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The global adoption of predominantly plant-based, sustainable, healthy diets will help reduce the risk of obesity-and malnutrition-related noncommunicable diseases while protecting the future health of our planet. This review examines the benefits and limitations of different types of plant-based diets in terms of health and nutrition, affordability and accessibility, cultural (ethical and religious) acceptability, and the environment (i.e., the 4 pillars underlying sustainable healthy diets). Results suggest that, without professional supervision, traditional plant-based diets (vegan, vegetarian, and pescatarian diets) can increase the risk of nutritional deficiencies among infants, children/adolescents, women, pregnant/lactating women, and the elderly. In contrast, flexitarian diets and territorial diversified diets (TDDs; e.g., Mediterranean and New Nordic diets) that include large quantities of plant-sourced foods, low amounts of red meat, and moderate amounts of poultry, fish, eggs, and dairy can meet the energy and nutrition needs of different populations without the need for dietary education or supplementation. Compared with vegan, vegetarian, and pescatarian diets, more diverse flexitarian diets and TDDs are associated with reduced volumes of food waste and may be more acceptable and easier to maintain for people who previously followed Western diets. Although flexitarian diets and TDDs have a greater impact on the environment than vegan, vegetarian, and pescatarian diets, the negative effects are considerably reduced compared with Western diets, especially if diets include locally sourced seasonal foods. Further studies are required to define more precisely optimal sustainable healthy diets for different populations and to ensure that diets are affordable and accessible to people in all countries. © 2021 The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.

Western diets are net acid-producing, based on their general characteristics of containing excessive amounts of grains in relation to their content of fruits and vegetables. The continuous consumption of acid-producing diets is countered by the renal excretion of the excess acid. However, when renal excretion is not adequate, as is the case in many older adults with mildly and moderately impaired renal function, other adaptations are employed to preserve neutrality. In adults who are unable to excrete the daily dietary acid load, the excess acid is buffered by bone. The mechanisms by which hydrogen ions affect bone have been well defined. Current evidence also indicates a role for muscle in preserving neutrality; however, the mechanism(s) by which this occurs have not been directly demonstrated. The evidence supporting the role of bone and muscle in defending against the development of frank metabolic acidosis are reviewed herein. This evidence stems from observational studies and randomized, controlled clinical trials. Gaps in the evidence that would be useful to fill are also indicated.

In this paper, we reviewed the role of dairy products in dietary zinc absorption. Dairy products can have a reasonable contribution for dietary zinc intake in Western diets, where dairy consumption is high. However, the co-ingestion of dairy products can also improve zinc absorption from other food products. Such improvements have been observed when dairy products (e.g., milk or yoghurt) were ingested together with food such as rice, tortillas or bread products, all of which are considered to be high-phytate foods with low inherent zinc absorption. For foods low in phytate, the co-ingestion of dairy products did not improve zinc absorption. Improved zinc absorption of zinc from high-phytate foods following co-ingestion with dairy products may be related to the beneficial effects of the citrate and phosphopeptides present in dairy products. Considering that the main dietary zinc sources in areas in the world where zinc deficiency is most prevalent are typically high in phytate, the inclusion of dairy products in meals may be a viable dietary strategy to improve zinc absorption.

Objective:To compare the dietary habits of children living in northern villages and in the capital of Greenland, given the reported transition from traditional to westernised diet in adults over recent decades, and to explore the association between consumption of marine mammals and fish (MMF) and the children’s metabolic profile and vitamin D status.Design:Children answered an FFQ encompassing sixty-four individual food types pooled into six food categories. Their pubertal stage, body fat, fitness level, metabolic profile (non-HDL-cholesterol, glycated Hb, insulin, glucose, high-sensitivity C-reactive protein) as well as serum 25-hydroxyvitamin D (25(OH)D) concentration were evaluated.Setting:Siorapaluk and Qaanaaq (north of Greenland) and Nuuk (west).Participants:Children aged 6–18 years (n 177).Results:MMF were most frequently eaten by children from Siorapaluk (mean (sd): 73·4 (14·1) times/month), followed by children from Qaanaaq (37·0 (25·0) times/month), and least often eaten by children from Nuuk (23·7 (24·6) times/month; P < 0·001). Children from Qaanaaq consumed ‘junk food’ more frequently (P < 0·001) and fruits and vegetables less frequently (P < 0·01) than children from Nuuk. MMF consumption was positively associated with serum 25(OH)D concentration (P < 0·05), but the overall prevalence of vitamin D deficiency was high (18 %). No association was found between MMF consumption and metabolic parameters.Conclusions:The dietary transition and influence of western diets have spread to the north of Greenland and only the most remote place consumed a traditional diet highly based on MMF. We found no strong associations of MMF consumption with metabolic health, but a positive association with vitamin D status.

Nutrition transition, defined as a shift in dietary patterns and energy expenditure, is a major concern worldwide and especially in low and middle-income countries. Nutrition transition is linked to an increased prevalence of metabolic disorders and non-communicable diseases such as obesity, diabetes and cardiovascular diseases. In regions such as the sub-Saharan Africa, prevalence of overweight and obesity has steadily increased in the recent years despite the high prevalence of hunger and malnutrition. Factors that have contributed to nutrition transition include urbanization, socio-economic developments and technological advancements. Food consumption in some households has shifted to diets rich in fats and oils, calorie-based sweeteners, and animal-based products high in saturated fats (referred to as “western diets”), from traditional African diets based on legumes, whole grain products and traditional vegetables. Opportunities to slow down the effects of nutrition transition in Africa may exist through education and policy changes that are culturally sensitive.

Food additives such as titanium dioxide (E171), iron oxides and hydroxides (E172), silver (E174), and gold (E175) are highly used as colorants while silicon dioxide (E551) is generally used as anticaking in ultra-processed foodstuff highly used in the Western diets. These additives contain nanosized particles (1–100 nm) and there is a rising concern since these nanoparticles could exert major adverse effects due to they are not metabolized but are accumulated in several organs. Here, we analyze the evidence of gastrotoxicity, hepatotoxicity and the impact of microbiota on gut-brain and gut-liver axis induced by E171, E172, E174, E175 and E551 and their non-food grade nanosized counterparts after oral consumption. Although, no studies using these food additives have been performed to evaluate neurotoxicity or alterations in animal behavior, their non-food grade nanosized counterparts have been associated with stress, depression, cognitive and eating disorders as signs of animal behavior alterations. We identified that these food additives induce gastrotoxicity, hepatotoxicity and alterations in gut microbiota and most evidence points out oxidative stress as the main mechanism of toxicity, however, the role of oxidative stress as the main mechanism needs to be explored further.

Fructose is a major component of Western diets and is implicated in the pathogenesis of obesity and type 2 diabetes. In response to an oral challenge, the majority of fructose is cleared during “first-pass” liver metabolism, primarily via phosphorylation by ketohexokinase (KHK). A rare benign genetic deficiency in KHK, called essential fructosuria (EF), leads to altered fructose metabolism. The only reported symptom of EF is the appearance of fructose in the urine following either oral or intravenous fructose administration. Here we develop and use a mathematical model to investigate the adaptations to altered fructose metabolism in people with EF. First, the model is calibrated to fit available data in normal healthy subjects. Then, to mathematically represent EF subjects, we systematically implement metabolic adaptations such that model simulations match available data for this phenotype. We hypothesize that these modifications represent the major metabolic adaptations present in these subjects. This modeling approach suggests that several other aspects of fructose metabolism, beyond hepatic KHK deficiency, are altered and contribute to the etiology of this benign condition. Specifically, we predict that fructose absorption into the portal vein is altered, peripheral metabolism is slowed, renal reabsorption of fructose is mostly ablated, and alternate pathways for hepatic metabolism of fructose are upregulated. Moreover, these findings have implications for drug discovery and development, suggesting that the therapeutic targeting of fructose metabolism could lead to unexpected metabolic adaptations, potentially due to a physiological response to high-fructose conditions.

Obesity afflicts 36.5% of the US population and 600 million individuals world-wide. Thus, it is imperative to understand the risk factors underlying metabolic disease including diet, activity level, sleep, and genetics. Another key contributory factor is the gut microbiota given its widely reported role in the development of metabolic disease. The gut microbiota, particularly its structure and function, is heavily influenced by Western style diets rich in a complex mixture of fats and high in simple sugars. In this review, the profound impact of obesity and Western diets on the gut microbiota will be illustrated, and the following research questions will be addressed: 1) to what extent do high fat diets (HFDs) alter community membership and function and does this depend upon the amount or type of fat consumed?, 2) how rapidly do dietary shifts alter gut microbial communities?, 3) are these alterations sustained or can the microbiome recover from dietary stress?, 4) how does diet drive host-microbe interactions leading to obesity?, and 5) what can be done to restore the detrimental impact of HFD on the gut microbiota? The goal of this review is to address these questions by parsing out the effects and underlying mechanisms of how Western diets impact the gut microbiota and host. By doing so, potential avenues for further exploration and strategies for microbiome-based interventions to prevent or treat diet-induced obesity may become more apparent.

Selected subpopulations of hypothalamic neurons play important roles in the regulation of whole body energy homeostasis. Studies have shown that the saturated fats present in large amounts in western diets can activate an inflammatory response in the hypothalamus, affecting the capacity of such neurons to respond appropriately to satiety and adipostatic signals. In the first part of this review, we will explore the mechanisms behind saturated fatty acid-induced hypothalamic dysfunction. Next, we will present and discuss recent studies that have identified the mechanisms that mediate some of the anti-inflammatory actions of unsaturated fatty acids in the hypothalamus and the potential for exploring these mechanisms to prevent or treat obesity.

Spirulina (Arthrospira platensis) is currently being increasingly researched for its usability and suitability in human nutrition. The inclusion of alternative protein sources, such as spirulina, in familiar products is a possible strategy to nudge consumers towards dietary change in Western societies. Filled pasta variants with three levels of spirulina-soy-extrudate in the filling (10%, 30% or 50%) were developed and investigated for their sensory characteristics and consumer liking. Recipe development was based on the concepts of flavor-flavor learning (beet-ginger or tomato) and masking (lemon-basil) to account for the musty and earthy notes of the alga. Consumer tests were conducted in Germany (n = 139), the Netherlands (n = 137) and France (n = 144), and conventional sensory profiling was accomplished with trained panelists (n = 12). Consumers preferred the lemon-basil flavor over tomato and beet-ginger flavored fillings. As expected, liking decreased with increased extrudate content, regardless of the flavor. For all flavors expected liking was higher than liking after product exposure; for the lemon-basil flavor the gap was the smallest. It was shown that low general food neophobia and familiarity with spirulina promoted consumer liking. The sensory profiling revealed that the spirulina-soy-extrudate content affected all sensory attributes identified across all flavors, but for the tomato flavor the most. Overall, this study confirms that it is important to consider differences in consumer motivation as well as the product’s conceptual and intrinsic sensory characteristics in new product development.

Recent studies report that microbiota in the human intestine play an important role in host health and that both long- and short-term diets influence gut microbiota. These findings have fueled interest in the potential of food to promote health by shaping the intestinal microbiota. Despite the fact that large populations in Asia consume high quantities of carbohydrates, such diets have been ignored in comparison to the attention received by Western diets containing high quantities of fat and animal protein. We gathered data that suggest an association between imbalanced high-carbohydrate intake and gut microbiota and host health. In this review, we identify not only the effect of total carbohydrates on the intestinal microbiota specifically and the health of their hosts in general, but also how specific types of carbohydrates influence both factors.

open access journal Exposure of UFA-containing culinary frying oils (CFOs), especially PUFA-rich ones, to high temperature frying episodes produces substantial, highly toxicologically-significant concentrations of reactive aldehydes, together with additional lipid oxidation products (LOPs), via a complex series of oxidative recycling bursts. Migration of thermally-stressed, peroxidised frying oils into foods during standard frying practices renders such LOP toxins available for human consumption, and concentrations of trans-2-alkenals, trans,trans-alka-2,4-dienals and n-alkanals present in potato chips obtained from fast-food retailers and further food outlets are all much greater than those of acrylamide and monochloropropanediol adducts detectable, for which a verisimilitude of high level public health concerns have been repeatedly stressed in the scientific literature available. In view of our observations, such LOPs are likely to play pivotal roles regarding the development, progression and incidence of wide range of human non-communicable diseases (NCDs), which undoubtedly will promote rising healthcare costs worldwide. Indeed, 30-35% of human cancers arising from environmental sources are attributable to diet alone, and it is therefore highly conceivable that dietary LOPs may impact significantly on this incidence level. Hence, exacting efforts to limit the consumption of foods fried in CFOs with high LOP contents are required. Since CFOs rich in peroxidation-resistant MUFAs, and especially SFAs, produce lower and much lower levels of such LOP toxins during frying episodes respectively, they offer safer, health-friendly alternatives to those laden with PUFAs. However, the future consideration, establishment and ratification of currently-unavailable minimal human daily intakes for LOPs of known molecular identities also represent major demands for action. Consumer concerns regarding the nutritional and health properties of their foods strongly support such requirements.

Milk is an important source of vitamins and minerals in Western diets. Both genetic and management factors influence the mineral content of milk. Furthermore, milk contains relatively high levels of riboflavin. However, little is known about factors influencing variation in riboflavin level in milk. The seasonal variation in the content of riboflavin, calcium, phosphorus and magnesium of bulk tank milk from one organic and two conventional dairies was therefore investigated. Results showed lower mineral contents for milk from the organic dairy compared with milk from the conventional dairies. For all minerals, there was a significant effect of season, whereas the riboflavin content varied only significantly across the year in milk from the organic dairy, resulting in lower levels during summer and higher levels during the indoor winter period. Despite this variation, milk from the organic dairy generally contained more riboflavin than milk from the two conventional dairies.

Obesity is becoming a major health issue in the world due to sedentary lifestyles and increasing intake of Western diets. Obesity is associated with metabolic abnormalities and atherosclerotic cardiovascular diseases. Adipose tissue has been increasingly considered to play a critical role in inducing metabolic disturbances and promoting atherogenesis. Arterial wall imaging permits direct visualization of atheroma burden in various vascular beds. In addition, recent advances in imaging technology help characterize components, microstructures and functional features of atherosclerotic plaques. These imaging modalities have contributed to elucidating factors associated with atherosclerosis in obese patients. Also, it provides opportunities to evaluate the effect of novel therapies on plaques in the setting of obesity. The findings of recent imaging studies and the clinical implications will be reviewed.

With the prevalence of western diets (i.e. high fat plus high protein foods), the morbidity of T2DM and metabolic syndrome are increasingly high. Accumulating evidences point out that plasma branched chain amino acids (BCAA, the essential amino acids compromising 20% of the protein intake) level is

Chronic disease is a major social challenge of the twenty-first century. In this review, we examine the evidence for discordance between modern diets and those on which humankind evolved as the cause of the increasing incidence of chronic diseases, and the evidence supporting consumption of plant foods as a way to reduce the risk of chronic disease. We also examine the evidence for avoiding certain components of plant-based foods that are enriched in Western diets, and review the mechanisms by which different phytonutrients are thought to reduce the risk of chronic disease. This body of evidence strongly suggests that consuming more fruits and vegetables could contribute both to medical nutrition therapies, as part of a package of treatments for conditions like type 2 diabetes, heart disease, cancer, and obesity, and to the prevention of these diseases. Plant science should be directed toward improving the quality of plant-based foods by building on our improved understanding of the complex relationships between plants, our diet, and our health.

C-reactive protein (CRP) is a marker of subclinical inflammation increased by Western diets and reduced by healthy dietary patterns, such as the Mediterranean diet. The role of dietary components is more controversial. Saturated and trans fatty acids may increase, whereas n-3 polyunsaturated fatty acids, either of plant and marine origin, may decrease CRP levels. Controversy in intervention studies may relate to differences in study design, including subjects' characteristics, dietary sources of fats, often-underpowered sample size, and type of comparator. Genetic factors influencing responses to dietary fats could contribute to interindividual heterogeneity. Available evidence does not allow envisaging in patients with diabetes different behaviors or mechanisms for dietary fats effects on inflammation than in nondiabetic populations. Although “ad hoc studies” are needed to clarify the role of confounding factors, the observed changes in CRP are in line with current recommended consumption of dietary fats.

El objetivo de la presente revisión es estudiar la relación entre los flavonoides y el cáncer de pulmón, postulando que su consumo habitual en la dieta occidental podría resultar beneficioso para proteger a los pacientes contra el cáncer de pulmón. Se realizó una extensa búsqueda de publicaciones científicas recientes en las siguientes bases de datos electrónicas especializadas: PubMed central (PMC)-NCBI, Elsevier Journal, SciELO España, Scirus y Science Direct, incluyendo estudios en células, animales y humanos sobre el efecto de los flavonoides en la prevención y el desarrollo de cáncer de pulmón. Pese a que los estudios in vitro y en modelos animales muestran la capacidad potencial de los flavonoides para actuar contra diferentes tipos de cáncer, y en especial contra el riesgo de padecer cáncer de pulmón, la presencia de datos contradictorios en los estudios epidemiológicos y la falta de estudios clínicos en humanos actualmente impiden realizar recomendaciones dietéticas basadas en la evidencia científica para los pacientes con cáncer de pulmón. Así, los autores del presente artículo recomiendan seguir los consejos de las guías de alimentación saludable, las cuales promocionan el consumo de alimentos ricos en flavonoides y reflejan el conocimiento necesario para tratar a los pacientes con cáncer de pulmón.Erratum in: Rev Esp Nutr Hum Diet. 2013;17(2):91-92Link: http://www.renhyd.org/index.php/renhyd/article/view/6/17

Magnesium is an essential cation for many important biological functions such as metabolism, muscle contraction, blood pressure, neurological function, to name just a few. Standard Western diets are low in magnesium due to the plethora of refined foods and the often low intake of fruit and vegetables. As a consequence, a modest to mild hypomagnesemia is observed in a large number of individuals [1]. A Korean research group [2] recently conducted a meta-analysis of epidemiological studies aimed at [...]

Fructose is consumed in significant amounts in Western diets. An increase in fructose consumption over the past 10-20 years has been linked with a rise in obesity and metabolic disorders. Fructose/sucrose produces deleterious metabolic effects in animal models. This raises concern regarding the short-term and long-term effects of fructose and its risk in humans.In rodents, fructose stimulates lipogenesis and leads to hepatic and extrahepatic insulin resistance, dyslipidaemia and high blood pressure. Insulin resistance appears to be related to ectopic lipid deposition. In humans, short-term fructose feeding increases de-novo lipogenesis and blood triglycerides and causes hepatic insulin resistance. There is presently no evidence for fructose-induced muscle insulin resistance in humans. The cellular mechanisms underlying the metabolic effects of fructose involve production of reactive oxygen species, activation of cellular stress pathways and possibly an increase in uric acid synthesis.Consuming large amounts of fructose can lead to the development of a complete metabolic syndrome in rodents. In humans, fructose consumed in moderate to high quantities in the diet increases plasma triglycerides and alters hepatic glucose homeostasis, but does not appear to cause muscle insulin resistance or high blood pressure in the short term. Further human studies are required to delineate the effects of fructose in humans.

Fats are prevalent in western diets; they have known deleterious effects on muscle insulin resistance and may contribute to bone loss most notably in the elderly population. Because current treatments for osteoporosis may lead to important side effects, several studies aimed at investigating the relevance of nutritional approaches and most notably the role of lipid diets on bone health status. Literature has widely linked lipid intake and inflammation status, a key protagonist involved in bone resorption. Regarding inflammation, lipids exhibit a duality, with both pro- and anti-inflammatory effects depending on their structures and metabolism. In this light, a growing body of evidence has revealed that ω-6 increase bone loss while ω-3 are believed to protect bone health. Nevertheless, this debate remains controversial and the mechanisms of action are poorly understood.

Both obesity and consumption of unhealthy, yet palatable ‘Western diets’ (those high in saturated fatty acids and simple sugars) are associated with cognitive impairment in humans and in experimental animal models. Here we review findings that link obesity and increased adiposity with impairment of specific domains of cognitive function in humans. Next, data from humans and animal models are discussed that attribute cognitive impairment to Western diet intake independent of obesity development. Finally, recent data are highlighted showing that impaired neuroendocrine signaling in the hippocampus may be causally related to Western diet-induced cognitive dysfunction.

Cholesterol and triglyceride-rich Western diets are typically associated with an increased occurrence of type 2 diabetes and vascular diseases. This study aimed to assess the relative impact of dietary cholesterol and triglycerides on glucose tolerance, insulin sensitivity, atherosclerotic plaque formation, and endothelial function. C57BL6 wild-type (C57) mice were compared with atherosclerotic LDLr−/− ApoB100/100 (LRKOB100) and atherosclerotic/diabetic IGF-II × LDLr−/− ApoB100/100 (LRKOB100/IGF) mice. Each group was fed either a standard chow diet, a 0.2% cholesterol diet, a high-fat diet (HFD), or a high-fat 0.2% cholesterol diet for 6 mo. The triglyceride-rich HFD increased body weight, glucose intolerance, and insulin resistance but did not alter endothelial function or atherosclerotic plaque formation. Dietary cholesterol, however, increased plaque formation in LRKOB100 and LRKOB100/IGF animals and decreased endothelial function regardless of genotype. However, cholesterol was not associated with an increase of insulin resistance in LRKOB100 and LRKOB100/IGF mice and, unexpectedly, was even found to reduce the insulin-resistant effect of dietary triglycerides in these animals. Our data indicate that dietary triglycerides and cholesterol have distinct metabolic and vascular effects in obese atherogenic mouse models resulting in dissociation between the impairment of glucose homeostasis and the development of atherosclerosis.

The methylnitrosourea-induced model of ER+ mammary cancer in female Sprague-Dawley rats has been routinely used to screen for chemopreventive agents. We recently reported that metformin was ineffective in reducing cancer formation in rats on a standard (4% fat) diet (Thompson, et al., Cancer Prev Res. 8, 231, 2015). In the present studies, rats were placed on a standard (Teklad) diet or on a Western diet (20% fat, low calcium) at 43 days of age (DOA), and administered MNU at 50 DOA. Rats were administered metformin or vehicle daily by gavage beginning at 57 days of age. Serum from the rats of the various groups was obtained both at 21 days following initial administration of metformin (or vehicle) and at the end of the study (when tumors had developed in most rats). We found an increase in the final body weights, number of mammary cancers, and the final weights of tumors in rats on western diet compared with standard diet. Furthermore, metformin failed to decrease tumor multiplicity in either diet, in fact, it increased final cancer weights (P Citation Format: Mark S. Miller, Matthew D. Thompson, Ronald A. Lubet, Vernon E. Steele, Harold E. Seifried, Clinton J. Grubbs. Effects of metfornin on mammary carcinogenesis and metabolic profiles in methylnitrosourea-treated rats on standard or Western diets. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 824.

The pathophysiology of atopic diseases, including asthma and allergy, is the result of complex gene–environment interactions. Since European colonization the Indigenous population of Australia has undergone significant changes with respect to their lifestyle as hunter-gatherers. These changes have had a detrimental effect on Aboriginal health, in part due to immunological modification. This review provides a comparative look at both the traditional Aboriginal/Indigenous diet and modern Western diets, examines some common allergies increasingly reported in contemporary Indigenous populations, and reviews concepts such the effect of vitamin deficiencies and changes in gut microbiota on immune function.

Modulation of the gut microbiota is an area of growing interest, particularly for its link to improving and maintaining the systemic health of the host. It has been suggested to have potential to reduce risk factors associated with chronic diseases, such as elevated cholesterol levels in coronary heart disease (CHD). Diets of our evolutionary ancestors were largely based on plant foods, high in dietary fiber and fermentable substrate, and our gut microbiota has evolved against a background of such diets. Therapeutic diets that mimic plant-based diets from the early phases of human evolution may result in drug-like cholesterol reductions. In contrast, typical Western diets low in dietary fiber and fermentable substrate, and high in saturated and trans fatty acids, are likely contributors to the increased need for pharmacological agents for cholesterol reduction. The gut microbiota of those consuming a Western diet are likely underutilized and depleted of metabolic fuels, resulting in a less than optimal gut microbial profile. As a result, this diet is mismatched to our archaic gut microbiota and, therefore, to our genome, which has changed relatively little since humans first appeared. While the exact mechanism by which the gut microbiota may modulate cholesterol levels still remains uncertain, end products of bacterial fermentation, particularly the short chain fatty acids (i.e., propionate), have been suggested as potential candidates. While more research is required to clarify the potential link between gut microbiota and CHD risk reduction, consuming a therapeutic diet rich in plant foods, dietary fiber, and fermentable substrate would be a useful strategy for improving systemic health, possibly by altering the gut microbiota.

Fructose consumption has increased dramatically in the last century in the Western diets, associated with a concomitant development of some physiopathologies like the metabolic syndrome, obesity and diabetes. While in rodent model the link between fructose consumption and the cited metabolic perturbations is today clear, the evidence that this could take place in humans at the current level of fructose consumption remains under debate. What is the significance of the data described in animal models when translated to humans? Can we trust on fructose?

Obesity is reaching pandemic proportions in Western society. It has resulted in increasing health care burden and decreasing life expectancy. Obesity is a complex, chronic disease, involving decades of pathophysiological changes and adaptation. Therefore, it is difficult ascertain the exact mechanisms for this long-term process in humans. To circumvent some of these issues, several surrogate models are available, including murine genetic loss-of-function mutations, transgenic gain-of-function mutations, polygenic models, and different environmental exposure models. The mouse model of diet-induced obesity has become one of the most important tools for understanding the interplay of high-fat Western diets and the development of obesity. The diet-induced obesity model closely mimics the increasingly availability of the high-fat/high-density foods in modern society over the past two decades, which are main contributors to the obesity trend in human. This model has lead to many discoveries of the important signalings in obesity, such as Akt and mTOR. The chapter describes protocols for diet induced-obesity model in mice and protocols for measuring insulin resistance and sensitivity.

Background : Colorectal cancer is a major cause of cancer death worldwide, and the prevalence in Nigeria appears to be increasing due to a shift to western diets. We undertook a retrospective analysis of colorectal cancers seen at the University of Benin Teaching Hospital, Benin City from January 1983 to December 2002. Methods : One hundred and two cases involving the large bowel were encountered. These were analysed for age, sex, site, histological type and clinical features. Results : The mean age was 44.5 +/-4.5 years. Males accounted for 56 (54.9%) cases, while 46(45.1%) were females. Seventy two (70.2%) of the tumours were located in the rectum. Adenocarcinoma was the predominant histological type, with 89 (87.2%) cases. Fifty two (51%) cases presented with intestinal obstruction. Conclusions : Conclusion, colorectal cancers are not rare in our environment as previously believed, though, the frequency in Benin City is relatively low.

Lipids include a diverse range of molecules, with triglycerides (also known as triacylglycerols) being the principal class in milk. Milk lipids typically contribute 8–10% of total energy intake in Western diets. Considerable research has been conducted on the positive nutritional effects of milk lipids in addition to investigation of their potential negative effects with respect to the so-called ‘diseases of affluence,’ including coronary heart disease (CHD), stroke, and certain cancers.

Historically, obesity was a disease of affluence; while the wealthy were able to afford ample, energy-dense food, the poor often went hungry. This pattern can still be seen in many developing countries, where lower socio-economic status (SES) is associated with food insecurity, inadequate energy intake, and malnutrition among both adults and children (UN FAO 2009). In such situations, obesity continues to be largely the preserve of those of greater affluence, although there is some evidence that this pattern is beginning to change as Western diets are increasingly adopted by middle and lower income urban populations within developing countries (Mendez et al. 2005; Wang and Lobstein 2006).

• Myalgic encephalomyelitis is a debilitating neurological disease affecting 3% of the adult population of Western countries.

• There is a rising prevalence of attention-deficit hyperactivity disorder defining the Richardson–Puri fatty acid model of attention-deficit hyperactivity disorder, suggesting association with fatty acid changes in the modern Western diet.

Western diets, which typically contain large amounts of energy-dense processed foods, together with a sedentary lifestyle are associated with increased cardiometabolic risk. We evaluated the long-term effects of consuming a low-calorie low-protein vegan diet or performing regular endurance exercise on cardiometabolic risk factors.In this cross-sectional study, cardiometabolic risk factors were evaluated in 21 sedentary subjects, who had been on a low-calorie low-protein raw vegan diet for 4.4 +/- 2.8 years, (mean age, 53.1 +/- 11 yrs), 21 body mass index (BMI)-matched endurance runners consuming Western diets, and 21 age- and gender-matched sedentary subjects, consuming Western diets.BMI was lower in the low-calorie low-protein vegan diet (21.3 +/- 3.1 kg/m(2)) and endurance runner (21.1 +/- 1.6 kg/m(2)) groups than in the sedentary Western diet group (26.5 +/- 2.7 kg/m(2)) (p0.005). Plasma concentrations of lipids, lipoproteins, glucose, insulin, C-reactive protein, blood pressure (BP), and carotid artery intima-media thickness were lower in the low-calorie low-protein vegan diet and runner groups than in the Western diet group (all p0.05). Both systolic and diastolic BP were lower in the low-calorie low-protein vegan diet group (104 +/- 15 and 62 +/- 11 mm Hg) than in BMI-matched endurance runners (122 +/- 13 and 72 +/- 9 mmHg) and Western diet group (132 +/- 14 and 79 +/- 8 mm Hg) (p0.001); BP values were directly associated with sodium intake and inversely associated with potassium and fiber intake.Long-term consumption of a low-calorie low-protein vegan diet or regular endurance exercise training is associated with low cardiometabolic risk. Moreover, our data suggest that specific components of a low-calorie low-protein vegan diet provide additional beneficial effects on blood pressure.

The relationship of dietary fatty acid intake and the risk of stroke has been the subject of numerous investigations. The results of studies of the effects of saturated fat have been conflicting making it difficult to reach a conclusion about saturated fat and stroke. Intake of n6 fatty acids, particularly linoleic acid, appears to be inversely related to stroke risk. Although concerns have been expressed about a possible increase in risk of hemorrhagic stroke related to long chain n3 intake caused by changes in the clotting ability of blood, the results suggest that these fatty acids, when consumed at levels found in typical Western diets, reduce the risk of ischemic stroke with no increase in risk of hemorrhagic stroke.

The treatment of psychiatric illness requires novel pharmacological strategies. There is a growing body of evidence examining the role of neuronal phospholipid abnormalities in the pathogenesis of psychiatric illness, particularly in schizophrenia. However, work in other conditions like mood disorders are also showing interesting outcomes with EPA supplementation. Diseases that are considered to have a genetic basis may be significantly influenced by environmental factors including dietary supplementation. The suggestion that EFA supplementation may prevent the onset of symptoms of a psychiatric disease or aberrant behaviour needs longitudinal randomized controlled research. In recent years the focus has shifted from omega-6 to omega-3. It is true that western diets have far more omega-6 than omega-3. In the 1980s, there were positive outcomes in research studies using GLA in schizophrenia (Vaddadi et al., 1989). Future research needs to incorporate studies using pure GLA. Research should not be restricted to parent fatty acid (omega-3) supplementation alone but be expanded to include bioactive down-the-chain metabolites. The recent identification of novel omega-3 derived mediators such as resolvins and neuroprotectins, which are a highly bioactive (1-10 nMol range), may well have some role to play in psychiatric disorders; however this remains highly speculative at this stage.

The statistics concerning weight, diet, and exercise in the United States are grim. Seventy-five percent of Americans fail to exercise at least 30 minutes a day. Obesity, low levels of physical activity, and Western diets rich in lipids and carbohydrates and poor in fruits and vegetables contribute to the intermediate medical conditions that increase stroke risk: hypertension, diabetes, and hyperlipidemia. The heartening aspect, however, is that these risk factors are potentially modifiable if clinicians identify and address the issues and patients comply with current recommendations.

G A A b st ra ct s diet alone group (p

There has been a disturbing increase in the incidence of pancreas cancer, especially in Western countries, during the present century. The only well-established aetiological factor of well-documented significance is the greater incidence of this cancer in tobacco smokers of all communities. Otherwise the reason for the increased incidence is not known but the pattern of increase has some similarities to the increased incidence of breast cancer in women and prostate cancer in men in Western communities. There is now well-documented evidence that the increase in breast and prostate cancers is at least partly related to diet. Typical modern Western diets have a low content of the naturally occurring plant hormones, the phyto-oestrogens, that are still plentiful in traditional diets of Asians and other communities with a low incidence of both breast and prostate cancer. This paper presents evidence to support the hypothesis that the increased incidence of pancreas cancer in Western communities may also be related to the relatively low dietary content and protective qualities of the naturally occurring plant hormones and related compounds. This paper presents evidence to support that hypothesis.

Obesity represents a major risk factor for the development of type 2 diabetes. Consumption of western diets and large amounts of soft-drinks contribute to excessive energy intake. Fructose, in the form of high-fructose-corn-syrup, is a component of soft-drinks and is thought to trigger hepatic lipotoxicity and insulin-resistance.

People in developed nations such as the United States and Canada have an increased risk of colon cancer. Fecal mutagens have been detected in the feces of individuals at high risk for colon cancer. We describe a rapid, sensitive, reliable, reproducible high-pressure liquid chromatography (HPLC) method for detecting fecapentaenes, the most active and chief mutagen found in human stool. We found fecapentaene in all the stool samples of adults on typical high-fat, low-fiber Western diets. These fecapentaene concentrations remained largely constant when subjects consumed constant diets. Fecapentaene concentrations were reduced for total-parenteral-nutrition (TPN) patients with severe intestinal malabsorption. This finding with TPN patients may reflect changes in important variables of gut microflora in fecapentaene production. Studies with newborns and children showed that fecapentaenes appeared very early in life but are not present in stool at birth.

There is increasing evidence that alkali therapy can retard progression of chronic kidney disease (CKD). We summarize recent studies and discuss a mechanism whereby alkali therapy may neutralize acid production associated with typical Western diets, which generate acid. We emphasize the rationale for using alkali therapy early in the course of CKD, even in the absence of overt metabolic acidosis, and we urge the pharmaceutical industry to develop palatable alkali-containing solutions.

Of all dietary factors associated epidemiologically with cancer of various sites, fat has been studied the most thoroughly and has produced the greatest number of direct associations. Dietary fat is highly correlated with consumption of other nutrients present in the same foods, especially protein, in Western diets. Therefore, it is not always possible to attribute these associations to intake per se with absolute certainty.

The first seriotis attempt to classify genetic hyperlipidemias was made by Fredrickson and Lees (1965), who phenotyped the genetic hyperlipidemias into five familial types numbered I-V. Due to the extensive and thorough work done by Goldstein et al. (1973) and Motulsky (1976), we can today classify genetic hyperlipidemias differently.

To the Editor.— Although we agree with most of the comments of Keith Dahlberg, MD (1980;243:1062), on the Cambodian refugees and their treatment for malnutrition and other medical conditions, his recommendations on personal care for refugee workers are subject to further comments. For newly arriving refugee workers from nontropical environments who are not acclimatized to the heat, adequate hydration is a must. However, the use of salt tablets should not be encouraged; rather, supplemental table salt taken with meals along with sufficient fluids is recommended. 1 Salt tablets are often taken needlessly, irregularly, and not always with adequate fluids; their rate of disintegration in the gastrointestinal tract is unpredictable. Western diets frequently include too much salt; therefore, continuing to use the same amount of salt as we use at home will probably suffice for most people while working in the tropics.

M ounting interest has been generated over the past decade concerning the potential beneficial effects of n-3 fatty acids on atherosclerosis and atherothrombotic disorders. Substantial quantities of epidemiological and laboratory data have accumulated regarding n-3 fatty acids and atherosclerosis. 1,2 The purpose of this review is to summarize recent studies that have sought to elucidate the biochemical and cellular effects by which n-3 fatty acids might favorably affect atherogenesis. We will begin with a very brief review of the clinical and epidemiological data. EPIDEMIOLOGICAL, CLINICAL, AND EXPERIMENTAL OBSERVATIONS Epidemiological studies of Greenland and Alaskan Eskimos have demonstrated a substantially reduced mortality rate of ischemic heart disease in these populations compared with European and North American cohorts. 3,4 Analysis of the Eskimo diet revealed differences from typical Western diets, especially in the fatty acid content, which contained substantial quantities of n-3 fatty acids derived from marine sources. 5 Similar studies in