The fungus Aspergillus flavus Link ex Fries can infect grains and oil seeds and develop Aflatoxin B1 (AfB1) in the fieldor in storage. Aflatoxin contamination is a serious health hazard — it is extremely toxic and hepatocarcinogenic for animals and humans. A practical approach to solve this problem is to use smectite clay as an amendment to animal feed. The objective of this research is to investigate smectite clay—AfB1 interactions by employing Fourier transform infrared (FTIR) spectroscopy to determine how clay composition influences AfB1 adsorption by smectites. When AfB1 was present in the clay, the spectral region from 1800 to 1300 cm−1 was altered, and the regions between 4000 and 1800 and 1300 and 400 cm−1 were unchanged except for the intensity in the broad region near 3400 cm−1 related to the abundance of water. The 1300–400 cm−1 region is attributed only to smectite clay properties, and it relates to the relative adsorption potential of the different smectites. Bonding between AfB1 and smectite clay appears to be in the furan rings. Other possible bonding is with the two oxygens in the coumarin ring of AfB1 and interlayer cations or their associated water molecules. The FTIR evidence of octahedral Fe in smectite and amorphous silica in the clays both indicate greater AfB1 adsorption potential. Other smectites with spectral absorption indicating predominantly Al in the octahedral positions adsorbed less AfB1.

Clinical trials conducted with incarcerated populations are rare. We present a case example of one such jail-based cancer prevention clinical trial to demonstrate the importance of including a theory-driven approach to intervention framing, novel experimental designs to boost access to low-risk trials, and retention strategies for long-term follow-up of hard-to-reach populations. As such we offer a social determinant of health framework to ensure cancer prevention research is conducted through the lenses of health promotion and health equity. Deviations from the gold-standard randomized control design, transparent systematic allotment, and street-based outreach retention strategies contribute to the feasibility of conducting clinical trials in carceral settings and after people leave jail. Best practices presented can be used in design and conduct of future clinical trials with criminal legal system-involved populations.

The present paper reviews progress in research on dietary fibre and human health over the past five decades. There is now convincing evidence from prospective cohort studies that diets low in dietary fibre are associated with increased risk of common non-communicable diseases including CVD, type 2 diabetes and colorectal cancer. These findings provide strong support for hypotheses proposed by Denis Burkitt 50 years ago, based on very limited evidence but with considerable imagination and insight. For the first two to three decades of this period, research on dietary fibre was hampered by the lack of consensus about the definition, and measurement, of this complex and diverse dietary component and by the lack of appropriate tools for investigating the gut microbiome that is central to understanding mechanisms of action. Recent technical and scientific advances in microbiome research (based on fast, low-cost, DNA sequencing) are facilitating investigation of the associations between dietary fibre, the gut microbiome and human health. Current challenges include the need for agreement about the characteristics of a healthy gut microbiome. Although the health benefits attributed to higher dietary fibre intake are likely to be shared with most types of dietary fibre, one should anticipate that different sources of dietary fibre and the other components (resistant starch and non-digestible oligosaccharides) that make up dietary fibre will have characteristically different effects on human physiology and disease risk. In conclusion, population-level intakes of dietary fibre are low and there is a public health priority to develop and implement more effective interventions to increase intake.

Inflammation is a central mechanism in metabolic disorders associated with morbidity and mortality and dietary factors can modulate inflammation. We aimed to prospectively investigate the association between an empirically developed, food-based dietary inflammatory pattern (EDIP) score and the risk of overall and cause-specific mortality, using data from the US National Health and Nutrition Examination Survey from 1999 to 2014. EDIP score was derived by entering thirty-nine predefined commonly consumed food groups into the reduced rank regression models followed by stepwise linear regression, which was most predictive of two plasma inflammation biomarkers including C-reactive protein and leucocyte count among 25 500 US adults. This score was further validated in a testing set of 9466 adults. Deaths from baseline until 31 December 2015 were identified through record linkage to the National Death Index. During a median follow-up of 7·8 years among 40 074 participants, we documented 4904 deaths. Compared with participants in the lowest quintile of EDIP score, those in the highest quintile had a higher risk of overall death (hazard ratio (HR) = 1·19, 95 % CI 1·08, 1·32, Ptrend = 0·002), and deaths from cancer (HR = 1·41, 95 % CI 1·14, 1·74, Ptrend = 0·017) and CVD (HR = 1·22, 95 % CI 0·98, 1·53, Ptrend = 0·211). When stratified by age, the association of EDIP with overall mortality was stronger among individuals under 65 years of age (Pinteraction = 0·001). Diets with a higher inflammatory potential were associated with increased risk of overall and cancer-specific mortality. Interventions to reduce the adverse effect of pro-inflammatory diets may potentially promote health and longevity.

During the 1960s and 1970s, the notion that the uterus is a useless and pathological organ after a woman has had ‘enough’ children emerged alongside news reports of excessive hysterectomy in Taiwan. This notion and hysterectomy became two sides of the same coin, the former pointing to the burden of birth control and cancer risk, and the latter to sterilization and removing cancer risk. I explore how, in post-war Taiwan, the notion became commonplace through the intersection of three historical formations: the medical tradition of employing surgery to manage risk (such as appendectomy for appendicitis), American-dominated family planning projects that intensified the surgical approach and promoted reproductive rationality, and cancer prevention campaigns that helped cultivate a sense of cancer risk. The gender politics operating in the family planning and cancer prevention projects were apparent. The burden of birth control fell mainly on women, and the cancer prevention campaign, centring almost exclusively on early detection of cervical cancer, made cancer into a woman’s disease. I argue that the discourses of reproductive rationality and disease risk were parallel and, in several key ways, intersecting logics that rendered the uterus useless and pathological and then informed surgeons’ practice of hysterectomy. Exploring the ways in which the uterus was envisioned and targeted in the history of medicine in Taiwan, this paper shows overlapping bio-politics in three strands of research in an East Asian context – namely women’s health, family planning and cancer prevention – and offers a case for global comparison.

Findings of epidemiological studies regarding the association between carrot consumption and lung cancer risk remain inconsistent. The present study aimed to summarise the current epidemiological evidence concerning carrot intake and lung cancer risk with a meta-analysis. We conducted a meta-analysis of case–control and prospective cohort studies, and searched PubMed and Embase databases from their inception to April 2018 without restriction by language. We also reviewed reference lists from included articles. Prospective cohort or case–control studies reporting OR or relative risk with the corresponding 95 % CI of the risk lung cancer for the highest compared with the lowest category of carrot intake. A total of eighteen eligible studies (seventeen case–control studies and one prospective cohort study) were included, involving 202 969 individuals and 5517 patients with lung cancer. The pooled OR of eighteen studies for lung cancer was 0·58 (95 % CI 0·45, 0·74) by comparing the highest category with the lowest category of carrot consumption. Based on subgroup analyses for the types of lung cancer, we pooled that squamous cell carcinoma (OR 0·52, 95 % CI 0·19, 1·45), small-cell carcinoma (OR 0·43, 95 % CI 0·12, 1·59), adenocarcinoma (OR 0·34, 95 % CI 0·15, 0·79), large-cell carcinoma (OR 0·40, 95 % CI 0·10, 1·57), squamous and small-cell carcinoma (OR 0·85, 95 % CI 0·45, 1·62), adenocarcinoma and large-cell carcinoma (OR 0·20, 95 % CI 0·02, 1·70) and mixed types (OR 0·61, 95 % CI 0·46, 0·81). Exclusion of any single study did not materially alter the pooled OR. Integrated epidemiological evidence from observational studies supported the hypothesis that carrot consumption may decrease the risk of lung cancer, especially for adenocarcinoma.

In 2014, the Food and Drug Administration approved a new human papillomavirus 9-valent vaccine (9vHPV), targeting nine HPV types: HPV types 6, 11, 16, and 18, which are also targeted by the quadrivalent HPV vaccine (qHPV), plus five additional high cancer risk HPV types (HPV types 31, 33, 45, 52, and 58). The aim of the current study was to systematically retrieve, qualitatively and quantitatively pool, as well as critically appraise all available evidence on 9vHPV from randomized controlled trials (RCTs). We conducted a systematic review of the literature on 9vHPV efficacy, immunogenicity and safety, as well as a systematic search of registered, completed, and ongoing RCTs. We retrieved and screened 227 records for eligibility. A total of 10 publications reported on RCTs’ results on 9vHPV and were included in the review. Sixteen RCTs on 9vHPV have been registered on RCT registries. There is evidence that 9vHPV generated a response to HPV types 6, 11, 16 and 18 that was non-inferior to qHPV. Vaccine efficacy against five additional HPV type-related diseases was directly assessed on females aged 16–26 years (risk reduction against high-grade cervical, vulvar or vaginal disease = 96·7%, 95% CI 80·9%–99·8%). Bridging efficacy was demonstrated for males and females aged 9–15 years and males aged 16–26 years (the lower bound of the 95% CIs of both the geometric mean titer ratio and difference in seroconversion rates meeting the criteria for non-inferiority for all HPV types). Overall, 9vHPV has been proved to be safe and well tolerated. Other RCTs addressed: 9vHPV co-administration with other vaccines, 9vHPV administration in subjects that previously received qHPV and 9vHPV efficacy in regimens containing fewer than three doses. The inclusion of additional HPV types in 9vHPV offers great potential to expand protection against HPV infection. However, the impact of 9vHPV on reducing the global burden of HPV-related disease will greatly depend on vaccine uptake, coverage, availability, and affordability.

For cancer prevention, the World Cancer Research Fund and American Institute for Cancer Research (WCRF/AICR) emphasise recommendations to improve individual behaviour, including avoidance of tobacco products, maintaining a lean body mass, participating in physical activity, consuming a plant-based diet, and minimising the consumption of energy-dense foods, such as sodas, red and processed meats and alcohol. In the present study of 275 healthy premenopausal women, we explored the association of adherence scores with levels of three biomarkers of antioxidant and inflammation status: serum C-reactive protein (CRP), serum γ-tocopherol and urinary F2-isoprostane. The statistical analysis applied linear regression across categories of adherence to WCRF/AICR recommendations. Overall, seventy-two women were classified as low ( ≤ 4), 150 as moderate (5–6), and fifty-three as high adherers ( ≥ 7). The unadjusted means for CRP were 2·7, 2·0 and 1·7 mg/l for low, moderate and high adherers (Ptrend= 0·03); this association was strengthened after adjustment for confounders (Ptrend= 0·006). The respective values for serum γ-tocopherol were 1·97, 1·63 and 1·45 μg/ml (Ptrend= 0·02 before and Ptrend= 0·03 after adjustment). Only for urinary F2-isoprostane, the lower values in high adherers (16·0, 14·5, and 13·3 ng/ml) did not reach statistical significance (Ptrend= 0·18). In an analysis by BMI, overweight and obese women had higher biomarker levels than normal weight women; the trend was significant for CRP (Ptrend< 0·001) and γ-tocopherol (Ptrend= 0·003) but not for F2-isoprostane (Ptrend= 0·14). These findings suggest that both adherence to the WCRF/AICR guidelines and normal BMI status are associated with lower levels of biomarkers that indicate oxidative stress and inflammation.

Vitamin D is unique among the vitamins in that man can synthesise it via the action of UV radiation upon the skin. This combined with its ability to act on specific target tissues via vitamin D receptors (VDR) make its classification as a steroid hormone more appropriate. While vitamin D deficiency is a recognised problem in some northern latitude countries, recent studies have shown that even in sunny countries, such as Australia, vitamin D deficiency may be more prevalent than first thought. Vitamin D is most well known for its role in bone health; however, the discovery of VDR on a wide variety of tissue types has also opened up roles for vitamin D far beyond traditional bone health. These include possible associations with autoimmune diseases such as multiple sclerosis and inflammatory bowel diseases, cancer, CVD and muscle strength. First, this paper presents an overview of the two sources of vitamin D: exposure to UVB radiation and food sources of vitamin D, with particular focus on both Australian and international studies on dietary vitamin D intake and national fortification strategies. Second, the paper reviews recent epidemiological and experimental evidence linking vitamin D and its role in health and disease for the major conditions linked to suboptimal vitamin D, while identifying significant gaps in the research and possible future directions for research.

Diet, nutritional status and lifestyle practices are significant determinants of the risk of certain cancers. In 1997 The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) developed a series of evidence-based recommendations to help reduce the population and individual risk of cancer. However, guidance for evaluating concordance or compliance with these recommendations is limited. To illustrate the challenges in evaluation, four publications were reviewed that explored the task of creating operative criteria from which to assess concordance with the tenets of the WCRF/AICR recommendations. Three documents dealt with secondary analysis, whereas one was a prospective inquiry, with procedures and instruments designed to obtain responses to WCRF/AICR cancer-prevention specification. One considered only population-goal criteria, and two dealt implicitly or explicitly with criteria at both population and individual levels. The assessment approaches used by the authors were compared with alternative semantic and conceptual interpretations of the WCRF/AICR population goals and individual guidelines. Attempts to develop operative criteria for assessment of concordance (reflecting either a more superficial or more in-depth parsing of recommendations) have been inconsistent. The results indicate that the language of the WCRF/AICR leaves a certain degree of semantic ambiguity for evaluation purposes. Future design of prospective studies for analyses of behaviours and relevant exposures (including those reported in the 2007 WCRF/AICR report) should carefully consider evaluation criteria and fully document detailed methodology.

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

While several effects beneficial to health have been attributed to the probiotic lactic acid bacteria, perhaps the most interesting and controversial remains that of anti-cancer activity. The vast majority of studies in this area deal with protective effects against colon cancer. There is no direct experimental evidence for cancer suppression in human subjects as a result of the consumption of probiotic cultures in fermented or unfermented dairy products. However, there is a wealth of indirect evidence, based largely on laboratory studies. Reports in the literature, regarding the anti-cancer effects of lactic acid bacteria, fall into the following categories: in vitro studies, animal studies, epidemiological studies and human dietary intervention studies. Examples of these reports will be given in the present review. The mechanisms by which probiotic bacteria may inhibit colon cancer are still poorly understood. However, several potential mechanisms are being discussed in the literature and these will also be addressed in the present review.

Although the biological requirement for vitamin D can be met by epidermal exposure to UV light, there are a number of conditions where this production does not occur or is not sufficient to meet biological needs. When this happens, vitamin D must be consumed and is a nutrient. However, two distinct observations have caused researchers to rethink certain dogma in vitamin D biology. First, it appears that in addition to the hormonally active form of 1,25 dihydroxyvitamin D (1,25(OH)2D), circulating levels of 25 hydroxyvitamin D have a critical importance for optimal human health. This and other data suggest that extra-renal production of 1,25(OH)2D contributes to Ca homeostasis and cancer prevention. Second, in addition to its role in the transcriptional activation of genes through the vitamin D receptor there is now compelling evidence that 1,25(OH)2D has a second molecular mode of action; the rapid activation of second-messenger and kinase pathways. The purpose of this second mode of action is only now being explored. The present review will discuss how these two areas are reshaping our understanding of vitamin D metabolism and action.

Over the past 20 years, a large number of epidemiological studies, particularly case-control and cohort studies, have been conducted to investigate the role of diet and the risk of developing different types of cancer. The most consistent finding so far is the association observed between consumption of vegetables and fruit and reduced risk of cancers of the digestive and respiratory tracts. More recently, evidence has accumulated indicating that high consumption of red meat (mainly beef, lamp and pork) and of preserved meat (‘charcuterie’) is specifically associated with a modest but significant increase in colorectal cancer risk. Finally, there is epidemiological evidence supporting an association between the risk of developing gastric cancer and the intake of salt and-preserved foods.

Cancer incidence and dietary habits vary substantially across Europe, and the expected benefit of dietary changes may be somewhat difference in different populations. Despite some uncertainly, it is generally agreed that an increase in the consumption of vegetables and fruits and a decrease in the intake of red meat, processed meat, alcoholic beverages, salt and salt-preserved foods should contribute to a reduction in the incidence of cancers of the digestive and respiratory tract.

Diet is an important factor in the causation of cancer. Previous systematic reviews of one-to-one interventions to encourage dietary change have found that such interventions can achieve modest improvements in diet. However, such interventions are resource intensive and unlikely to be good value for money at a population level. Interventions that address groups, communities or whole populations may be less resource intensive and effect change in a wider population. We report a systematic review of such interventions. We set wide inclusion criteria, including before-and-after studies and studies with a non-randomized comparison group as well as randomized trials. We found eighteen studies based in the community, seventeen based on worksites, five based in churches and one based in a supermarket. Interventions which targeted fruit and vegetable intake were most likely to be successful, particularly in worksites and churches. There was also evidence of small positive effects on reducing fat intake in worksites and churches. Overall the community-based interventions showed little effect. The studies included in the present review were generally poorly reported. Dietary changes are reported in the relatively short-term studies reviewed here but may not be sustained in the long term. The effects that we have identified are small but the reach is potentially very wide, in some cases as wide as a whole country. The cost effectiveness of such strategies remains to be evaluated.

Cancer is the major cause of death in the UK, and the Government has set a target to reduce death rate from cancer in individuals 75 years by ≥20% by 2010. Whilst earlier diagnosis and more effective treatments will contribute to meeting this target, there are considerable opportunities to prevent cancer by improving diet and other aspects of lifestyle. There is now a good understanding of the biological basis of carcinogenesis, which is providing the basis for mechanistic investigation of the chemo-preventive properties of certain foods and food components. It is becoming increasingly clear that there are important interactions between an individual's genotype (characterised by single nucleotide polymorphisms in particular genes) and habitual diet that modulate the risk of developing cancer. The technology to support this post-genomic revolution in nutrition research is now widely available, but brings with it considerable challenges in terms of study design and ethics. However, in the absence of a robust body of evidence on which dietary strategies will benefit which individuals, soundly based genetically-targeted nutrition advice to the public on cancer prevention is a little way in the future.

Insulin-like growth factor I (IGF-I) and its main binding protein 3 (IGFBP-3) are multi-regulatory peptides important in tumour cell growth and survival. In the circulation, they occur in large quantities and are readily measured. Across a population, concentrations vary and this may impact on risk of cancers common in western societies. Emerging epidemiological evidence supports the notion that higher levels of IGF-I are associated with increased risk of pre-menopausal, but not post-menopausal, breast cancer. Higher levels of IGFBP-3 may also predict for increased risk of pre-menopausal breast cancer, but this is contrary to the conventional view that this peptide is tumour protective. Nutritional and lifestyle factors, important in breast cancer risk, also inter-relate with circulating levels of IGF-I, but in many circumstances, the relationships are complex. It is becoming increasingly important that the clinical breast oncologist understands the physiology of the IGF system and its potential role in cancer risk assessment and prevention.