Green tea and breast cancer

The identification of modifiable lifestyle factors that could reduce the risk of breast cancer is a research priority. Despite the enormous chemopreventive potential of green tea and compelling evidence from animal studies, its role in breast cancer development in humans is still unclear. Part of the uncertainty is related to the relatively small number of epidemiological studies on green tea and breast cancer and that the overall results from case-control studies and prospective cohort studies are discordant. In addition, the mechanisms by which green tea intake may influence risk of breast cancer in humans remain not well studied. We review the human studies that have evaluated the relationship between green tea intake and four biomarkers (sex steroid hormones, mammographic density, insulin-like growth factor, adiponectin) that are believed to be important in breast cancer development. Results from these biomarker studies are also inconclusive. Limitations of observational studies and areas of further investigations are discussed.     

Overview of the epidemiology methods and applications: strengths and limitations of observational study designs

The impact of study design on the results of medical research has long been an area of both substantial debate and a smaller body of empirical research. Examples come from many disciplines within clinical and public health research. Among the early major contributions in the 1970s was work by Mosteller and colleagues (Gilbert et al., 1997), who noted that innovations in surgery and anesthesia showed greater gains than standard therapy when nonrandomized, controlled trials were evaluated compared with the gains reported in randomized, controlled trials. More recently, we and others have evaluated the impact of design in medical and surgical research, and concluded that the mean gain comparing new therapies to established therapies was biased by study design in nonrandomized trials (Colditz et al., 1989; Miller et al., 1989). Benson and Hartz (2000) conducted a study in which they focused only on studies reported after 1985. On the basis of 136 reports of 19 diverse treatments, Benson and Hartz concluded that in only 2 of the 19 analyses did the combined data from the observational studies lie outside the 95% confidence interval for the combined data from the randomized trials. A similar study drew only on data reported from 1991 to 1995, which showed remarkably similar results among observational studies and randomized, controlled trials (Concato et al., 2000). These more recent data suggest that advancing the study design and analytic methods may reduce bias in some evaluations of medical and public health interventions. Such methods apply not only to the original studies, but also to the approaches that are taken to quantitatively combine results by using meta-analytic approaches such as random effects meta-regression, Bayesian meta-analysis, and the like (Normand, 1999). By focusing attention on thorough data analysis, design issues can be understood and their impact or bias can be estimated, on average, and then ideally accounted for in the interpretation of data. Before discussing dietary data, let us first consider some of the more clearly delineated preventive exposures. Issues of study design have been addressed in terms of combining randomized trials and observational studies in evaluating preventive interventions such as Bacillus Calmette-Guerin vaccination (Colditz et al., 1994) and mammography screening (Desmissie et al., 1998). When one is interpreting the apparent heterogeneity in the results, it is important to step back and ask what is the relationship being evaluated under these different study designs? For example, a randomized, controlled trial uses the intention-to-treat analysis to preserve the merit of randomization. Such an analysis does not evaluate the exposure-disease relationship, but rather examines the impact of offering a new therapy versus an alternative therapy (regardless of adherence to the intervention, or control or placebo). On the other hand, a case-control study or a prospective cohort study will evaluate the impact of the screening test among those participants who were screened as compared with those who were never screened. In prevention studies, the design raises major issues of the timing of the exposure in the natural history of disease and also the adherence to therapy by healthy research volunteers. Case-control studies of preventive interventions such as screening mammography and prospective population-based studies of pap smears have capitalized on this variation in time since the last screen to evaluate the protective interval for a screening test (IARC Work Group, 1986). In contrast, a trial must choose a level of exposure, such as annual mammography screenings or colon screenings every 10 years with a colonoscopy, regardless of the evolving evidence on the duration of protection after a negative screening test. Continuing with the mammography example, a detailed study by Demissie and colleagues (1998) combined data from seven randomized trials and six case-control studies that investigated the association between participation in breast cancer screening programs and breast cancer mortality. The authors showed that if one assumes noncompliance with mammography (approaching 30%) and 20% of the control group is screened, then the benefit of mammography in terms of reduced mortality is comparable in randomized, controlled trials and epidemiologic studies after adjusting for nonadherence (Demissie et al., 1998). Thus, the different designs fundamentally measure different constructs of the impact of screening. Zelen (1988) considered the challenges of primary prevention trials and addressed both compliance and models of carcinogenesis as major impediments to the use of randomized, controlled trials to evaluate cancer prevention strategies. It is important to contrast these issues in both treatment trials and prevention trials. In treatment trials, recently diagnosed patients, who are often in life-threatening situations, are typically offered the option to participate in a trial of a new therapy compared with standard therapy or placebo. Compliance or adherence to therapy is usually very high among these highly motivated patients and their outcomes are generally in the short- to mid-term. In contrast, prevention trials recruit large numbers of healthy participants, offer them a therapy, and then follow them over many years because the chronic diseases being prevented are relatively rare. With substantial noncompliance (often in the range of 20% to 40% over the duration of the trial), an intention-to-treat analysis is no longer unbiased, but rather gives a biased estimate of the effect, typically underestimating the magnitude of the association that is seen in observation studies in which those participants who have had exposure to a particular lifestyle component are compared with those without such an exposure. There are additional challenges for nutritional interventions, including the timing of diet as a preventive agent in the disease process and the range of nutrient intakes in the population. In retrospective case-control studies, recall bias of past diet is an additional issue with which to contend. Unlike smoking or screening tests in which the exposure is finite and can be completely stopped and started, one's diet, physical activity, and weight change cannot go to zero for prolonged periods and sustain life. The range of nutrient intake is a major issue when enrolling participants into prevention trials and observational studies. Health-conscious volunteers are more often identified and screened as eligible for a trial. The epidemiology of diet and colon cancer has been extensively studied. For example, Cho et al. (2004) conducted a combined analysis of prospective dietary studies of calcium and vitamin D intake data from 10 cohorts. The dose-response relationship for calcium showed that the greatest benefit for increasing calcium intake was for those participants who had a reported daily intake below 1000 mg/d. Increasing the intake of those individuals with low intake to the level of 1000 mg/day would yield a 20% reduction in risk. Beyond this level of intake, there was little additional reduction in the risk of colon cancer. In the Women's Health Initiative, participants had a mean calcium intake of 1150 mg/d at baseline and increased this intake in the intervention arm to 2250 mg/d on average. This magnitude of increase was of limited association in the combined, prospective, cohort studies and was not related to risk in the randomized trial (Wactawski-Wende et al., 2006). Similar findings apply to the interpretation of the vitamin D intervention and highlight the role of dietary intake at randomization when evaluating dietary components. Returning to the time frame of exposure in the carcinogenic process, the null randomized, controlled trials of fiber (Alberts et al., 2000) and fruit and vegetables (Schatzkin et al., 2000) for the prevention of polyp recurrence amply illustrate Zelen's concerns regarding the timing of the preventive intervention in the disease process. The extent of DNA damage accumulated across the colonic mucosa at the time of detecting the "eligibility polyp" was certainly not limited only to the removed polyp. Rather, these observations beg the question that at what stage in the disease process may fiber play a role in protecting against colon cancer? This contrasts with the richness of epidemiologic studies that can address exposure over the life course and relate such exposure to disease risk. Perhaps the best-known example is the radiation follow-up effects cohort in Japan in which a radiation dose was estimated for each woman who had been exposed to the effects of the atomic bombs on Hiroshima and Nagasaki and followed-up over 40 years. The results of this study showed a clear and strong relationship between the increased risk of breast cancer with higher exposure among those participants who were exposed before the age of 20 years (Land et al., 2003). Retrospective assessment of diet after disease diagnosis has been demonstrated to introduce bias into the evaluation of exposure-disease relationships. For example, Giovannucci et al. (1993) evaluated retrospective recall of diet after breast cancer diagnosis within the ongoing Nurses' Health Study. In contrast with the prospective analysis in which no relationship between dietary fat and breast cancer was observed, the retrospective analysis yielded a positive relationship for total fat and saturated fat (Giovannucci et al., 1993). By comparing the top quintile versus the bottom quintile of reported intake, the retrospective assessment yielded odds ratios of 1.43 for total fat and 1.38 for saturated fat. Therefore, the magnitude of bias was sufficient to distort evaluation of the diet-disease relationship. (ABSTRACT TRUNCATED)     

Context is everything: Mining the normal and preneoplastic microenvironment for insights into the diet and cancer risk conundrum

This review highlights the context-dependence of epithelial carcinogenesis in order to illuminate the potential for progress in the field of diet and cancer prevention. Estimates drawn from observational epidemiology imply that diet and lifestyle changes have the potential to prevent 30-40% of cancer cases. However, the application of knowledge gleaned from observational epidemiology applied to randomized clinical trials (RCT) has yielded equivocal or negative results. Resolving this conundrum requires: (i) advances in diet assessment methodologies and the design of clinical trials; (ii) greater knowledge of the active components within foods which may impact cancer risk; and (iii) knowledge about the effects of dietary components on susceptible tissues throughout the disease process (Meyskens, F. L., Jr., Szabo, E., Diet and cancer: The disconnect between epidemiology and RCT. Cancer Epidemiol. Biomarkers Prev. 2005, 14, 1366-1369). Explicit consideration of the causal criteria will pay tangible benefits in the design of basic, clinical, and epidemiologic studies in cancer prevention. The rational identification of diet-dependent physiologic targets for cancer prevention is best pursued by appreciating context-dependence of epithelial carcinogenesis. Five contexts, or paradigms useful in understanding the multifactorial nature of carcinogenesis, are offered which describe the potential diet-associated physiologic influences on normal and preneoplastic cells and tumor microenvironments. Taken together with the interactions of systemic, endocrine, and autocrine/paracrine signals that may modulate the process of carcinogenesis, we can appreciate how dietary factors may act collectively in normal tissues or at early stages of carcinogenesis to prevent cancer. Only by understanding the effect of dietary components on the cellular and stromal components of the tissue microenvironment early in the process of epithelial carcinogenesis will yield clues useful for the development of improved strategies for cancer prevention.     

Nutritional factors and colon cancer

During the last 2 decades, substantial progress has been made in understanding the relationship between dietary constituents and the development of colon cancer in man. Unlike studies of cancer among smokers and nonsmokers, nutritional epidemiologic studies are confronted with the inherent difficulty of assessing reasonably precise exposures. The lack of consistency between international correlation studies and case‐control studies does not necessarily negate a dietary etiology of colon cancer because these inconsistencies may have arisen, at least in part, from methodological limitations. Some of these deficiencies in epidemiological studies of diet and cancer have been corrected; recent case‐control studies demonstrated that high dietary fat is a risk factor for colon cancer development and that an overall increase in intake of foods high in fiber might decrease the risk for colon cancer. The results of epidemiologic studies may be assumed to present conservative estimates of the true risk for cancer associated with diet. The populations with high incidences of colon cancer are characterized by high consumption of dietary fat, which may be a risk factor in the absence of factors that are protective, such as whole‐grain cereals and of other high fiber. Laboratory‐animal model studies have shown that certain dietary lipids and fibers influence tumorigenesis in the colon. The data of metabolic epidemiological and laboratory‐animal model studies are sufficiently convincing with respect to the enhancement of colon cancer by type of fat and protection by certain dietary fibers.     

Phytosterols as anticancer compounds

Phytochemicals have been proposed to offer protection against a variety of chronic ailments including cardiovascular diseases, obesity, diabetes, and cancer. As for cancer protection, it has been estimated that diets rich in phytochemicals can significantly reduce cancer risk by as much as 20%. Phytosterols are specific phytochemicals that resemble cholesterol in structure but are found exclusively in plants. Phytosterols are absorbed from the diet in small but significant amounts. Epidemiological data suggest that the phytosterol content of the diet is associated with a reduction in common cancers including cancers of the colon, breast, and prostate. The means by which dietary phytosterols may be achieving these effects is becoming clearer from molecular studies with tumorigenic research models. Phytosterols affect host systems potentially enabling more robust antitumor responses, including the boosting of immune recognition of cancer, influencing hormonal dependent growth of endocrine tumors, and altering sterol biosynthesis. In addition, phytosterols have effects that directly inhibit tumor growth, including the slowing of cell cycle progression, the induction of apoptosis, and the inhibition of tumor metastasis. This review summarizes the current state of knowledge regarding the anticancer effects of phytosterols.     

Mycotoxin exposure and human cancer risk: A systematic review of epidemiological studies

In recent years, there has been an increasing interest in investigating the carcinogenicity of mycotoxins in humans. This systematic review aims to provide an overview of data linking exposure to different mycotoxins with human cancer risk. Publications (2019 and earlier) of case–control or longitudinal cohort studies were identified in PubMed and EMBASE. These articles were then screened by independent reviewers and their quality was assessed according to the Newcastle–Ottawa scale. Animal, cross‐sectional, and molecular studies satisfied criteria for exclusion. In total, 14 articles were included: 13 case–control studies and 1 longitudinal cohort study. Included articles focused on associations of mycotoxin exposure with primary liver, breast, and cervical cancer. Overall, a positive association between the consumption of aflatoxin‐contaminated foods and primary liver cancer risk was verified. Two case–control studies in Africa investigated the relationship between zearalenone and its metabolites and breast cancer risk, though conflicting results were reported. Two case–control studies investigated the association between hepatocellular carcinoma and fumonisin B1 exposure, but no significant associations were observed. This systematic review incorporates several clear observations of dose‐dependent associations between aflatoxins and liver cancer risk, in keeping with IARC Monograph conclusions. Only few human epidemiological studies investigated the associations between mycotoxin exposures and cancer risk. To close this gap, more in‐depth research is needed to unravel evidence for other common mycotoxins, such as deoxynivalenol and ochratoxin A. The link between mycotoxin exposures and cancer risk has mainly been established in experimental studies, and needs to be confirmed in human epidemiological studies to support the evidence‐based public health strategies.     

The meaning of food to breast cancer survivors.

Although a definitive relationship between diet and breast cancer remains controversial, many women adopt dietary change after diagnosis. To understand factors motivating dietary change, we explored the meanings that breast cancer survivors attached to food during recovery. Six women who were breast cancer survivors for six to 19 years participated in semi-structured interviews exploring personal meanings attached to food, dietary changes after diagnosis, factors influencing dietary change, and experiences with food in relation to breast cancer. Two distinct phases emerged. These corresponded to active treatment, when women used food to gain control, to cope, for comfort, and for hope, and to post-treatment, when the meanings that women attached to food were shaped by the perception of food's role in breast cancer causation. Women who believed that diet prevents a first diagnosis adopted change to prevent recurrence, while those who did not believe in the relationship between diet and breast cancer adopted change to improve health. In women with breast cancer, food can be an important coping mechanism. Women may benefit from counselling grounded in the meanings they attach to food over the recovery continuum.     

Anticarcinogenecity of microbiota and probiotics in breast cancer

Breast cancer is one of the most important causes of cancer related morbidity and mortality in the world. Along with genetic, environmental factors also play a multifaceted role in the development of disease. Breast contains several bacterial species performing specialized functions. Probiotics, as functional food, play pivotal role against breast cancer development in vivo and in vitro. Current review summarized all the available data related to diet, probiotics, and their association with breast cancer risk along with underlying mechanisms. Presently, it was believed that many of the commercially available probiotic products were safe to use and had some beneficial health effects for the host. Probiotics had a potential to act against breast cancer progression evidenced by many animal model and cell-based experiments. Some probiotics strains may be useful as an adjuvant therapy for breast cancer prevention or treatment, by modulating immune response or breast microbial community. However, large-scale clinical trials and intense research are mandatory to explore probiotics-related metabolic and molecular mechanisms in breast cancer.     

Major scientific advances with dairy foods in nutrition and health

A large body of scientific evidence collected in recent decades demonstrates that an adequate intake of calcium and other nutrients from dairy foods reduces the risk of osteoporosis by increasing bone acquisition during growth, slowing age-related bone loss, and reducing osteoporotic fractures. These results have culminated in the new (2005) Dietary Guidelines for Americans that now recommend 3 servings of milk products per day to reduce the risk of low bone mass and contribute important amounts of many nutrients that may have additional health attributes beyond bone health. A number of animal, observational, and clinical studies have shown that dairy food consumption can help reduce the risk of hypertension. Clinical trials indicate that the consumption of recommended levels of dairy products, as part of a healthy diet, can contribute to lower blood pressure in individuals with normal and elevated blood pressure. Emerging data also indicate that specific peptides associated with casein and whey proteins can significantly lower blood pressure. In addition, a growing body of evidence has provided support for a beneficial effect of dairy foods on body weight and fat loss. Clinical studies have demonstrated that during caloric restriction, body weight and body fat loss occurs when adequate calcium is provided by supplements and that this effect is further augmented by an equivalent amount of calcium supplied from dairy foods. Several studies support a role for calcium, vitamin D, and dairy foods against colon cancer. Additionally, conjugated linoleic acid, a fatty acid found naturally in dairy fat, confers a wide range of anticarcinogenic benefits in experimental animal models and is especially consistent for protection against breast cancer.     

Vegetarian,vegan diets and multiple health outcomes: A systematic review with meta-analysis of observational studies

Background: Beneficial effects of vegetarian and vegan diets on health outcomes have been supposed in previous studies. Objectives: Aim of this study was to clarify the association between vegetarian, vegan diets, risk factors for chronic diseases, risk of all-cause mortality, incidence, and mortality from cardio-cerebrovascular diseases, total cancer and specific type of cancer (colorectal, breast, prostate and lung), through meta-analysis. Methods: A comprehensive search of Medline, EMBASE, Scopus, The Cochrane Library, and Google Scholar was conducted. Results: Eighty-six cross-sectional and 10 cohort prospective studies were included. The overall analysis among cross-sectional studies reported significant reduced levels of body mass index, total cholesterol, LDL-cholesterol, and glucose levels in vegetarians and vegans versus omnivores. With regard to prospective cohort studies, the analysis showed a significant reduced risk of incidence and/or mortality from ischemic heart disease (RR 0.75; 95% CI, 0.68 to 0.82) and incidence of total cancer (RR 0.92; 95% CI 0.87 to 0.98) but not of total cardiovascular and cerebrovascular diseases, all-cause mortality and mortality from cancer. No significant association was evidenced when specific types of cancer were analyzed. The analysis conducted among vegans reported significant association with the risk of incidence from total cancer (RR 0.85; 95% CI, 0.75 to 0.95), despite obtained only in a limited number of studies. Conclusions: This comprehensive meta-analysis reports a significant protective effect of a vegetarian diet versus the incidence and/or mortality from ischemic heart disease (?25%) and incidence from total cancer (?8%). Vegan diet conferred a significant reduced risk (?15%) of incidence from total cancer.     

Red meat consumption: An overview of the risks and benefits

Red meat is long established as an important dietary source of protein and essential nutrients including iron, zinc and vitamin B12, yet recent reports that its consumption may increase the risk of cardiovascular disease (CVD) and colon cancer have led to a negative perception of the role of red meat in health. The aim of this paper is to review existing literature for both the risks and benefits of red meat consumption, focusing on case–control and prospective studies. Despite many studies reporting an association between red meat and the risk of CVD and colon cancer, several methodological limitations and inconsistencies were identified which may impact on the validity of their findings. Overall, there is no strong evidence to support the recent conclusion from the World Cancer Research Fund (WCRF) report that red meat has a convincing role to play in colon cancer. A substantial amount of evidence supports the role of lean red meat as a positive moderator of lipid profiles with recent studies identifying it as a dietary source of the anti-inflammatory long chain (LC) n−3 PUFAs and conjugated linoleic acid (CLA). In conclusion, moderate consumption of lean red meat as part of a balanced diet is unlikely to increase risk for CVD or colon cancer, but may positively influence nutrient intakes and fatty acid profiles, thereby impacting positively on long-term health.     

食用油中脂肪伴随物的营养与功能

我国油脂营养和食用油消费领域存在片面强调脂肪酸平衡而忽视脂肪伴随物营养与功能的误区.本文从法国悖论、地中海式饮食、爱斯基摩人膳食的角度出发,阐述了脂肪伴随物与人体健康的密切关系.并且采用饱和脂肪与心血管病之间关系、脂肪摄入与乳腺癌的相关性、高脂膳食氧化应激与抗氧化剂的干预作用等营养学的最新研究结果,表明饱和脂肪酸与心血管疾病之间不存在显著的相关性,摄入富含有益脂肪伴随物、营养全面的食用油是油脂营养的关键所在.     

Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009)

Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004-2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel's full report (http://www.otru.org/pdf/special/expert_panel_tobacco_breast_cancer.pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex/current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality.     

Correlations of dietary patterns with prostate health

Both genetic and environmental influences may be involved in etiology of prostate health and prostate cancer. These include ethnic origin, family history, smoking, and diet. Adiposity and excess energy intake are potentially distinct risk factors and positive associations with prostate cancer risk for both were observed among case-control and cohort studies. Some epidemiological studies support an association between dietary fat, particularly saturated or animal fats, and prostate cancer risk. Of these, several suggest reduced risk with low-fat diets high in n-3 fatty acids and increased risk with high-fat diets rich in n-6 fatty acids. Others suggested association with higher meat intake, possibly due to heterocyclic amines and polycyclic aromatic hydrocarbons, produced during grilling or frying. Positive association of prostate cancer risk with dairy intake could involve alpha-methylacyl-CoA racemase activity (required for beta-oxidation of phytanic acid present in dairy products and red meat) or the suppression of vitamin D activity by calcium. Inverse associations were observed with dietary intake of plant foods. These include cereals, soy products, and fruit and vegetable sources of carotenoids. Numerous plant constituents may act synergistically in the prevention and inhibition of prostate disorders. These diet-risk associations may lead to future individualized diet recommendations based upon genetic polymorphisms.     

Dietary patterns and the risk of obesity,type 2 diabetes mellitus,cardiovascular diseases,asthma, and neurodegenerative diseases

Diet and lifestyle play a significant role in the development chronic diseases; however the full complexity of this relationship is not yet understood. Dietary pattern investigation, which reflects the complexity of dietary intake, has emerged as an alternative and complementary approach for examining the association between diet and chronic diseases. Literature on this association has largely focused on individual nutrients, with conflicting outcomes, but individuals consume a combination of foods from many groups that form dietary patterns. Our objective was to systematically review the current findings on the effects of dietary patterns on chronic diseases. In this review, we describe and discuss the relationships between dietary patterns, such as the Mediterranean, the Dietary Approach to Stop Hypertension, Prudent, Seventh-day Adventists, and Western, with risk of obesity, type-2 diabetes mellitus, cardiovascular diseases, asthma, and neurodegenearive diseases. Evidence is increasing from both observational and clinical studies that plant-based dietary patterns, which are rich in fruits, vegetables, and whole grains, are valuable in preventing various chronic diseases, whereas a diet high in red and processed meat, refined grains and added sugar seems to increase said risk. Dietary pattern analysis might be especially valuable to the development and evaluation of food-based dietary guidelines.     

谷物膳食纤维抑制红肉胆碱代谢及其加工适应性

流行病学研究表明,谷物膳食纤维对慢性代谢性疾病,如肥胖、Ⅱ型糖尿病、心脑血管疾病以及结肠癌等具有预防作用。在典型红肉膳食结构中补充膳食纤维,在提高膳食营养、促进肠道益生菌增殖的同时,可抑制胆碱成分向三甲胺的转化进而减少动脉粥样硬化等潜在疾病的发生。膳食纤维分子结构特征和介观性质会影响其微生物可利用性和作用方式,并影响其在机体内发挥干预功能,因而多元强化方式的定向改性理论和技术及构效关系的建立对于目标膳食纤维产品的获得至关重要。基于谷物膳食纤维补充与调节肠道菌群和宿主效应的“精准饮食”研究将颠覆传统的红肉膳食营养原则,为 “健康中国”的实施提供坚实健康基础。     

Diet, nutrition, and cancer

Evidence pertaining to the role of dietary factors in carcinogenesis comes from both epidemiological studies and laboratory experiments. In 1982, the Committee on Diet, Nutrition, and Cancer of the National Research Council conducted a comprehensive evaluation of this evidence. That assessment as well as recent epidemiological and laboratory investigations suggest that a high fat diet is associated with increased susceptibility to cancer of different sites, particularly the breast and colon, and to a lesser extent, the prostate. Current data permit no definitive conclusions about other dietary macroconstituents including cholesterol, total caloric intake, protein, carbohydrates and total dietary fiber. Specific components of fiber, however, may have a protective effect against colon cancer. In epidemiological studies, frequent consumption of certain fruits and vegetables, especially citrus fruits and carotene-rich and cruciferous vegetables, is associated with a lower incidence of cancers at various sites. The specific components responsible for these effects are not clearly identified, although the epidemiological evidence appears to be most consistent for a protective effect of carotene on lung cancer and less so for vitamins A and C and various cancer sites. The laboratory evidence is most consistent for vitamin A deficiency and enhanced tumorigenesis, and for the ability of various nonnutritive components in cruciferous vegetables to block in-vivo carcinogenesis. The data for minerals and carcinogenesis are extremely limited, although preliminary evidence from both epidemiological and laboratory studies suggests that selenium may protect against overall cancer risk. Frequent consumption of cured, pickled, or smoked foods, possibly because they may contain nitrosamines or polycyclic aromatic hydrocarbons, appears to increase the risk of esophageal or stomach cancer, however, the specific causative agents in these foods are not clearly identified. Excessive alcohol consumption among smokers appears to be associated with an elevated risk of cancers of the oral cavity, esophagus, larynx, and respiratory tract. The mechanisms of action of dietary factors on carcinogenesis are poorly understood. The NRC committee, and more recently, the National Cancer Institute and the American Cancer Society have proposed interim dietary guidelines to lower the risk of cancer. These guidelines are consistent with general dietary recommendations proposed by U.S. government agencies for maintenance of good health.(ABSTRACT TRUNCATED AT 400 WORDS)     

饮食与新冠病毒感染的研究进展

COVID-19新型冠状病毒是以前从未发现的线性单链的RNA冠状病毒。COVID-19世界范围内大流行带来了无数经济、政治、社会后果,尤其是人类健康后果。饮食在新冠病毒感染风险和症状严重程度的作用正在凸显。大量证据表明,均衡健康的饮食模式可以减少COVID-19感染及重症的风险。该文就国内外饮食与新冠病毒感染风险及严重程度研究进行汇总,指出益生菌或益生元、膳食纤维、十字花科蔬菜、维生素C和膳食多酚的膳食模式是COVID-19感染及重症的保护因素;而过加工食品和高糖（果糖、葡萄糖）高脂高蛋白饮食模式是新冠病毒感染的风险因素。该文提倡的饮食模式可能为通过饮食干预预防或治疗新冠病毒感染提供指导。     

Healthy indexes in public health practice and research: a review

The scientific community has long been interested in the overall quality of diets owing to the fact that it is important for each individual's health through a healthy, varied, and balanced diet. Much research has been conducted on methods used to measure dietary quality. These studies led to the determination of numerous indices, some very simple and some much more complex. Indices that examine diets for several attributes concurrently are able to provide a measure of overall diet quality that is not possible when only single nutrients or food groups are examined. Using these indices, diet quality may be evaluated in relation to nutrient adequacy, compliance with dietary guidelines, or nutrition recommendations, association with risk of chronic diseases, or mortality, and used to assess interventions. However, there are several factors that should be taken into consideration for the design of an index, like the purpose of its use, as well as its simplicity in daily practice. The general purpose of an index is to synthesize a large amount of information into a single useful indicator. The purpose of this review was to present and to critically review the most commonly used dietary indices, and how they reflect various aspects of diet quality. The majority of these indices fail to recognize the various inter-relationships between their components, as well as their accuracy for estimating specific health outcomes. Thus, the development of weighted dietary indices that adequately assess a dietary pattern and its relationship to the burden of a disease is considered essential.     

100% citrus juice: Nutritional contribution,dietary benefits,and association with anthropometric measures

Citrus juices such as 100% orange (OJ) and grapefruit juice (GJ) are commonly consumed throughout the world. This review examines the contributions of OJ and GJ to nutrient intake, diet quality, and fruit intake, and supports citrus juices as nutrient-dense beverages. This review also explores the research examining associations between OJ and GJ intake and anthropometric measures. Citrus juices are excellent sources of vitamin C and contribute other key nutrients such as potassium, folate, magnesium, and vitamin A. OJ intake has been associated with better diet quality in children and adults. OJ intake has not been associated with adverse effects on weight or other body measures in observational studies in children and adults. In adults, some observational studies report more favorable body mass index or body measure parameters in OJ consumers compared to nonconsumers. Intervention studies in adults report no negative impacts of OJ or GJ consumption on anthropometric measures, although these measures were typically not the primary outcomes examined in the studies. Moderate consumption of citrus juices may provide meaningful nutritional and dietary benefits and do not appear to negatively impact body weight, body composition, or other anthropometric measures in children and adults.