.91‐1.08). In the prospective observational studies, high processed meat consumption was associated with increased breast cancer risk.
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Background: Carcinogenic exposure in early life may be critical for subsequent breast cancer risk. Dairy consumption was examined during adolescence and early adulthood in relation to incident breast cancer in the Nurses' Health Study II cohort.
Methods: For the analyses of early adulthood dairy consumption, we included 90,503 premenopausal women ages 27 to 44 years in 1991 who reported dairy consumption using a validated food-frequency questionnaire. From 1991 to 2013, 3,191 invasive breast cancer cases were identified. In 1998, 44,264 women recalled adolescent dairy consumption. This subgroup of women was followed up from 1998 to 2013; 1,318 invasive breast cancer cases were identified. Multivariate hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using the Cox proportional hazard regression.
Results: Adolescent and early adulthood total dairy consumption was not associated with overall breast cancer risk (each serving/day during adolescence, total dairy HR = 1.02, 95% CI, 0.97–1.07; for early adulthood total dairy HR = 1.01, 95% CI, 0.97–1.04), as were intakes of calcium, vitamin D, and lactose. Adolescent consumption of total and high-fat dairy was associated with higher risk of estrogen and progesterone receptor negative (each serving/day: total dairy HR = 1.11, 95% CI, 1.00–1.24; high-fat dairy HR = 1.17, 95% CI, 1.04–1.31). However, higher adolescent high-fat dairy consumption was associated with lower risk of estrogen and progesterone receptor positive tumors (each serving/day HR = 0.91, 95% CI, 0.86–0.97).
Conclusions: Our results suggest no overall association between dairy consumption during adolescence or early adulthood and breast cancer risk, but the findings may differ by hormone receptor status of tumors.
Impact: Dairy consumption in adolescence or early adulthood may not be a significant predictor of breast cancer incidence.
Replacement of saturated fat by the major dietary polyunsaturated fat linoleic acid reduces blood cholesterol concentrations and the risk of coronary artery disease. However, there is concern that long-term consumption of large amounts of linoleic acid might increase cancer risk. We reviewed the epidemiologic and experimental literature on linoleic acid intake and cancer risk and performed additional meta-analyses of risk estimates from case-control and prospective cohort studies. None of the combined estimates from within-population studies indicated a significantly increased risk of cancer with high compared with low intakes of linoleic acid or polyunsaturated fat. For case-control studies, the combined relative risks were 0.84 (95% CI: 0.71, 1.00) for breast, 0.92 (95% CI: 0.85, 1.08) for colorectal, and 1.27 (95% CI: 0.97, 1.66) for prostate cancer. For prospective cohort studies, combined relative risks were 1.05 (95% CI: 0.83, 1.34) for breast, 0.92 (95% CI: 0.70, 1.22) for colon, and 0.83 (95% CI: 0.56, 1.24) for prostate cancer. Ecologic comparisons of populations showed positive associations between cancer rates and per capita use of animal or saturated fat, but less so with per capita use of vegetable oil or polyunsaturated fat. Controlled studies of coronary artery disease in men did not, except for 1 study, show an increased cancer incidence after consumption of diets with a very high linoleic acid content for several years. Animal experiments indicated that a minimum amount of linoleic acid is required to promote growth of artificially induced tumors in rodents; but above this threshold, linoleic acid did not appear to have a specific tumor-promoting effect. Although current evidence cannot exclude a small increase in risk, it seems unlikely that a high intake of linoleic acid substantially raises the risks of breast, colorectal, or prostate cancer in humans.
Changes in hormone levels in postmenopausal women increase the risk of noncommunicable diseases such as cardiovascular disease, poor bone health, and cancer. Postmenopausal vegetarian women may obtain various health benefits from plant food–based diets, but studies have also observed poor nutritional conditions in postmenopausal vegetarian women, such as poor nutrient absorption and nutritional status. These changes may be due to the characteristics of the overall dietary patterns, making it difficult to draw consistent conclusions. In this chapter, we examine the effect of a vegetarian diet on bone health, breast cancer, diabetes, and cardiovascular disease in postmenopausal women. Conflicting or nonmeaningful results have been reported regarding the association between a vegetarian diet and these diseases with respect to several nutrient intakes, type of vegetarian diet, hormone levels, etc. Despite differences among types of vegetarian diets, previous studies and the health benefits observed in vegetarians suggest that a vegetarian diet might reduce postmenopausal health risks.
Protein is important to the human body,and different sources of protein may have different effects on the risk of breast cancer. Thus,we conducted a meta-analysis to investigate the association between different dietary protein sources and breast cancer risk. PubMed and several databases were searched until December 2015. Relevant articles were retrieved according to specific searching criteria. Forty-six prospective studies were included. The summary relative risk (RR) for highest versus lowest intake was 1.07 (95% confidence interval (CI) 1.01-1.14,I² = 34.6%) for processed meat,0.92 (95% CI 0.84-1.00,I² = 0%) for soy food,0.93 (95% CI 0.85-1.00,I² = 40.1%) for skim milk,and 0.90 (95% CI 0.82-1.00,I² = 0%) for yogurt. Similar conclusions were obtained in dose-response association for each serving increase: total red meat (RR: 1.07; 95% CI 1.01-1.14,I² = 7.1%),fresh red meat (RR: 1.13; 95% CI 1.01-1.26,I² = 56.4%),processed meat (RR: 1.09; 95% CI 1.02-1.17,I² = 11.8%),soy food (RR: 0.91; 95% CI 0.84-1.00,I² = 0%),and skim milk (RR: 0.96; 95% CI 0.92-1.00,I² = 11.9%). There was a null association between poultry,fish,egg,nuts,total milk,and whole milk intake and breast cancer risk. Higher total red meat,fresh red meat,and processed meat intake may be risk factors for breast cancer,whereas higher soy food and skim milk intake may reduce the risk of breast cancer.
Childhood obesity is associated with a greater chance of a lifetime of obesity. Evidence suggests dairy at recommended levels could be beneficial in maintaining normal weight and body composition. We assessed whether dairy consumption is associated with anthropometric indicators of health (z-scores for weight-for-age (WAZ); height-for-age (HAZ) and body mass index (BMIZ); waist-to-height ratio (WHtR); fat-free mass (FFM); and fat mass (FM)) in adolescents. In a cross-sectional study, 536 males and females ages 12-18 completed a 151-item semi-quantitative web-based food frequency questionnaire that included 34 dairy-containing foods. Dairy foods were categorized into milk, cheese, sweetened dairy, and total dairy. Anthropometrics were measured during school visits. Total dairy intake was associated with WAZ (β = 0.25 (95% CI: 0.01, 0.49), p = 0.045) and HAZ (β = 0.28 (95% CI: 0.04, 0.52), p = 0.021). In boys, total dairy was associated with WHtR (β = 0.02 (95% CI: 0.00, 0.04), p = 0.039), FFM (β = 4.83 (95% CI: 1.79, 7.87), p = 0.002), and FM (β = 3.89 (95% CI: 0.58, 7.21), p = 0.021), and cheese was associated with FFM (β = 4.22 (95% CI: 0.98, 7.47), p = 0.011). Dairy consumption seems to influence growth in both genders, and body composition and central obesity in boys. Prospective studies are needed to identify how types of dairy relate to growth, body composition, and central obesity of adolescents.
For a very long time, food has been recognized as being important in the development of disease, at least back to the time of Hippocrates 2500 years ago when he said, “Whoever gives these things (food) no consideration, and is ignorant of them, how can he understand the diseases of man?” Much later, in 1849, John Hughes Bennett, Senior Professor of Clinical Medicine, whose textbook on medicine appears to have been the standard of its day in Britain, pursued the idea that dietary fat was important in the causation of cancer when he first stated that, “The circumstances which diminish obesity, and a tendency to the formation of fat, would seem a priori to be opposed to the cancerous tendency” (p. 250) (1), then later, in 1865, urged that, “In carcinoma... a diminution of this element (fat) in the food should be aimed at” (2). In more modern times, the studies of Tannenbaum and his colleagues (2–4) during the 1940s and 1950s on the role of nutrition in the development of tumors in experimental animals and the research of Ancel Keys and colleagues on diet and cardiovascular disease (5,6) often have been assigned landmark status.
Le cancer du sein reste un problème de santé publique majeur de par sa fréquence, en effet on estime que 52 588 femmes ont été atteintes en France en 2010 (http://www.ins.sante.fr) et que plus de 11 000 en sont décédées. Le taux reste faible avant l’âge de 30 ans puis croît jusqu’à 60–69 ans où il dépasse les 320 pour 100 000 femmes par an. Les taux diminuent légèrement après 85 ans (245 pour 100 000).
In order to motivate women to take a positive approach towards the prevention of breast cancer, it is necessary to provide them with information. Moreover, an informed population is more likely to respond and take action if such action is perceived to be both effective and of personal benefit. Of the many reasons by which a woman might be persuaded to take preventive action, the best are likely to be related to something close and personal to her, and a variety of methods should be used to bring about such motivation [1].
Prostate cancer is an important public health problem with over a quarter of a million new cases diagnosed worldwide in 1985 (Parkin et al. 1993). The incidence of the disease is increasing rapidly in most regions of the world (Boyle 1994; Alexander and Boyle, this volume) although the mortality rate has remained constant in generations of men born since the early years of this century (Boyle et al. 1994). The evidence that prostate cancer risk has important environmental determinants is compelling. Briefly, different populations around the world experience different levels of prostate cancer, and these levels change with time usually in an orderly and predictable manner: international variation in incidence is around two orders of magnitude (Boyle et al. 1994). However, when migration takes place, groups of migrants tend to acquire the prostate cancer pattern of their new home (Haenszel 1961). Furthermore, groups within a community whose life-style habits differentiate them from other members of the same community generally have notably different prostate cancer rates, for example, Seventh Day Adventists and Mormons (Zaridze and Boyle 1987).
Breast cancer is the most significant cancer occurring among women in the United States in terms of incidence. In 1995 it has been estimated that there were 182,000 new cases of the disease among women and 46,000 deaths attributable to breast cancer (1). High rates of breast cancer are also seen in Western European and similar populations, including Canada and Australia. Rates of this disease are generally lower in Asian countries, such as Japan and China, but in these latter populations rates have substantially increased over the past several decades (2).
Readily grasped concepts such as lifetime risk of, and expected age at onset of, a disease, cannot be easily estimated by the relative risk methods commonly used in epidemiology. Here we develop a method for estimating these quantities with confidence intervals, where the likelihood is a multivariate function of exposure variables. The model is basically non-parametric, except for a proportional hazards assumption on exposures, and except for the youngest data-poor ages, where an exponential model in age is assumed. Tests of goodness-of-fit of the model are described, these allowing for product terms between exposures and age. Application of the method is made to the Adventist Health Study cohort, where the independent effects of several exposures on these outcomes are demonstrated. Copyright (C) 1999 John Wiley & Sons, Ltd.
Among cancers in American women, breast cancer (BC) has the second highest incidence and mortality. The association of BC with diet has been inconsistent. Studies that evaluate associations with dietary patterns are less common and reflect an individual’s whole diet. We associated dietary patterns with the risk of BC in American women of the Adventist Health Study-2 (AHS-2), a prospective cohort of 96 001 subjects recruited between 2002 and 2007. Answers to a previously validated FFQ were used to classify subjects to vegan, lacto-ovo-vegetarian, pesco-vegetarian, semi-vegetarian and non-vegetarian dietary patterns. Incident BC were identified by matching AHS-2 subjects to data from forty-eight state cancer registries. Statistical analyses used proportional hazard regression analyses with covariates that were chosen
a priori
. From 50 404 female participants (26 193 vegetarians), we identified 892 incident BC cases, with 478 cases among vegetarians. As compared with non-vegetarians, all vegetarians combined did not have a significantly lower risk (hazard ratio (HR) 0·97; CI 0·84, 1·11;
P=
0·64). However, vegans showed consistently lower (but non-significant) point estimates when compared with non-vegetarians (all cases: HR 0·78; CI 0·58, 1·05;
P=
0·09). In summary, participants in this cohort who follow a vegetarian dietary pattern did not experience a lower risk of BC as compared with non-vegetarians, although lower risk in vegans is possible. These findings add to the very limited literature associating vegetarian diets with BC risk and can assist nutritionists when evaluating the impact of these diets. The findings will also motivate further evaluation of vegan diets and their special characteristics.
Background: Conjugated linoleic acid (CLA), which is present in milk products and meat from ruminants, appears to have anticarcinogenic activity against breast cancer in animal and in vitro experiments. To date, few epidemiologic data are available in humans. Objective: This study evaluated the relation between intakes of CLA and other fatty acids and breast cancer incidence in the Netherlands Cohort Study. Design: Intake data derived from a validated 150-item food-frequency questionnaire were linked to an existing database with analytic data on specific fatty acids in European foods (the TRANSFAIR study). With 6.3 y of follow-up and 941 incident cases of breast cancer, multivariate rate ratios and 95% CIs were calculated for energy-adjusted intakes of fatty acids and CLA-containing food groups (eg, butter, cheese, milk, other milk products, and meat). Results: CLA intake showed a weak, positive relation with breast cancer incidence (rate ratio for highest compared with lowest quintile: 1.24, 95% CI: 0.91, 1.69; P for trend = 0.02). Statistically significant positive associations were found with total trans fatty acids and (borderline) with saturated fatty acids. Significant inverse associations were found with monounsaturated and cis unsaturated fatty acids, whereas total fat and energy intake of CLA-containing food groups were not related to breast cancer incidence. Conclusion: The suggested anticarcinogenic property of CLA in animal and tissue culture models could not be confirmed in this epidemiologic study in humans.
Introduction Case study 1: Association between red meat consumption and breast cancer Case study 2: Trends in fish growth rate and size Acknowledgements References
The associations between saturated fatty acid (SFA) consumption and risk of breast cancer (BC) remains inconclusive. Therefore, we conducted this meta-analysis to determine the quantitative relations between dietary SFA intake and incidence of BC.
Literatures published up to April 2015 were systematically screened through Pubmed and Web of Science. Relevant publication quality was evaluated by conducting the Newcastle-Ottawa scale. We used fixed effects models or random effect models to calculate the summary relative risks (RRs) and odds ratios (ORs), and conducted sensitivity analyses and evaluated the publication bias.
We identified a total of 52 studies (24 cohort studies and 28 case–control studies), with over 50,000 females diagnosed with BC. The associations between dietary SFA intake and risk of BC were 1.18 for case–control studies (high vs low intake, 95% confidence interval [CI] = 1.03–1.34) and 1.04 for cohort studies (95% CI = 0.97–1.11). When restricted analyses to population-based studies, positive associations were observed for both cohort (RR [95% CI] = 1.11 [1.01–1.21]) and case–control studies (OR [95% CI] = 1.26 [1.03–1.53]). Additionally, for case–control studies, significant positive associations between higher SFA intake and BC risk were observed for Asian (OR [95% CI] = 1.17 [1.02–1.34]) and Caucasian (OR [95% CI] = 1.19 [1.00–1.41]), as well as for postmenopausal women (OR = 1.33, 95% CI: 1.02–1.73). In contrast, higher dietary SFA intake was not associated with risk of BC among premenopausal women, in cohort studies or hospital-based studies.
A positive association between higher dietary SFA intake and postmenopausal BC risk was observed in case–control but not in cohort studies. More studies are warranted to confirm these findings.
Epidemiological findings indicate that the consumption of tomatoes and tomato products is linked to a reduced risk for prostate cancer. Since prostate cancer is still a severe health problem throughout the Western world, and the success in treating advanced prostate cancer remains poor, the importance of dietary prevention is growing. Lycopene, the red pigment of tomatoes and known as a potent antioxidant, is considered to be the major active component in tomatoes. In several preclinical studies, lycopene has been demonstrated not only to improve oxidative stress defense and activates phase II drug metabolism, but also to improve intercellular communication by enhancing gap junctional communication. Moreover, lycopene modulates intracellular signaling pathways, e.g. IGF-I and androgen signaling, leading to reduced proliferation of normal and cancerous prostate epithelial cells. The finding that lycopene reduces local androgen signaling in both rat prostate tumors and healthy prostate tissue suggests a role for lycopene in primary prevention of prostate cancer as well as benign prostate hyperplasia. Down-regulation of inflammatory markers in rat prostate indicate an anti-inflammatory action of lycopene, which may also contribute to a cancer-preventive effect of lycopene. Long-term intervention trials in humans are required to finally prove clinical efficacy of the lycopene molecule in prostate health.
Breast cancer develops in both men and women. This chapter discusses the classic features of breast cancer in both sexes highlighting the differences and more often the similarities between them. In the chapter, there is description of various hormonal, lifestyle, and genetic factors reported to play a role in the development of breast carcinoma. However, most individuals of either gender who develop breast cancer have no apparent risk factor for the disease, and most male patients have no detectable hormonal imbalances. Breast cancer in males generally occurs a decade later than breast cancer in females with a mean age of presentation ranging from 60 to 65 years. Because of the proximity of breast ducts to the skin, other manifestations, such as, nipple retraction, fixation, ulceration, edema, and discharge can also occur frequently in men. The most common histology of male breast cancer is infiltrating ductal carcinoma. Male breast cancer is classically described as having a poorer prognosis than female breast cancer suggesting that, in males, it is a more aggressive disease. However, evidence is accumulating, which suggests that the disease is biologically similar in the two genders. Despite this, a poorer survival in men is a consistent finding.
The amount and type of fat consumed in the diet may be important in the development of human cancer. Several organizations have advocated decreasing the fat content of the diet as a means of Preventing the development of cancer. For example, the American Institute for Cancer Research states to “limit consumption of fatty foods, particularly those of animal origin” (World Cancer Research Fund/American Institute for Cancer Research, 1997). On the other hand, the American Cancer Society no longer speci, cally recommends lowering fat intake, and instead advises individuals to eat a variety of healthy foods, with an emphasis on plant sources (American Cancer Society, 2006).
Evidence suggests that egg intake may be implicated in the aetiology of sex hormone-related cancers. However, dose-response relationships between egg intake and such cancers are unclear. Thus, we conducted a dose-response meta-analysis to summarise the dose-response relationships between egg consumption and the risk of breast, prostate and gynaecological cancers. A literature search was performed using PubMed and Embase up to April 2015 to identify relevant prospective observational studies. Summary relative risk (RR) and 95 % CI were estimated using a random-effects model. For breast cancer, the linear dose-response meta-analysis found a non-significantly increased risk (RR for an increase of 5 eggs consumed/week: 1·05, 95 % CI 0·99, 1·11, n 16 023 cases). Evidence for non-linearity was not statistically significant (P non-linearity= 0·50, n 15 415 cases) but consuming ≥ 5 eggs/week was significantly associated with an increased risk of breast cancer compared with no egg consumption, with the summary RR being 1·04 (95 % CI 1·01, 1·07) for consuming 5 eggs/week and 1·09 (95 % CI 1·03, 1·15) for consuming about 9 eggs/week. For other cancers investigated, the summary RR for an increase of 5 eggs consumed/week was 1·09 (95 % CI 0·96, 1·24, n 2636 cases) for ovarian cancer; 1·47 (95 % CI 1·01, 2·14, n 609 cases) for fatal prostate cancer, with evidence of small-study effects (P Egger= 0·04). No evidence was found for an association with the risk of total prostate cancer. While our conclusion was tempered by the potential for publication bias and confounding, high egg intake may be associated with a modestly elevated risk of breast cancer, and a positive association between egg intake and ovarian and fatal prostate cancers cannot be ruled out.
Breast cancer is a disease that develops in both men and women. While there are similarities in this disease between the two genders, there are also differences. It is the most commonly diagnosed malignancy in women, second only to skin cancer, with associated immense socioeconomic ramifications. However, in men, breast cancer is rare. Is this disease biologically different in men and women? Or is it similar between the sexes with the same etiologic, prognostic, and clinical features? The data to date suggest that breast cancer in men is fundamentally identical to breast cancer in women with few exceptions. This chapter explores the classic features of breast cancer in both sexes, highlighting the differences and the similarities between them and what is as yet unknown. Despite the clear disparity in the incidence of breast cancer between the sexes, once it occurs in either a man or a woman its clinical presentation, pathologic appearance, response to treatment, and overall prognosis are not that different. Given that breast cancer in women is a prevalent disease and the second leading cause of cancer-related death, there is a great socioeconomic burden. This has led to extensive research into this disease. The risk factors, prognostic factors, and treatment algorithm have all been thoroughly explored, and clinicians have resources to draw on when treating their female patients. This is the major difference between the sexes. Breast cancer is a rarity in males; therefore, it is much less studied. Although there have been some emerging data in male breast cancer, most knowledge and treatment approaches for this disease in males come from the extrapolation of information about female patients with breast cancer.
The relationship between egg consumption and breast cancer risk has been inconsistent, so it is necessary to conduct a meta-analysis to evaluate the relationship. PubMed, EMBASE and ISI Web of Knowledge were searched to find cohort studies or case control studies that evaluated the relationship between egg consumption and breast cancer risk. A comprehensive meta-analysis software was used to conduct the meta-analysis. 13 studies were included. The meta-analysis results showed that egg consumption was associated with increased breast cancer risk (RR 1.04, 95 % CI 1.01-1.08). Subgroup analyses showed egg consumption was also associated with increased breast cancer risk based on cohort studies (RR 1.04, 95 % CI 1.00-1.08), among European population (RR 1.05, 95 % CI 1.01-1.09), Asian population (RR 1.09, 95 % CI 1.00-1.18), postmenopausal population (RR 1.06, 95 % CI 1.02-1.10), and those who consumed ≥2, ≤5/week (RR 1.10, 95 % CI 1.02-1.17), but not in case-control studies (RR 1.06, 95 % CI 0.97-1.15), among American population (RR 1.04, 95 % CI 0.94-1.16), premenopausal population (RR 1.04, 95 % CI 0.98-1.11) and those who consumed ≥1, <2/week (RR 1.04, 95 % CI 0.97-1.11) or >5 eggs/week (RR 0.97, 95 % CI 0.88-1.06). Egg consumption was associated with increased breast cancer risk among the European, Asian and postmenopausal population and those who consumed ≥2, ≤5/week.
The present article reviews the literature about trans fatty acids and the controversy about their effects on carcinogenesis. Experimental studies on animals are related to mammary tumors, colon tumors and liver tumors: it seems that there is no relation beetween trans fatty acids and mammary tumors, as well as liver tumors ; however, results about trans fatty acids and colon tumors are much debated. Studies on humans are related to breast cancer, prostate cancer and colon tumor: results about trans fatty acids, breast cancer and colon tumor are much debated ; yet, it seems there would be no relation beetween trans fatty acids and prostate cancer. A critical analysis about available data is proposed.
To investigate the association between intake of fish and n-3 polyunsaturated fatty acids (n-3 PUFA) and the risk of breast cancer and to evaluate the potential dose-response relation.
Meta-analysis and systematic review of prospective cohort studies.
PubMed and Embase up to December 2012 and references of retrieved relevant articles.
Prospective cohort studies with relative risk and 95% confidence intervals for breast cancer according to fish intake, n-3 PUFA intake, or tissue biomarkers.
Twenty six publications, including 20 905 cases of breast cancer and 883 585 participants from 21 independent prospective cohort studies were eligible. Eleven articles (13 323 breast cancer events and 687 770 participants) investigated fish intake, 17 articles investigated marine n-3 PUFA (16 178 breast cancer events and 527 392 participants), and 12 articles investigated alpha linolenic acid (14 284 breast cancer events and 405 592 participants). Marine n-3 PUFA was associated with 14% reduction of risk of breast cancer (relative risk for highest v lowest category 0.86 (95% confidence interval 0.78 to 0.94), I(2)=54), and the relative risk remained similar whether marine n-3 PUFA was measured as dietary intake (0.85, 0.76 to 0.96, I(2)=67%) or as tissue biomarkers (0.86, 0.71 to 1.03, I(2)=8%). Subgroup analyses also indicated that the inverse association between marine n-3 PUFA and risk was more evident in studies that did not adjust for body mass index (BMI) (0.74, 0.64 to 0.86, I(2)=0) than in studies that did adjust for BMI (0.90, 0.80 to 1.01, I(2)=63.2%). Dose-response analysis indicated that risk of breast cancer was reduced by 5% per 0.1g/day (0.95, 0.90 to 1.00, I(2)=52%) or 0.1% energy/day (0.95, 0.90 to 1.00, I(2)=79%) increment of dietary marine n-3 PUFA intake. No significant association was observed for fish intake or exposure to alpha linolenic acid.
Higher consumption of dietary marine n-3 PUFA is associated with a lower risk of breast cancer. The associations of fish and alpha linolenic acid intake with risk warrant further investigation of prospective cohort studies. These findings could have public health implications with regard to prevention of breast cancer through dietary and lifestyle interventions.
To compare the mortality rates of vegetarians and non-vegetarians.
Collaborative analysis using original data from five prospective studies. Death rate ratios for vegetarians compared to non-vegetarians were calculated for ischaemic heart disease, cerebrovascular disease, cancers of the stomach, large bowel, lung, breast and prostate, and for all causes of death. All results were adjusted for age, sex and smoking. A random effects model was used to calculate pooled estimates of effect for all studies combined.
USA, UK and Germany.
76,172 men and women aged 16-89 years at recruitment. Vegetarians were those who did not eat any meat or fish (n = 27,808). Non-vegetarians were from a similar background to the vegetarians within each study.
After a mean of 10.6 years of follow-up there were 8330 deaths before the age of 90 years, including 2264 deaths from ischaemic heart disease. In comparison with non-vegetarians, vegetarians had a 24% reduction in mortality from ischaemic heart disease (death rate ratio 0.76, 95% CI 0.62-0.94). The reduction in mortality among vegetarians varied significantly with age at death: rate ratios for vegetarians compared to non-vegetarians were 0.55 (95% CI 0.35-0.85), 0.69 (95% CI 0.53-0.90) and 0.92 (95% CI 0.73-1.16) for deaths from ischaemic heart disease at ages <65, 65-79 and 80-89 years, respectively. When the non-vegetarians were divided into regular meat eaters (who ate meat at least once a week) and semi-vegetarians (who ate fish only or ate meat less than once a week), the ischaemic heart disease death rate ratios compared to regular meat eaters were 0.78 (95% CI 0.68-0.89) in semi-vegetarians and 0.66 (95% CI 0.53-0.83) in vegetarians (test for trend P< 0.001). There were no significant differences between vegetarians and non-vegetarians in mortality from the other causes of death examined.
Vegetarians have a lower risk of dying from ischaemic heart disease than non-vegetarians.
The relationship between fish consumption and risk of major cancers such as cancer of the breast, colon, rectum and prostate has been insufficiently clarified. The present literature review of epidemiological studies shows somewhat inconsistent results, but overall there seems to be either no association or an inverse association between fish consumption and risk of breast, colorectal and prostate cancer. However, very few of the published studies have been designed to investigate properly hypotheses regarding fish consumption and cancer risk. Rather, the studies have focused on cancer risk related to meat or fat consumption. Common methodological weaknesses in the studies are combined consumption of lean and fatty fish, or even mixed fish consumption with consumption of chicken, ignoring seasonal variation and different ways of storing, preparing and serving fish, and narrow ranges of exposure. The methodological weaknesses should be borne in mind when evaluating current knowledge on the impact of fish consumption on cancer risk, and when designing new studies.
Willett WC (Harvard Medical School and Brigham and Women’s Hospital, Boston, MA, USA). Diet and Breast Cancer. J Intern Med 2001; 249: 395–411.
Analyses of dairy consumption and breast cancer incidence have yielded conflicting results. In this prospective cohort study of 48,844 premenopausal Norwegian women, we examined the relationship between childhood and adult milk consumption and breast cancer incidence. During a mean follow-up time of 6.2 years, 317 incident cases of breast cancer were diagnosed. Information on childhood and adult milk consumption was obtained from frequency questions mailed to the participants in 1991–92. Milk consumption as a child was negatively associated with subsequent breast cancer among the youngest women (34–39 years) (p for trend = 0.001), but not among older ones (40–49 years). Adult milk consumption tended to be negatively related to breast cancer incidence (p for trend = 0.12) after adjustment for age, reproductive and hormonal factors, body mass index, education, physical activity, and alcohol consumption. Women drinking more than 3 glasses of milk per day had an incidence rate ratio of breast cancer of 0.56 (95% confidence interval 0.31–1.01) compared with women not drinking milk. Analyses according to type of milk consumed and milk fat consumption did not reveal any clear associations. A combination of childhood and adult milk consumption produced a clear negative trend in breast cancer incidence rate ratios with increasing milk consumption (p = 0.03). © 2001 Wiley-Liss, Inc.
Recently, there has been interest in whether intakes of specific types of fat are associated with breast cancer risk independently of other types of fat, but results have been inconsistent. We identified 8 prospective studies that met predefined criteria and analyzed their primary data using a standardized approach. Holding total energy intake constant, we calculated relative risks for increments of 5% of energy for each type of fat compared with an equivalent amount of energy from carbohydrates or from other types of fat. We combined study-specific relative risks using a random effects model. In the pooled database, 7,329 incident invasive breast cancer cases occurred among 351,821 women. The pooled relative risks (95% confidence intervals [CI]) for an increment of 5% of energy were 1.09 (1.00–1.19) for saturated, 0.93 (0.84–1.03) for monounsaturated and 1.05 (0.96–1.16) for polyunsaturated fat compared with equivalent energy intake from carbohydrates. For a 5% of energy increment, the relative risks were 1.18 (95% CI 0.99–1.42) for substituting saturated for monounsaturated fat, 0.98 (95% CI 0.85–1.12) for substituting saturated for polyunsaturated fat and 0.87 (95% CI 0.73–1.02) for substituting monounsaturated for polyunsaturated fat. No associations were observed for animal or vegetable fat intakes. These associations were not modified by menopausal status. These data are suggestive of only a weak positive association with substitution of saturated fat for carbohydrate consumption; none of the other types of fat examined was significantly associated with breast cancer risk relative to an equivalent reduction in carbohydrate consumption. © 2001 Wiley-Liss, Inc.
Key Points
Staying lean and physically active throughout adult life has major health benefits.
Diets low in the percentage of energy from fat have not been associated with lower risks of heart disease, cancer, or better long-term weight control.
Replacing trans and saturated fats with unsaturated fats substantially reduces risks of heart disease.
Consuming grains in their original high-fiber/whole grain form is likely to reduce risks of type 2 diabetes and heart disease.
High intake of fruits and vegetables reduces risks of cardiovascular disease, but the benefits for cancer reduction appear modest.
The incidence of breast cancer varies dramatically across different populations (Parkin et al. 1999), and migrants from low-incidence
geographic areas take on the incidence rates of the new area to which they migrate (Ziegler et al. 1993). Lifestyle appears
to be a strong determinant of breast cancer risk and diet composition and nutritional status are important candidates. Understanding
the role of diet in breast cancer is important because dietary factors are potentially modifiable risk factors on which preventive
efforts may focus. New insights Into breast cancer etiology have revealed additional complexities of the potential relevance
of diet.
To assess more precisely the relative risks associated with established risk factors for breast cancer, and whether the association between dietary fat and breast cancer risk varies according to levels of these risk factors, we pooled primary data from six prospective studies in North America and Western Europe in which individual estimates of dietary fat intake had been obtained by validated food-frequency questionnaires. Based on information from 322,647 women among whom 4,827 cases occurred during follow-up: the multivariate-adjusted risk of late menarche (age15 years or more compared with under 12) was 0.72 (95 percent confidence interval [CI]=0.62-0.82); of being postmenopausal was 0.82 (CI=0.69-0.97); of high parity (three or more births compared with none) was 0.72 (CI=0.61-0.86); of late age at first birth (over 30 years of age compared with 20 or under) was 1.46 (CI=1.22-1.75); of benign breast disease was 1.53 (CI=1.41-1.65); of maternal history of breast cancer was 1.38 (CI=1.14-1.67); and history of a sister with breast cancer was 1.47 (CI=1.27-1.70). Greater duration of schooling (more than high-school graduation compared with less than high-school graduation) was associated significantly with higher risk in age-adjusted analyses, but was attenuated after controlling for other risk factors. Total fat intake (adjusted for energy consumption) was not associated significantly with breast cancer risk in any strata of these non-dietary risk factors. We observed a marginally significant interaction between total fat intake and risk of breast cancer according to history of benign breast disease, with fat intake being associated nonsignificantly positively with risk among women with a previous history of benign breast disease; no other significant interactions were observed. Risks for reproductive factors were similar to those observed in case-control studies; relative risks for family history of breast cancer were lower. We found no clear evidence in any subgroups of a major relation between total energy-adjusted fat intake and breast cancer.
The aim of this case-control study was to compare two different statistical methods in the identification of dietary patterns by use of principal component analysis (PCA) and variable clustering (VC) and to examine their association with the risk of breast cancer (BC).
A dose-response association was then performed by the use of an adaptation of free knot spline function in logistic models.
A "Western" pattern was revealed by PCA and VC and was then shown to be associated with a nonsignificant increase of BC risk. Only PCA identified a "meat/alcohol" pattern. Above the spline threshold, BC risk increased significantly (OR ≥ s vs. < s = 2.56, 95% CI 1.54-4.27). When we used PCA, a "Mediterranean" pattern was identified, but no association between BC risk and this pattern was shown. VC split the "Mediterranean" dietary pattern in two: "raw vegetables and olive oil" and "fish." Above the spline threshold, the "fish" pattern tended to protect against BC risk (OR ≥ s vs. < s = 0.77, 95% CI 0.58-1.01), whereas an excess of raw vegetables and olive oil increased BC risk (OR 1 se = 1.22, 95% CI = 1.06-1.32).
Some results from the PCA and the VC methods were similar, whereas others were different but gave complementary results.
In previous reports concerning cancer among Seventh-Day Adventists (SDA), comparisons were made only with the general population. This report compared California SDA to a sample of non-SDA who were demographically similar to SDA. The study consisted of 17 years of follow-up (1960–76) on 22,940 white California SDA and 13 years of follow-up (1960–72) on 112,725 white California non-SDA. Both groups completed the same base-line questionnaire in 1960. Deaths were ascertained by annual contacts with each study member and by computer-assisted record linkage with the California State death certificate file. Results indicated that, with the exception of colon-rectal cancer and smoking-related cancers, the difference in risk of fatal cancer between SDA and non-SDA was substantially reduced when SDA were compared with a more socioeconomically similar population. The persistence of the low risk for colon-rectal cancer can probably be attributed to some aspect of the diet or life-style of the SDA.
Experimental studies have shown that, when combinations of the oestrogen fractions are administered, the net effect is influenced by the relative amounts of the several fractions as well as by the total dose. Specifically, it appears that the non-carcinogenic, impeded fraction (œstriol) partly inhibits the action of the carcinogenic, unimpeded fractions (oestrone, œstradiol). However, attempts to demonstrate differences in the ratio of impeded to unimpeded oestrogens between breast cancer cases and controls have been inconclusive. Epidemiological evidence suggests that early reproductive life is a time when events of significance to future breast-cancer risk occur. In particular, pregnancy at a young age is associated with both favourable oestrogen fraction ratios and decreased breast-cancer risk. We therefore suggest that the relative levels of the individual oestrogen fractions produced in the first decade or so after puberty are important determinants of a woman's life-time breast-cancer risk. This hypothesis allows reconciliation of several sets of observations which have previously seemed inconsistent, including the varied results of case-control studies. While a direct test of this hypothesis is not likely to be forthcoming in the next decade, several investigations could be undertaken immediately to provide persuasive evidence for or against it.
The relationship between dietary factors and the age of menarche (AOM) was investigated using prospective data. Dietary intake was assessed by multiple 24-hour recalls during 1 or more years immediately prior to menarche for each of 230 white, non-hispanic girls from southern California. The study population was well nourished with an average intake of calories and 13 nutrients well within the recommended dietary allowances of the National Research Council. The data show a significant association between meat and age of menarche (p<0.025) resulting in a 6 month earlier AOM among meat users compared to vegetarians. Conversely, those using meat analogues had menarche 9 months later than those who did not use meat analogues (p<0.001). The use of grains, nuts, beans and other legumes is associated (p<0.025) with 5–6 months later AOM compared to a more restricted use of these foods. The upper quartile of intake of carbohydrate, thiamine, and iron is associated with a 7–8 month later AOM than those in the lowest quartile of intake of these nutrients. Total intake of protein or fat was not associated with AOM. These results are consistent with the hypothesis that diet affects the AOM. The present prospective data from well nourished girls support previous retrospective studies which associate meat use with earlier AOM. These data point to a vegetarian dietary lifestyle as an important factor in retarding the onset of menarche among well nourished girls.
As part of a case-control study in northern Alberta, Canada, 577 women aged 30–80 with breast cancer diagnosed during 1976–77 and a population-based agestratified random sample of 826 disease-free female controls were questioned about certain aspects of their diet. Computing relative risks (RRs) by tertiles, significant increasing trends were found with more frequent consumption of beef (RRs of 1.0, 2.3, 1.5; test for trend, p <0.001), pork (RRs of 1.0, 1.6, 2.2; test for trend, p <0.001), and sweet desserts (RRs of 1.0, 1.3, 1.5; test for trend, p = 0.01). Elevated risks were also noted for use of butter at the table and for frying with butter or margarine, as opposed to vegetable oils. The association of total beef and pork consumption with breast cancer was not materially affected by controlling for age at first birth, family history of breast cancer, previous benign breast biopsy or socioeconomic status. Nor was the association reduced by controlling for ages of menarche and menopause, even though within the control series the intake of beef and pork reported in adult life was higher among those with a lower age at menarche or a older age at natural menopause.
Thesis (Dr. P.H.)--Loma Linda University, 1980. Includes bibliographical references (p. 180-209). Facsimile.
In interview data from the U.S.A.'s Third National Cancer Survey, alcohol ingestion was associated with a higher occurrence of cancers of the breast, thyroid, and amlignant melanoma. Data from other studies support the first two associations. A unifying hypothesis to explain these seemingly diverse associations suggests that alcohol stimulates anterior pituitary secretion of prolactin, thyroid-stimulating hormone (T.S.H.), and melanocyte-stimulating hormone (M.S.H.). Under the stimulations of these hormones, the three target tissues exhibit increased mitotic activity and hence an increase susceptibility to the development of a malignancy. A wide variety of findings from other studies indicate plausibility for this hypothesis. The implications could be grave. In addition to alcohol, several common drugs acting in similar manner could be cancer promoters, including: resperine, methyldopa, phenothiaznes, d-amphetamine, tricyclic antidepressants, and antihistamines. Over 20000 (25%) ofall new breast-cancer cases each year in the U.S.A. could be preventable if this hypothesis is correct.
A prospective epidemiologic study of prostate cancer was conducted in Japan. The 10-year follow-up study of 122,261 men aged 40 years and above, who constitute 94.5% of the census population of 29 Health Center Districts, revealed a significantly lower age-standardized death rate for prostate cancer in men who daily ate green and yellow vegetables. This association is consistently observed in each age-group, in each socioeconomic class, and in each prefecture. Selected epidemiologic phenomena, such as the upward trend of the prostate cancer death rate in Japan, intracountry variation of death rate, the significantly lower incidence rate in Japan compared with that of the United States, and elevated risk in Japanese migrants to Hawaii, appear to be explained by the variation in diet and change in amount of green and yellow vegetables ingested. The possible role of vitamin A is considered as a factor in preventing and inhibiting growth of prostate cancer. Most of the other factors studied appear noncontributory, except for marital status; a higher risk was observed in "ever married" men.
Breast cancer is still relatively infrequent in Japan. However, both mortality and morbidity rates have sharply increased in recent years, especially in ages 45–59. The risk was noted to be 8.5 times higher in women of high socioeconomic strata eating meat daily compared with women of low socioeconomic strata who do not eat meat daily, when 142,857 women aged 40 years were followed for 10 years. A high positive correlation was found between per capita fat intake and adjusted death rates of breast cancer in different districts of Japan. It was estimated that the breast cancer death rate will rise to the U.S. level when Japanese dietary fat intake approaches present day U.S. levels. The close correlation with fat intake was noted to come mainly from the consumption of pork and animal fat. The ratio of recent increase in breast cancer death rates was also found to be under the combined influence of animal fat and AF2, a highly mutagenic food additive widely used in Japan from 1965 to 1975 and shown to produce mammary carcinoma in rats. A series of case-control studies reveals the higher risk of breast cancer with the increase in body size especially in postmenopausal women. The recent breast cancer increase could therefore be a reflection of the fact that women in Japan are becoming heavier, especially after age 30.
The Adventist Health Study is a prospective cohort study of 34,198 non-Hispanic white Seventh-day Adventists (13,857 men; 20,341 women, age 25-100 years) followed for 6 years (1977-1982). Within this population, 55.2% were lacto-ovovegetarian (consumed meat, poultry, or fish less than one time per week with no restrictions as to egg or dairy product consumption) in 1976 and most abstained from alcohol, tobacco, and pork products. Baseline data included demographic variables, information on current and past dietary habits, exercise patterns, use of prescription drugs, use of alcohol and tobacco, measures of religiosity, occupation and residential histories, anthropometric data, and menstrual and reproductive histories. Nonfatal case ascertainment was completed through review of self-reported hospitalizations obtained from annual self-administered mailed questionnaires and through computerized record linkage with two California population-based tumor registries. Fatal case ascertainment was completed via record linkage with computerized California state death certificate files, the National Death Index, and individual follow-up. During the 6 years of follow-up, 52.8% of the 34,198 study subjects reported at least one hospitalization. A total of 20,702 medical charts were reviewed for cancer and cardiovascular disease incidence and 1406 incident cancer cases and 2716 deaths from all causes were identified after baseline data collection.
We evaluated the risk of breast cancer in relation to the frequency of consumption of a few selected dietary items. Data were used from a case-control study of 1,108 histologically confirmed breast cancer patients and 1,281 control subjects who were in the hospital for acute conditions unrelated to any of the established or suspected risk factors for breast cancer. Moderately elevated risk estimates were associated with higher levels of fat consumption in seasonings [butter, margarine, and oil, relative risk (RR) = 1.34, 95% confidence interval (CI) = 1.06-1.71] and meat (RR = 1.36, 95% CI = 1.12-1.65), whereas a reduced risk (RR = 0.42, 95% CI = 0.34-0.51) was associated with a more frequent green vegetable consumption. It was not possible to show that these associations were incidental, because allowance for several identified potential confounding factors, including the major identified or potential risk factors for breast cancer, did not materially modify the risk estimates. Further, no appreciable interaction emerged with age or menopausal status, because the diet-related risk estimates were similar in pre- or postmenopausal women. However, the implications of these findings in terms of specific micronutrients (e.g., retinol or beta-carotene) and biological correlates are still unclear. Alcohol consumption was significantly greater among breast cancer cases, with a multivariate risk estimate of 2.92 for the highest level. Thus, the present findings confirm that various aspects of diet may influence the risk of breast cancer, although the small amount of available knowledge does introduce serious uncertainties in any discussion of the potential implications in terms of prevention on a public health scale.
Seventh-day Adventist women experience lower mortality rates from breast cancer than other white females in the United States. To evaluate the role of diet in relation to breast cancer within this unique population (more than one-half of all Adventist women are lacto-ovo-vegetarians), a nested case-control study was conducted including 142 cases of fatal breast cancer and 852 matched controls among California Seventh-day Adventist women in 1960-1980. No significant relations between the consumption of animal products (meat, milk, cheese, and eggs) and breast cancer were evident. Odds ratios of 1.00, 1.22, and 1.03 were observed for meat consumption categories of none or occasional, 1-3 days/week, and 4+ days/week, respectively. However, among those women who experienced a relatively early age at natural menopause (less than or equal to 48 years), a suggestive though nonsignificant, positive association between meat consumption and risk was noted. These relations remained unchanged after simultaneously controlling for the effects of other covariates (menstrual characteristics and obesity) via conditional logistic regression analysis. Risk was not related to age at first exposure to the vegetarian lifestyle nor to duration of exposure to the vegetarian lifestyle.
A case-control study was done to examine the relationship between childhood and recent eating practices and risk of breast cancer. Eight hundred forty-six cases and 862 controls returned questionnaires indicating their menopausal status. In premenopausal women, breast cancer risk was increased with recent consumption of foods high in fat content (gravy, beef, pork) and reduced with foods low in fat content (fish); in postmenopausal women, risk was increased with pork consumption only. Regarding carotene sources, risk was reduced with carrot consumption in postmenopausal women only. Similar trends in risk were not found for childhood eating practices. Body weight influenced the breast cancer risk differently for pre- and postmenopausal women: Heavier weight in childhood and teens reduced the risk of premenopausal breast cancer, and heavier weight in adulthood increased the risk of postmenopausal breast cancer. We conclude that fat consumption is associated with breast cancer, especially in premenopausal women.
Dietary fat has been suggested as a risk factor for breast cancer in women, but the available data on humans are sparse and inconsistent. In 1980, 89,538 U.S. registered nurses who were 34 to 59 years of age and had no history of cancer completed a previously validated dietary questionnaire designed to measure individual consumption of total fat, saturated fat, linoleic acid, and cholesterol, as well as other nutrients. In a subsample of 173 participants studied in detail, those in the highest quintile of fat intake consumed a mean of 44 percent of calories from fat, as compared with 32 percent for those in the lowest quintile. During four years of follow-up, 601 cases of breast cancer were diagnosed among the 89,538 nurses in the study. After adjustment for known determinants in multivariate analyses, the relative risk of breast cancer among women in the highest quintile of calorie-adjusted total fat intake, as compared with women in the lowest quintile, was 0.82 (95 percent confidence limits, 0.64 and 1.05). The corresponding relative risks were 0.84 (confidence limits, 0.66 and 1.08) for saturated fat, 0.88 (0.69 and 1.12) for linoleic acid, and 0.91 (0.70 and 1.18) for cholesterol intake. Similar results were found for both postmenopausal and premenopausal women. These data are based on a limited period of follow-up and do not exclude a possible influence of fat intake before adulthood or at levels lower than 30 percent of calories. They suggest, however, that a moderate reduction in fat intake by adult women is unlikely to result in a substantial reduction in the incidence of breast cancer.
The relation between total caloric intake, body weight, and tumorigenesis, as well as the independence of these effects from those of dietary fat, were evaluated using data from 82 published experiments involving several tumor sites in mice. Comparing experimental (calorie restricted) to control (ad libitum) groups showed that the former consumed 29% fewer calories (experimental groups consumed fewer calories than control groups in all but a few isocaloric experiments), 50% less total fat, 11% less protein, and weighed 25% less than control animals. Adult body weight was highly correlated to caloric intake in both males (r = 0.85) and females (r = 0.74), although this correlation decreased with increasing caloric intake. Cumulative tumor incidence was, on average, 42% lower in the restricted groups. Multivariate regression analyses revealed that, regardless of the level of dietary fat, tumor incidence increased with increasing caloric intake and body weight over a wide range of intakes, including moderate caloric restriction (i.e., 7-20%). These data indicate that total caloric intake is an important determinant of tumorigenesis in mice, and that body weight may be a more sensitive indicator for this effect than is caloric intake alone.
Breslow N E (Department of Biostatisties, SC-32, University of Washigton, Seattle, WA 98195, USA). Elementary methods of cohort analysis. International Journal of Epidemiology 1984, 13: 112– 115.
The Mantel-Haenszel procedure offers a simple and efficient means of estimating a common rate ratio from incidence density data in cohort studies. A new formula is provided for the variance of its logarithm, comparisons are made with the method of maximum likehood, and associated tests for heterogeneity and trend in the component rate ratios are described.
Survival rates were compared among 282 Seventh-day Adventists and 1675 other white female cancer cases following diagnosis during the 30-year period, 1946 to 1976, at two California hospitals owned and operated by the Seventh-day Adventist Church. The Adventist women had a more favorable 5-year relative survival pattern than the other women (69.7% vs. 62.9%) as well as a higher probability of not dying of breast cancer. The differences, however, were no longer significant when stage at diagnosis was taken into account. It seems likely that the lower breast cancer death rates reported among Seventh-day Adventist women as compared with the general population result in part from better survival patterns due to earlier diagnosis and treatment.
In previous reports concerning cancer among Seventh-Day Adventists (SDA), comparisons were made only with the general population. This report compared California SDA to a sample of non-SDA who were demographically similar to SDA. The study consisted of 17 years of follow-up (1960--76) on 22,940 white California SDA and 13 years of follow-up (1960--72) on 112,725 white California non-SDA. Both groups completed the same base-line questionnaire in 1960. Deaths were ascertained by annual contacts with each study member and by computer-assisted record linkage with the California State death certificate file. Results indicated that, with the exception of colon-rectal cancer and smoking-related cancers, the difference in risk of fatal cancer between SDA and non-SDA was substantially reduced when SDA were compared with a more socioeconomically similar population. The persistence of the low risk for colon-rectal cancer can probably be attributed to some aspect of the diet or life-style of the SDA.
A variety of studies have shown that diets high in fat, particularly polyunsaturated, have enhanced the production of tumors in animals challenged with chemical carcinogens. Other studies have found an apparent contradiction of no difference in the incidence of breast cancer among women with varying levels of serum cholesterol as measured decades earlier. The present study concerns 2024 breast cancer cases and 1463 control patients without neoplasms or pathology of the reproductive and digestive organs, seen at Roswell Park Memorial Institute from 1958 to 1965. Based upon the assessments of their varying ingestion of fats from their own reports of diets, no difference in risk was found. Similarly, there was no difference in risk of breast cancer associated with ingesting diets containing various levels of either vitamin C or the cruciferous vegetables. Risk for breast cancer in women 55 years of age and older increased somewhat with decreases in ingestion of foods containing vitamin A.
Chronic disease among Seventhday Adventists. A low-risk group. Rationale, methodology, and description of the population Estimating major nutrient intake from self-administered food fresuency questionnaires (Abstr)
- Wl Beeson
- Mills
- Pk
- Phillips
- Phillips Rl
- Kuzma
Beeson WL, Mills PK, Phillips RL ef al. Chronic disease among Seventhday Adventists. A low-risk group. Rationale, methodology, and description of the population. Cancer 1989; 64570-581, 8. Phillips RL, Kuzma JW. Estimating major nutrient intake from self-administered food fresuency questionnaires (Abstr). Am J Epidemiol 1976; 104:3540.
Elementary methods of cohort analysis Diet in the etiology of breast cancer
- N Breslow
- Rohan Te
- Bain
Breslow, N. Elementary methods of cohort analysis. Znt J Epidemiol 1984; 13:112-115. 11. Rohan TE, Bain CJ. Diet in the etiology of breast cancer. Epi-demiol Rev 1987; 9:120-145.
Blot WJ ef al. Dietary factors and breast cancer risk
- Jh Lubin
- Bums
Lubin JH, Bums PE, Blot WJ ef al. Dietary factors and breast cancer risk. fnf J Cancer 1981; 28685-689.
The association of dietary factors with the age of menarche The bimodel age distribution of patients with mammary carcinoma: Evidence for the existence of two types of human breast cancer Breast cancer
- Dg Kissinger
- Sanchez
- F Dewaard
- Baandess
- Halewijn Ea
- J Huizinga
Kissinger DG, Sanchez A. The association of dietary factors with the age of menarche. Nutr Res 1987; 7:471-479. 2 1. DeWaard F, Baandess-Van Halewijn EA, Huizinga J. The bimodel age distribution of patients with mammary carcinoma: Evidence for the existence of two types of human breast cancer. Cancer 1964; 17:141- 151. 22. Pike MC, Ross RK. Breast cancer. Br Med Bull 1984; 40:351- 354.
Validity and reproducibility of alternative nutrient indices based on a mailed food frequency questionnaire. Presented at the Society for Epidemiologic Research annual meeting
- Andress M Fraser
- Morgan J Ge
- Kuzma
Abbey DE, Andress M, Fraser GE, Morgan J, Kuzma J. Validity and reproducibility of alternative nutrient indices based on a mailed food frequency questionnaire. Presented at the Society for Epidemiologic Research annual meeting. Vancouver, British Columbia, 1988.
Cancer in vegetarians Environ-mental Aspects of Cancer: The Role of Macro and Micro Components of Foods
- Phillips Rl Da Snowdon
- Brin
- El Wynder
- Ga Leveille
- Jh Weisburger
- Livingston
Phillips RL, Snowdon DA, Brin BN. Cancer in vegetarians. In: Wynder EL, Leveille GA, Weisburger JH, Livingston GE, eds. Environ-mental Aspects of Cancer: The Role of Macro and Micro Components of Foods. Westport, CT: Food and Nutrition Press, 1983; 53-72.
Diet in the epidemiology of breast cancer Dietary factors and the risk of breast cancer
- S Graham
- J Marshall
- C Mettlin
- C Lavecchia
- A Decarli
- S Franchexhi
Graham S, Marshall J, Mettlin C ef al. Diet in the epidemiology
of breast cancer. Am J Epidemiol 1982; 1 16:68-75.
15. LaVecchia C, DeCarli A, Franchexhi S el al. Dietary factors and
the risk of breast cancer. Nutr Cancer 1987; 10205-214.
Environmental Aspects of Cancer: The Role of Macro and Micro Components of Foods
- El Wynder
- Ga Leveille
- Jh Weisburger
- Ge Livingston
Wynder EL, Leveille GA, Weisburger JH, Livingston GE, eds. Environmental Aspects of Cancer: The Role of Macro and Micro Components
of Foods. Westport, CT: Food and Nutrition Press, 1983; 53-72.
Validity and reproducibility of alternative nutrient indices based on a mailed food frequency questionnaire. Presented at the Society for Epidemiologic Research annual meeting. Vancouver, British Columbia, 1988. 10. Breslow, N. Elementary methods of cohort analysis
- De Abbey
- M Andress
- Ge Fraser
- J Morgan
- J Kuzma
Abbey DE, Andress M, Fraser GE, Morgan J, Kuzma J. Validity
and reproducibility of alternative nutrient indices based on a mailed
food frequency questionnaire. Presented at the Society for Epidemiologic
Research annual meeting. Vancouver, British Columbia, 1988.
10. Breslow, N. Elementary methods of cohort analysis. Znt J Epidemiol 1984; 13:112-115.
Childhood and recent eating patterns and risk of breast cancer Kissinger DG, Sanchez A. The association of dietary factors with the age of menarche
- Tg Hislop
- Aj Coldman
- Jm Elwood
Hislop TG, Coldman AJ, Elwood JM ef al. Childhood and recent
eating patterns and risk of breast cancer. Cancer Detect Prev 1986; 9:
20. Kissinger DG, Sanchez A. The association of dietary factors with
the age of menarche. Nutr Res 1987; 7:471-479.
The bimodel age distribution of patients with mammary carcinoma: Evidence for the existence of two types of human breast cancer
- F Dewaard
- Ea Baandess-Van Halewijn
- J Huizinga