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 conclusion.,; with grades of confidence in the causality of associations and made recommendations. Recommendations are given as public health goals as well as for individuals.
Immunomodulatory actions of vitamin D have been recognised for over a quarter of a century, but it is only in the last few years that the significance of this to normal human physiology has become apparent. Two key factors have underpinned this revised perspective. Firstly, there are increasing data linking vitamin insufficiency with prevalent immune disorders. Improved awareness of low circulating levels of precursor 25-hydroxyvitamin D in populations across the globe has prompted epidemiological investigations of health problems associated with vitamin D insufficiency. Prominent among these are autoimmune diseases such as multiple sclerosis, type 1 diabetes and Crohn's disease, but more recent studies indicate that infections such as tuberculosis may also be linked to low 25-hydroxyvitamin D levels. The second factor expanding the link between vitamin D and the immune system is our improved knowledge of the mechanisms that facilitate this association. It is now clear that cells from the immune system contain all the machinery needed to convert 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D, and for subsequent responses to 1,25-dihydroxyvitamin D. Mechanisms such as this are important for promoting antimicrobial responses to pathogens in macrophages, and for regulating the maturation of antigen-presenting dendritic cells. The latter may be a key pathway by which vitamin D controls T-lymphocyte (T-cell) function. However, T-cells also exhibit direct responses to 1,25-dihydroxyvitamin D, notably the development of suppressor regulatory T-cells. Collectively these observations suggest that vitamin D is a key factor linking innate and adaptive immunity, and both of these functions may be compromised under conditions of vitamin D insufficiency.
Epidemiological evidence suggests that a high intake of plant foods is associated with lower risk of chronic diseases. However, the mechanism of action and the components involved in this effect have not been identified clearly. In recent years, the scientific community has agreed to focus its attention on a class of secondary metabolites extensively present in a wide range of plant foods: the flavonoids, suggested as having different biological roles. The anti-inflammatory actions of flavonoids in vitro or in cellular models involve the inhibition of the synthesis and activities of different pro-inflammatory mediators such as eicosanoids, cytokines, adhesion molecules and C-reactive protein. Molecular activities of flavonoids include inhibition of transcription factors such as NF-κB and activating protein-1 (AP-1), as well as activation of nuclear factor-erythroid 2-related factor 2 (Nrf2). However, the in vitro evidence might be somehow of limited impact due to the non-physiological concentrations utilized and to the fact that in vivo flavonoids are extensively metabolized to molecules with different chemical structures and activities compared with the ones originally present in the food. Human studies investigating the effect of flavonoids on markers of inflammation are insufficient, and are mainly focused on flavonoid-rich foods but not on pure molecules. Most of the studies lack assessment of flavonoid absorption or fail to associate an effect on inflammation with a change in circulating levels of flavonoids. Human trials with appropriate placebo and pure flavonoid molecules are needed to clarify if flavonoids represent ancillary ingredients or key molecules involved in the anti-inflammatory properties of plant foods. [PUBLICATION ABSTRACT
The terminology used for describing intervention groups in randomised controlled trials (RCT) on the effect of intravenous fluid on outcome in abdominal surgery has been imprecise, and the lack of standardised definitions of the terms 'standard', 'restricted' and 'liberal' has led to some confusion and difficulty in interpreting the literature. The aims of this paper were to clarify these definitions and to use them to perform a meta-analysis of nine RCT on primarily crystalloid-based peri-operative intravenous fluid therapy in 801 patients undergoing elective open abdominal surgery. Patients who received more or less fluids than those who received a 'balanced' amount were considered to be in a state of 'fluid imbalance'. When 'restricted' fluid regimens were compared with 'standard or liberal' fluid regimens, there was no difference in post-operative complication rates (risk ratio 0.96 (95% CI 0.56, 1.65), P = 0.89) or length of hospital stay (weighted mean difference (WMD) -1.77 (95% CI -4.36, 0.81) d, P = 0.18). However, when the fluid regimens were reclassified and patients were grouped into those who were managed in a state of fluid 'balance' or 'imbalance', the former group had significantly fewer complications (risk ratio 0.59 (95% CI 0.44, 0.81), P = 0.0008) and a shorter length of stay (WMD -3.44 (95% CI -6.33, -0.54) d, P = 0.02) than the latter. Using imprecise terminology, there was no apparent difference between the effects of fluid-restricted and standard or liberal fluid regimens on outcome in patients undergoing elective open abdominal surgery. However, patients managed in a state of fluid balance fared better than those managed in a state of fluid imbalance.
Vitamin D status may influence the risk of developing metabolic diseases such as Type 2 diabetes (T2D), metabolic syndrome (MetS) and insulin resistance (IR). Several studies have assessed vitamin D in relationship with metabolic outcomes; however, results remain inconsistent. A systematic review and meta-analysis using multiple databases (MEDLINE, Web of Science and EMBASE), was performed up to 10 August 2012. Prospective studies reporting association of circulating or dietary vitamin D with incident T2D, MetS and IR outcomes were included. Relative risks (RR) were pooled using random effects and subgroup analysis by pertinent study-level characteristics was performed. A total of seventeen articles based on eighteen unique prospective studies, and comprising 210 107 participants with 15 899 metabolic events, collected during a median follow up of 10 years (range 3-22 years), were included. RR for individuals in top v. bottom thirds of baseline vitamin D were 0.81 (95% CI 0.71, 0.92); 0.86 (95% CI 0.80, 0.92); and 0.84 (95% CI 0.64, 1.12) for T2D, MetS and IR outcomes, respectively. Moderate heterogeneity was found between fourteen studies (I-2 = 67%, P<0.001) reporting on T2D. Findings were generally consistent across various study-level characteristics. In conclusion, vitamin D status at baseline in apparently healthy adults is inversely associated with future risks of T2D and MetS. Interventions aimed at maintaining adequate levels of vitamin D in addition to preventing deficiency may be a useful preventive measure for metabolic diseases. However, reliable evidence from carefully designed intervention studies, particularly those based on healthy populations, is needed to confirm observational findings.
For nutrition practitioners and researchers, assessing dietary intake of children and adults with a high level of accuracy continues to be a challenge. Developments in mobile technologies have created a role for images in the assessment of dietary intake. The objective of this review was to examine peer-reviewed published papers covering development, evaluation and/ or validation of image-assisted or image-based dietary assessment methods from December 2013 to January 2016. Images taken with handheld devices or wearable cameras have been used to assist traditional dietary assessment methods for portion size estimations made by dietitians (image-assisted methods). Image-assisted approaches can supplement either dietary records or 24-h dietary recalls. In recent years, image-based approaches integrating application technology for mobile devices have been developed (image-based methods). Image-based approaches aim at capturing all eating occasions by images as the primary record of dietary intake, and therefore follow the methodology of food records. The present paper reviews several image-assisted and image-based methods, their benefits and challenges; followed by details on an image-based mobile food record. Mobile technology offers a wide range of feasible options for dietary assessment, which are easier to incorporate into daily routines. The presented studies illustrate that image-assisted methods can improve the accuracy of conventional dietary assessment methods by adding eating occasion detail via pictures captured by an individual (dynamic images). All of the studies reduced underreporting with the help of images compared with results with traditional assessment methods. Studies with larger sample sizes are needed to better delineate attributes with regards to age of user, degree of error and cost.
Se is an unusual trace element in having its own codon in mRNA that specifies its insertion into selenoproteins as selenocysteine (SeCys), by means of a mechanism requiring a large SeCys-insertion complex. This exacting insertion machinery for selenoprotein production has implications for the Se requirements for cancer prevention. If Se may protect against cancer, an adequate intake of Se is desirable. However, the level of intake in Europe and some parts of the world is not adequate for full expression of protective selenoproteins. The evidence for Se as a cancer preventive agent includes that from geographic, animal, prospective and intervention studies. Newly-published prospective studies on oesophageal, gastric-cardia and lung cancer have reinforced previous evidence, which is particularly strong for prostate cancer. Interventions with Se have shown benefit in reducing the risk of cancer incidence and mortality in all cancers combined, and specifically in liver, prostate, colo-rectal and lung cancers. The effect seems to be strongest in those individuals with the lowest Se status. As the level of Se that appears to be required for optimal effect is higher than that previously understood to be required to maximise the activity of selenoenzymes, the question has been raised as to whether selenoproteins are involved in the anti-cancer process. However, recent evidence showing an association between Se, reduction of DNA damage and oxidative stress together with data showing an effect of selenoprotein genotype on cancer risk implies that selenoproteins are indeed implicated. The likelihood of simultaneous and consecutive effects at different cancer stages still allows an important role for anti-cancer Se metabolites such as methyl selenol formed from gamma-glutamyl-selenomethyl-SeCys and selenomethyl-SeCys, components identified in certain plants and Se-enriched yeast that have anti-cancer effects. There is some evidence that Se may affect not only cancer risk but also progression and metastasis. Current primary and secondary prevention trials of Se are underway in the USA, including the Selenium and Vitamin E Cancer Prevention Trial (SELECT) relating to prostate cancer, although a large European trial is still desirable given the likelihood of a stronger effect in populations of lower Se status.
Progressive involuntary weight loss, in particular the loss of lean tissue, is common in patients with advanced cancer and has long been recognised to result in a deterioration in performance status and quality of life, increased morbidity and mortality. The aetiology of such weight loss or cachexia is complex and involves both tumour and host responses. Thus, identification of patients who are or are likely to become cachectic has been problematic. In addition to a reduction in appetite and increased satiety leading to poor dietary intake, there is now increasing clinical evidence that the activation of a chronic ongoing systemic inflammatory response is one of the earliest and most important contributory factors to cachexia. Such findings help to explain the failure of simple nutritional programmes to reverse weight loss adequately in patients with cancer. In the present paper the development of an inflammation-based score is described, which is derived from the acute-phase proteins C-reactive protein and albumin and is termed the Glasgow prognostic score (GPS). Its value as a predictor Of Survival, independent of tumour stage, performance status and treatment (active or palliative), has been shown in a variety of advanced common solid tumours. The nature of the relationship between the GPS, appetite, body composition, performance status and quality of life of the patient with advanced cancer will be described. Recently, it has become evident that the systemic inflammatory response is also present in a smaller proportion of patients with primary operable cancer and is also predictive of disease progression and poor survival. The role of GPS in clinical decision making will be discussed.
Epidemiological evidence suggests that a high intake of plant foods is associated with lower risk of chronic diseases. However, the mechanism of action and the components involved in this effect have not been identified clearly. In recent years, the scientific community has agreed to focus its attention on a class of secondary metabolites extensively present in a wide range of plant foods: the flavonoids, suggested as having different biological roles. The anti-inflammatory actions of flavonoids in vitro or in cellular models involve the inhibition of the synthesis and activities of different pro-inflammatory mediators such as eicosanoids, cyfokines, adhesion molecules and C-reactive protein. Molecular activities of flavonoids include inhibition of transcription factors such as NF-kappa B and activating protein-1 (AP-1), as well as activation of nuclear factor-erythroid 2-related factor 2 (Nrf2). However, the in vitro evidence might be somehow of limited impact due to the non-physiological concentrations utilized and to the fact that in vivo flavonoids are extensively metabolized to molecules with different chemical structures and activities compared with the ones originally present in the food. Human studies investigating the effect of flavonoids on markers of inflammation are insufficient, and are mainly focused on flavonoid-rich foods but not on pure molecules. Most of the studies lack assessment of flavonoid absorption or fail to associate an effect on inflammation with a change in circulating levels of flavonoids. Human trials with appropriate placebo and pure flavonoid molecules are needed to clarify if flavonoids represent ancillary ingredients or key molecules involved in the anti-inflammatory properties of plant foods.
This paper aims to describe different approaches for studying the overall diet with advantages and limitations. Studies of the overall diet have emerged because the relationship between dietary intake and health is very complex with all kinds of interactions. These cannot be captured well by studying single dietary components. Three main approaches to study the overall diet can be distinguished. The first method is researcher-defined scores or indices of diet quality. These are usually based on guidelines for a healthy diet or on diets known to be healthy. The second approach, using principal component or cluster analysis, is driven by the underlying dietary data. In principal component analysis, scales are derived based on the underlying relationships between food groups, whereas in cluster analysis, subgroups of the population are created with people that cluster together based on their dietary intake. A third approach includes methods that are driven by a combination of biological pathways and the underlying dietary data. Reduced rank regression defines linear combinations of food intakes that maximally explain nutrient intakes or intermediate markers of disease. Decision tree analysis identifies subgroups of a population whose members share dietary characteristics that influence (intermediate markers of) disease. It is concluded that all approaches have advantages and limitations and essentially answer different questions. The third approach is still more in an exploration phase, but seems to have great potential with complementary value. More insight into the utility of conducting studies on the overall diet can be gained if more attention is given to methodological issues.
Increasing evidence from the EU Project EARNEST and many other investigators demonstrates that early nutrition and lifestyle have long-term effects on later health and the risk of common non-communicable diseases (known as 'developmental programming'). Because of the increasing public health importance and the transgenerational nature of the problem, obesity and associated disorders are the focus of the new EU funded project 'EarlyNutrition'. Currently, three key hypotheses have been defined: the fuel mediated 'in utero' hypothesis suggests that intrauterine exposure to an excess of fuels, most notably glucose, causes permanent changes of the fetus that lead to obesity in postnatal life; the accelerated postnatal weight gain hypothesis proposes an association between rapid weight gain in infancy and an increased risk of later obesity and adverse outcomes; and the mismatch hypothesis suggests that experiencing a developmental 'mismatch' between a sub-optimal perinatal and an obesogenic childhood environment is related to a particular predisposition to obesity and corresponding co-morbidities. Using existing cohort studies, ongoing and novel intervention studies and a basic science programme to investigate those key hypotheses, project EarlyNutrition will provide the scientific foundations for evidence-based recommendations for optimal nutrition considering long-term health outcomes, with a focus on obesity and related disorders. Scientific and technical expertise in placental biology, epigenetics and metabolomics will provide understanding at the cellular and molecular level of the relationships between early life nutritional status and the risk of later adiposity. This will help refine strategies for intervention in early life to prevent obesity.
Proceedings of the Nutrition Society Non-alcoholic fatty liver disease (NAFLD) is considered to be the hepatic component of the metabolic syndrome and its prevalence is rapidly increasing due to its strong association with insulin resistance and obesity. At present, given that NAFLD is highly prevalent and therapies are limited, much attention is focused on identifying effective dietary strategies for the prevention and treatment of the disease. Polyphenols are a group of plant bioactive compounds whose regular consumption have been associated with a reduction in the risk of a number of metabolic disorders associated with NAFLD. Here we review the emerging and relatively consistent evidence from cell culture and rodent studies showing that select polyphenols positively modulate a variety of contributors to the NAFLD phenotype, through diverse and complementary mechanisms of action. In particular, the reduction of de novo lipogenesis (via sterol regulatory element-binding protein 1c) and increased fatty acid beta-oxidation, presumably involving AMP-activated protein kinase activation, will be discussed. The indirect antioxidant and anti-inflammatory properties of polyphenols which have been reported to contribute to the amelioration of NAFLD will also be addressed. In addition to a direct study of the liver, rodent studies have provided insight into the impact of polyphenols on adipose tissue function and whole body insulin sensitivity, which are likely to in part modulate their impact on NAFLD development. Finally an overview of the limited data from clinical trials will be given along with a discussion of the dose extrapolation from animal studies to human subjects.
Compelling evidence exists for the cardioprotective benefits resulting from consumption of fatty acids from fish oils, EPA (20:5n-3) and DHA (22:6n-3). EPA and DHA alter membrane fluidity, interact with transcription factors such as PPAR and sterol regulatory element binding protein, and are substrates for enzymes including cyclooxygenase, lipoxygenase and cytochrome P450. As a result, fish oils may improve cardiovascular health by altering lipid metabolism, inducing haemodynamic changes, decreasing arrhythmias, modulating platelet function, improving endothelial function and inhibiting inflammatory pathways. The independent effects of EPA and DHA are poorly understood. While both EPA and DHA decrease TAG levels, only DHA appears to increase HDL and LDL particle size. Evidence to date suggests that DHA is more efficient in decreasing blood pressure, heart rate and platelet aggregation compared to EPA. Fish oil consumption appears to improve arterial compliance and endothelial function; it is not yet clear as to whether differences exist between EPA and DHA in their vascular effects. In contrast, the beneficial effect of fish oils on inflammation and insulin sensitivity observed in vitro and in animal studies has not been confirmed in human subjects. Further investigation to clarify the relative effects of consuming EPA and DHA at a range of doses would enable elaboration of current understanding regarding cardioprotective effects of consuming oily fish and algal sources of long chain n-3 PUFA, and provide clearer evidence for the clinical therapeutic potential of consuming either EPA or DHA-rich oils.
There is now compelling evidence that growth patterns in early life are associated with risk of the metabolic syndrome in adulthood, although the relative importance of prenatal v. postnatal growth for such associations remains controversial. Body composition may play a key role in the 'programming' of such diseases, through itself being programmed by early growth, and perhaps also by being a mediator of the programming process. Early studies reporting positive associations between birth weight and adult BMI suggested a tendency for large babies to become obese adults. Such findings appeared contradictory to the many studies linking low birth weight with increased risk of the metabolic syndrome. Recent studies now indicate that birth weight is strongly predictive of later lean mass, and has a much weaker association with later fatness. Studies that link low birth weight with a more central adipose distribution in later life remain controversial, and require confirmation using more sophisticated methodologies. Findings for infant growth rate appear population-specific, with infant weight gain predicting subsequent lean mass in developing countries, but predicting subsequent fat mass and obesity in industrialised populations. Further studies are required on this issue, to ensure that appropriate public health policies are recommended for countries across the range of economic development. Although the links between early growth and later disease risk implicate early-life nutrition, either in utero or during infancy, few prospective studies have explored the influence of early diet on later body composition. Many studies have associated breast-feeding with a reduced prevalence of obesity categorised by BMI; however, the few studies directly evaluating childhood fatness provide little support for this hypothesis. Recent advances in the ability to measure body composition during the infant period offer a major opportunity to improve the understanding of the nutritional programming of body composition and its contribution, or lack thereof, to subsequent disease risk.
This paper presents emerging evidence linking visceral adiposity and the metabolic syndrome (MetSyn) with carcinogenesis. The link between obesity and cancer has been clearly identified in a multitude of robust epidemiological studies. Research is now focusing on the role of visceral adipose tissue in carcinogenesis; as it is recognised as an important metabolic tissue that secretes factors that systemically alter the immunological, metabolic and endocrine milieu. Excess visceral adipose tissue gives rise to a state of chronic systemic inflammation with associated insulin resistance and dysmetabolism, collectively known as the MetSyn. Prospective cohort studies have shown associations between visceral adiposity, the MetSyn and increased risk of breast cancer, colorectal cancer and oesophageal adenocarcinoma. Furthermore, visceral adiposity and the MetSyn have been associated with increased tumour progression and reduced survival. The mechanisms by which visceral adiposity and the MetSyn are thought to promote tumorigenesis are manifold. These include alterations in adipokine secretion and cell signalling pathways. In addition, hyperinsulinaemia, subsequent insulin resistance and stimulation of the insulin-like growth factor-1 axis have all been linked with visceral adiposity and promote tumour progression. Furthermore, the abundance of inflammatory cells in visceral adipose tissue, including macrophages and T-cells, create systemic inflammation and a pro-tumorigenic environment. It is clear from current research that excess visceral adiposity and associated dysmetabolism play a central role in the pathogenesis of certain cancer types. Further research is required to elucidate the exact mechanisms at play and identify potential targets for intervention.
Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease in both adults and children worldwide. As a disease spectrum, NAFLD may progress from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. An estimated 20-35% of the general population has steatosis, 10% of whom will develop the more progressive non-alcoholic steatohepatitis associated with markedly increased risk of cardiovascular- and liver-related mortality. Development of NAFLD is strongly linked to components of the metabolic syndrome including obesity, insulin resistance, dyslipidaemia and type 2 diabetes. The recognition that NAFLD is an independent risk factor for CVD is a major public health concern. There is a great need for a sensitive non-invasive test for the early detection and assessment of the stage of NAFLD that could also be used to monitor response to treatment. The cellular and molecular aetiology of NAFLD is multi-factorial; genetic polymorphisms influencing NAFLD have been identified and nutrition is a modifiable environmental factor influencing NAFLD progression. Weight loss through diet and exercise is the primary recommendation in the clinical management of NAFLD. The application of systems biology to the identification of NAFLD biomarkers and factors involved in NAFLD progression is an area of promising research.
In recent years focus-group interviews, as a means of qualitative data collection, have gained popularity amongst professionals within the health and social care arena. Despite this popularity, analysing qualitative data, particularly focus-group interviews, poses a challenge to most practitioner researchers. The present paper responds to the needs expressed by public health nutritionists, community dietitians and health development specialists following two training sessions organised collaboratively by the Health Development Agency, the Nutrition Society and the British Dietetic Association in 2003. The focus of the present paper is on the concepts and application of framework analysis, especially the use of Krueger's framework. It provides some practical steps for the analysis of individual data, as well as focus-group data using examples from the author's own research, in such a way as to assist the newcomer to qualitative research to engage with the methodology. Thus, it complements the papers by Draper (2004) and Fade (2004) that discuss in detail the complementary role of qualitative data in researching human behaviours, feelings and attitudes. Draper (2004) has provided theoretical and philosophical bases for qualitative data analysis. Fade (2004) has described interpretative phenomenology analysis as a method of analysing individual interview data. The present paper, using framework analysis concentrating on focus-group interviews, provides another approach to qualitative data analysis.
Nutritional epigenetics has emerged as a novel mechanism underlying gene-diet interactions, further elucidating the modulatory role of nutrition in aging and age-related disease development. Epigenetics is defined as a heritable modification to the DNA that regulates chromosome architecture and modulates gene expression without changes in the underlying bp sequence, ultimately determining phenotype from genotype. DNA methylation and post-translational histone modifications are classical levels of epigenetic regulation. Epigenetic phenomena are critical from embryonic development through the aging process, with aberrations in epigenetic patterns emerging as aetiological mechanisms in many age-related diseases such as cancer, CVD and neurodegenerative disorders. Nutrients can act as the source of epigenetic modifications and can regulate the placement of these modifications. Nutrients involved in one-carbon metabolism, namely folate, vitamin B-12, vitamin B-6, riboflavin, methionine, choline and betaine, are involved in DNA methylation by regulating levels of the universal methyl donor S-adenosylmethionine and methyltransferase inhibitor S-adenosylhomocysteine. Other nutrients and bioactive food components such as retinoic acid, resveratrol, curcumin, sulforaphane and tea polyphenols can modulate epigenetic patterns by altering the levels of S-adenosylmethionine and S-adenosylhomocysteine or directing the enzymes that catalyse DNA methylation and histone modifications. Aging and age-related diseases are associated with profound changes in epigenetic patterns, though it is not yet known whether these changes are programmatic or stochastic in nature. Future work in this field seeks to characterise the epigenetic pattern of healthy aging to ultimately identify nutritional measures to achieve this pattern.
In nutritional epidemiology, development of valid dietary assessment instruments specific to populations in diverse settings is of paramount importance. Such instruments are essential when trying to characterise dietary patterns and intake, investigate diet-disease associations, inform and evaluate nutrition interventions, assess nutrient-gene interactions, conduct cross-country comparison studies and monitor nutrition transitions. The FFQ is a relatively inexpensive tool for measuring long-term dietary intake for large populations and for allowing researchers to track dietary changes over time. However, FFQ must be population specific to capture the local diet and available foods. Collecting 24-h dietary recalls and utilising community feedback to build the FFQ ensures that a culturally appropriate instrument is developed. This article presents several examples describing FFQ development and utilisation in different settings globally. In the Canadian Arctic, FFQ were developed and utilised to inform and evaluate a community-based intervention programme, characterise the diet and track dietary changes occurring among Inuit and Inuvialuit, populations experiencing rising rates of chronic disease and likely to be extremely vulnerable to the potential effects of climate change. Another example is an FFQ developed to assess sodium intake and evaluate a sodium reduction trial in a high-risk population in Barbados. An example is provided from Brazil, where an FFQ was developed to assess associations between diet, heterocyclic aromatic amines and colorectal adenoma among Japanese Brazilians and to conduct cross-country comparisons. These and other case studies highlight the diversity in dietary intake between populations and the need for FFQ to be developed to capture this diversity.
In recent years, there has been a renewed interest in the role of dietary fibre in obesity management. Much of this interest stems from animal and human studies which suggest that an increased intake of fermentable fibre can suppress appetite and improve weight management. A growing number of reports have demonstrated that the principal products of colonic fermentation of dietary fibre, SCFA, contribute to energy homeostasis via effects on multiple cellular metabolic pathways and receptor-mediated mechanisms. In particular, over the past decade it has been identified that a widespread receptor system exists for SCFA. These G-protein-coupled receptors, free fatty acid receptor (FFAR) 2 and FFAR3 are expressed in numerous tissue sites, including the gut epithelium and adipose tissue. Investigations using FFAR2-or FFAR3-deficient animal models suggest that SCFA-mediated stimulation of these receptors enhances the release of the anorectic hormones peptide tyrosine tyrosine and glucagon-like peptide-1 from colonic L cells and leptin from adipocytes. In addition, the SCFA acetate has recently been shown to have a direct role in central appetite regulation. Furthermore, the SCFA propionate is a known precursor for hepatic glucose production, which has been reported to suppress feeding behaviour in ruminant studies through the stimulation of hepatic vagal afferents. The present review therefore proposes that an elevated colonic production of SCFA could stimulate numerous hormonal and neural signals at different organ and tissue sites that would cumulatively suppress short-term appetite and energy intake.