Published Science

Changing food consumption patterns and associated greenhouse gas (GHG) emissions have been a matter of scientific debate for decades. The agricultural sector is one of the major GHG emitters and thus holds a large potential for climate change mitigation through optimal management and dietary changes. We assess this potential, project emissions, and investigate dietary patterns and their changes globally on a per country basis between 1961 and 2007. Sixteen representative and spatially differentiated patterns with a per capita calorie intake ranging from 1,870 to >3,400 kcal/day were derived. Detailed analyses show that low calorie diets are decreasing worldwide, while in parallel diet composition is changing as well: a discernable shift towards more balanced diets in developing countries can be observed and steps towards more meat rich diets as a typical characteristics in developed countries. Low calorie diets which are mainly observable in developing countries show a similar emission burden than moderate and high calorie diets. This can be explained by a less efficient calorie production per unit of GHG emissions in developing countries. Very high calorie diets are common in the developed world and exhibit high total per capita emissions of 3.7-6.1 kg CO(2eq.)/day due to high carbon intensity and high intake of animal products. In case of an unbridled demographic growth and changing dietary patterns the projected emissions from agriculture will approach 20 Gt CO(2eq.)/yr by 2050.

Primates have proportionately three times larger brain as compared to that of other mammals of comparable size and humans, in turn, have three times larger brain as compared to that of all other primates of similar size. So we need to meet higher energy demands because brain is energetically expensive. This has a significant impact on our dietary patterns in addition to shaping of our body composition. Here we propose that our dietary patterns to meet our higher energy demands have been ultimately set by the instinct of higher energy intake and our larger brains have a stress effect on our metabolic organs (organs involved in energy metabolism like gut, liver, pancreas etc.). We discuss these two points from evolutionary (Evolutionary instinct) and physiological (Metabolic stress) point of view and argue that these two points explain the manifestation of diabetes primarily as a human disease and enhance our understanding of its mechanism.

Periods of deliberate fasting with restriction of solid food intake are practiced worldwide, mostly based on traditional, cultural or religious reasons. There is large empirical and observational evidence that medically supervised modified fasting (fasting cure, 200-500 kcal nutritional intake per day) with periods of 7-21 days is efficacious in the treatment of rheumatic diseases, chronic pain syndromes, hypertension, and metabolic syndrome. The beneficial effects of fasting followed by vegetarian diet in rheumatoid arthritis are confirmed by randomized controlled trials. Further beneficial effects of fasting are supported by observational data and abundant evidence from experimental research which found caloric restriction and intermittent fasting being associated with deceleration or prevention of most chronic degenerative and chronic inflammatory diseases. Intermittent fasting may also be useful as an accompanying treatment during chemotherapy of cancer. A further beneficial effect of fasting relates to improvements in sustainable lifestyle modification and adoption of a healthy diet, possibly mediated by fasting-induced mood enhancement. Various identified mechanisms of fasting point to its potential health-promoting effects, e.g., fasting-induced neuroendocrine activation and hormetic stress response, increased production of neurotrophic factors, reduced mitochondrial oxidative stress, general decrease of signals associated with aging, and promotion of autophagy. Fasting therapy might contribute to the prevention and treatment of chronic diseases and should be further evaluated in controlled clinical trials and observational studies.

Flavonoids or bioflavonoids are unique low molecular weight ubiquitous polyphenolic compounds produced by plants during their metabolic activities as a secondary metabolites and responsible for major organoleptic characteristics and health benefits of plant derived foods. The flavonoids are potent antioxidants agents and protect the cells by scavenging and inhibiting the production and initiation of free radicals, superoxide anions and lipid peroxy radicals. Besides potent antioxidant capacity, flavonoids also shows antimicrobial, antimutagenic, antidiabetic, antithrombosis, antirheumatic, antiatherosclerotic, antiallergic, anti-inflammatory, antiulcers and hepatoprotectives and better termed as neutraceuticals. The antioxidant capacity of meat is very low and this can be increased by adding flavonoids in meat during processing in the form of plant parts rich in flavonoids such as seeds, fruit skin or peel, bark and flower as raw or in extract form without comprising the sensory attributes of meat and meat products.

Objective Short sleep duration has been reported to be associated with obesity, type 2 diabetes, and pre-diabetes. Since excess weight, glucose abnormalities, and insulin resistance tend to cluster, the individual role insulin resistance may have in habitual shortened sleep is unclear. The study purpose was to assess whether habitual sleep curtailment is independently related to insulin resistance in obese individuals. Materials/Methods Non-diabetic, overweight/obese individuals from the community were stratified as insulin-resistant (n = 35) or insulin-sensitive (n = 21) based on steady-state plasma glucose concentrations (SSPG) during the insulin suppression test. Seventy-five gram oral glucose tolerance tests were performed. Participants were asked, "On average, how many hours of sleep do you get per night?" Shortened sleep duration was defined as less than 7 h of sleep per night. Results SSPG concentrations differed 2.5-fold (P \textless 0.001) between insulin-resistant and insulin-sensitive individuals. Impaired fasting glucose and glucose intolerance were prevalent in both groups (\textgreater 40%); however, body mass index, waist circumference, mean fasting or 2-h post-glucola glucose concentrations were not significantly different. Insulin-resistant individuals reported (mean ± SD) fewer hours of sleep than did insulin-sensitive individuals (6.53 ± 1.1 vs 7.24 ± 0.9 h, P \textless 0.05). Shortened sleep duration was more prevalent among insulin-resistant as compared with insulin-sensitive individuals (60% vs 24%, P \textless 0.05). Conclusions Non-diabetic, insulin-resistant individuals averaged fewer hours of sleep and were more likely to report shortened sleep duration as compared with similarly obese insulin-sensitive individuals. There appears to be an independent association between habitual shortened sleep and insulin resistance among obese, dysglycemic adults without diabetes. © 2013 Elsevier Inc.

Diabetes is a national health problem, and the burden of the disease and its consequences particularly affect Hispanics. While social determinants of health models have improved our conceptualization of how certain contexts and environments influence an individual's ability to make healthy choices, a structural violence framework transcends traditional uni-dimensional analysis. Thus, a structural violence approach is capable of revealing dynamics of social practices that operate across multiple dimensions of people's lives in ways that may not immediately appear related to health. Working with a Hispanic immigrant community in Albuquerque, New Mexico, we demonstrate how structural forces simultaneously directly inhibit access to appropriate healthcare services and create fear among immigrants, acting to further undermine health and nurture disparity. Although fear is not normally directly associated with diabetes health outcomes, in the community where we conducted this study participant narratives discussed fear and health as interconnected.

Glycation of low-density lipoprotein (LDL) increases its atherogenicity, but whether high-density lipoprotein (HDL) can protect LDL against glycation is not known. LDL and HDL were isolated from 32 volunteers with serum HDL cholesterol concentrations ranging from 0.76 to 2.01 (mean = 1.36) mmol/L. Glycation of LDL was induced by incubation with 0-80 mmol/L glucose for 7 days at 37°C under nitrogen in the presence of and absence of human HDL. Glycation of LDL apolipoprotein B (apoB) doubled at glucose 50 and 80 mmol/L (both p \textless 0.001), and this increase was ameliorated by HDL. In the absence of glucose, 0.11 (0.01) [mean (standard error, SE)] mg apoB/mg LDL protein was glycated increasing to 0.22 (0.02) mg/mg at glucose 80 mmol/L in the absence of HDL, but remaining at 0.13 (0.01) mg/mg when autologous HDL was present. Heterologous HDL from a further study of 12 healthy participants was similarly effective in impeding LDL apoB glycation. HDL impeded not only glycation but also the lipid peroxidation, free amino group consumption and increased electrophoretic mobility of LDL which accompanied glycation. HDL from participants with higher serum paraoxonase1 (PON1) was more effective in impeding glycation and the related processes. In conclusion, HDL can impede the glucose-induced glycoxidation of LDL. PON1 may be important for this function of HDL.

Consumption of added sugar has increased over recent decades and is correlated with numerous diseases. Rodent models have elucidated mechanisms of toxicity, but only at concentrations beyond typical human exposure. Here we show that comparatively low levels of added sugar consumption have substantial negative effects on mouse survival, competitive ability, and reproduction. Using Organismal Performance Assays--in which mice fed human-relevant concentrations of added sugar (25% kcal from a mixture of fructose and glucose, modeling high fructose corn syrup) and control mice compete in seminatural enclosures for territories, resources and mates--we demonstrate that fructose/glucose-fed females experience a twofold increase in mortality while fructose/glucose-fed males control 26% fewer territories and produce 25% less offspring. These findings represent the lowest level of sugar consumption shown to adversely affect mammalian health. Clinical defects of fructose/glucose-fed mice were decreased glucose clearance and increased fasting cholesterol. Our data highlight that physiological adversity can exist when clinical disruptions are minor, and suggest that Organismal Performance Assays represent a promising technique for unmasking negative effects of toxicants.

Debate concerning the environmental impact of human arrival in Australia has continued for more than a century. Here we review the evidence for human impact and the mechanisms by which humans may have affected the environment of tropical Australia. We limit our review to tropical Australia because, over three decades ago, it was proposed that the imposition of an anthropogenic fire regime upon human occupation of the Australian continent may have resulted in profound changes in regional vegetation and climate across this region. We conclude that ecological processes and vegetation–fire–climate–human feedbacks do exist that could have driven a significant shift in boundary conditions and ecosystem state at the sub-continental scale through the sustained imposition of an anthropogenic fire regime over tens of millennia. These potential feedbacks operate through the inhibition of forest expansion both directly, by targeted burning at established forest edges and newly irrupted forest patches, and indirectly, through lengthening of the dry season because of changes to the timing of burning. However, the impact of any such anthropogenic forcing may have been entirely overshadowed by the effects of natural climate change and variability, as well as the generally low nutrient status of Australian soils. A robust assessment of the degree to which the environment of tropical Australia at the large scale has been modified from its ‘natural’ state because of human occupation will require new, coordinated collaborations between indigenous traditional landowners, archaeologists, anthropologists, geochronologists, geoscientists, ecologists, climatologists and modellers.

Abstract Background: Fasting during the month of Ramadan is a religious obligation that is practiced by millions of people around the world yet there is no clear scientific consensus on its effects on cardiovascular disease. This study was performed to inform physicians as well as patients of evidence based recommendations on this subject. Aim: The study was undertaken to assess (1) Any alteration in the incidence of acute cardiac illness during Ramadan fasting? (2) Whether fasting during the month of Ramadan alter the clinical status of patients with stable cardiac disease? And (3) The impact of Ramadan fasting on cardiovascular risk factors in normal subjects, in patients with stable cardiac disease, metabolic syndrome, dyslipidemia, type 2 diabetes and systemic hypertension. Study design: Systematic review of the literature. Method: A Medline search of the English literature published between January 1980 and September 2012. Results: The incidence of acute cardiac illness during Ramadan fasting was sim...

OBJECTIVE: The optimal diet for weight loss in type 2 diabetes remains controversial. This study examined a low-carbohydrate, high-fat diet with detailed physiological assessments of insulin sensitivity, glycemic control, and risk factors for cardiovascular disease. METHODS: Fourteen obese patients (body mass index [BMI] 40.6 ± 4.9 kg/m(2)) with type 2 diabetes were recruited for an "Atkins"-type low-carbohydrate diet. Measurements were made at 0, 12, and 24 weeks of weight, insulin sensitivity, HbA1c, lipids, and blood pressure. RESULTS: Twelve completers lost a mean of 9.7 ± 1.8 kg over 24 weeks attributable to a major reduction in carbohydrates and resultant reduction in total energy intake. Glycemic control significantly improved (HbA1c -1.1 ± 0.25%) with reductions in hypoglycemic medication. Fasting glucose, homeostasis model assessment (HOMA), and area under the curve (AUC) glucose (intravenous glucose tolerance test [IVGTT]) were significantly reduced by week 12 ( p

Objective: To assess recent trends in nonalcoholic fatty liver disease (NAFLD) prevalence among US adolescents. Study design: Cross-sectional data from 12 714 12-19 year olds (exclusions: chronic hepatitis, hepatotoxic medications) in the National Health and Examination Survey between 1988-1994 and 2007-2010 were used to estimate trends in suspected NAFLD, defined as overweight (body mass index ≥85th percentile) plus elevated alanine aminotransferase levels (boys \textgreater25.8 U/L; girls \textgreater22.1 U/L). Linear trends in prevalence and the independent effect of demographic indicators and adiposity on NAFLD risk were tested using regression models. Complex sampling methods and P values of \textless.05 were used to assess statistical significance. Results: Suspected NAFLD prevalence (SE) rose from 3.9% (0.5) in 1988-1994 to 10.7% (0.9) in 2007-2010 (P \textless .0001), with increases among all race/ethnic subgroups, males and females, and those obese (P trend ≤.0006 for all). Among those obese, the multivariate adjusted odds of suspected NAFLD were higher with increased age, body mass index, Mexican American race, and male sex; the adjusted odds in 2007-2010 were 2.0 times those in 1988-1994. In 2007-2010, 48.1% (3.7) of all obese males and 56.0% (3.5) of obese Mexican American males had suspected NAFLD. Conclusion: Prevalence of suspected NAFLD has more than doubled over the past 20 years and currently affects nearly 11% of adolescents and one-half of obese males. The rapid increase among those obese, independent of body mass index, suggests that other modifiable risk factors have influenced this trend. Copyright © 2013 Mosby Inc.

Insulin signalling is uniquely required for storing energy as fat in humans. While de novo synthesis of fatty acids and triacylglycerol occurs mostly in liver, adipose tissue is the primary site for triacylglycerol storage. Insulin signalling mechanisms in adipose tissue that stimulate hydrolysis of circulating triacylglycerol, uptake of the released fatty acids and their conversion to triacylglycerol are poorly understood. New findings include (1) activation of DNA-dependent protein kinase to stimulate upstream stimulatory factor (USF)1/USF2 heterodimers, enhancing the lipogenic transcription factor sterol regulatory element binding protein 1c (SREBP1c); (2) stimulation of fatty acid synthase through AMP kinase modulation; (3) mobilisation of lipid droplet proteins to promote retention of triacylglycerol; and (4) upregulation of a novel carbohydrate response element binding protein β isoform that potently stimulates transcription of lipogenic enzymes. Additionally, insulin signalling through mammalian target of rapamycin to activate transcription and processing of SREBP1c described in liver may apply to adipose tissue. Paradoxically, insulin resistance in obesity and type 2 diabetes is associated with increased triacylglycerol synthesis in liver, while it is decreased in adipose tissue. This and other mysteries about insulin signalling and insulin resistance in adipose tissue make this topic especially fertile for future research.

Colorectal cancer (CRC) is the most common gastrointestinal cancer, and a significant health care problem globally. Dietary factors, for example high meat consumption and deficiency of fiber, calcium, vitamin D, and folate, are well-recognized to be associated with a risk of developing CRC. Colonic microbiota, by living in a mutual relationship and participating in key metabolic functions that compliment host physiology, is crucially important in the maintenance of our health. A state of imbalance in host-microbe homeostasis, termed dysbiosis, is associated with several diseases, including CRC. Epidemiological studies have revealed strong associations between diet, microbiota, and CRC. Substantial in-vitro and in-vivo evidence suggests that the dynamic composition and diversity of colonic microbiota are affected by alteration of the diet, and that the balance between the beneficial and detrimental microbial metabolites is of crucial importance in mediation of the dietary risk factors of colonic carcinogenesis. A better understanding of complex diet-microbiota-CRC relationships can help us understand how diet affects the risk of CRC and will provide a more scientific approach to the development of novel strategies to prevent CRC. © 2013 Springer Science+Business Media New York.

Increasingly, patients and members of the public are involved in the design, conduct and dissemination of research. INVOLVE, the UK's national body for patient and public involvement, usefully defines this sort of involvement as: 'research being carried out " with " or " by " members of the public rather than " to " , " about " or " for " them' (INVOLVE, 2012). At the Musculoskeletal Research Unit in Bristol, we are often asked about our patient involvement work. In light of the questions that we are asked, this editorial highlights some current practice and guidance. We also reflect on the impact of our patient involvement activity and hope that this serves as a useful in-troduction and points interested readers to further reading. Why involve patients in research? Rationale for involving patients in study design are multi-ple, and include moral and ethical arguments about citi-zens' rights, increasing relevance of research, and the view that doing so can improve research quality, although this may be hard to define (Fudge et al., 2008; Gibson et al., 2012; Ward et al., 2010). There are many examples of pa-tient involvement in research, and patients have been in-volved at different stages in the research process, including: • Identification of research priorities and agenda

BACKGROUND/AIM: In Poland, vegetarian diets are becoming more and more popular. The aim of this study was to examine the effect of iron intake on iron status in vegetarian children. METHODS: Dietary iron intake, iron food sources, blood count, serum iron, ferritin level and total iron-binding capacity were estimated in two groups of children, namely vegetarians (n = 22) and omnivores (n = 18) of both sexes, aged from 2 to 18 years. Seven-day food records were used to assess their diet. RESULTS: Dietary iron intake in vegetarians and omnivores was low (up to 65.0 and 60.1% of the recommended dietary allowance). A significantly higher intake of vitamin C was observed in vegetarians compared with omnivores (p = 0.019). The main sources of iron in vegetarians were cereal products, followed by vegetables and mushroom products, then fruit. The prevalence of iron deficiency (ID) was higher in the vegetarian group (p = 0.023). The serum ferritin level and mean corpuscular volume in the vegetarians were also lower than in the omnivores (p = 0.01 and p = 0.014, respectively). CONCLUSIONS: Children who follow a vegetarian diet may suffer from ID in spite of having a high vitamin C intake. This indicates the need to introduce dietary education and iron status monitoring.

Autism spectrum disorders share three core symptoms: impaired sociability, repetitive behaviors and communication deficits. Incidence is rising, and current treatments are inadequate. Seizures are a common comorbidity, and since the 1920's a high-fat, low-carbohydrate ketogenic diet has been used to treat epilepsy. Evidence suggests the ketogenic diet and analogous metabolic approaches may benefit diverse neurological disorders. Here we show that a ketogenic diet improves autistic behaviors in the BTBR mouse. Juvenile BTBR mice were fed standard or ketogenic diet for three weeks and tested for sociability, self-directed repetitive behavior, and communication. In separate experiments, spontaneous intrahippocampal EEGs and tests of seizure susceptibility (6 Hz corneal stimulation, flurothyl, SKF83822, pentylenetetrazole) were compared between BTBR and control (C57Bl/6) mice. Ketogenic diet-fed BTBR mice showed increased sociability in a three-chamber test, decreased self-directed repetitive behavior, and improved social communication of a food preference. Although seizures are a common comorbidity with autism, BTBR mice fed a standard diet exhibit neither spontaneous seizures nor abnormal EEG, and have increased seizure susceptibility in just one of four tests. Thus, behavioral improvements are dissociable from any antiseizure effect. Our results suggest that a ketogenic diet improves multiple autistic behaviors in the BTBR mouse model. Therefore, ketogenic diets or analogous metabolic strategies may offer novel opportunities to improve core behavioral symptoms of autism spectrum disorders.

The research presented here is primarily concerned with human-environment interactions on the tropical coast of northern Australia during the late Holocene. Based on the suggestion that significant change can occur within short time-frames as a direct result of interactive processes, the archaeological evidence from the Point Blane Peninsula, Blue Mud Bay, is used to address the issue of how much change and variability occurred in hunter-gatherer economic and social structures during the late Holocene in coastal northeastern Arnhem Land. The suggestion proposed here is that processes of environmental and climatic change resulted in changes in resource distribution and abundance, which in turn affected patterns of settlement and resource exploitation strategies, levels of mobility and, potentially, the size of foraging groups on the coast. The question of human behavioural variability over the last 3000 years in Blue Mud Bay has been addressed by examining issues of scale and resolution in archaeological interpretation, specifically the differential chronological and spatial patterning of shell midden and mound sites on the peninsula in conjunction with variability in molluscan resource exploitation. To this end, the biological and ecological characteristics of the dominant molluscan species is considered in detail, in combination with assessing the potential for human impact through predation. Investigating pre-contact coastal foraging behaviour via the archaeological record provides an opportunity for change to recognised in a number of ways. For example, a differential focus on resources, variations in group size and levels of mobility can all be identified. It has also been shown that human-environment interactions are non-linear or progressive, and that human behaviour during the late Holocene was both flexible and dynamic.

OBJECTIVE: Low-carbohydrate diets and their combination with high-protein diets have been gaining widespread popularity to control weight. In addition to weight loss, they may have favorable short-term effects on the risk factors of cardiovascular disease (CVD). Our objective was to elucidate their long-term effects on mortality and CVD incidence.$\backslash$n$\backslash$nDATA SOURCES: MEDLINE, EMBASE, ISI Web of Science, Cochrane Library, and ClinicalTrials.gov for relevant articles published as of September 2012. Cohort studies of at least one year's follow-up period were included.$\backslash$n$\backslash$nREVIEW METHODS: Identified articles were systematically reviewed and those with pertinent data were selected for meta-analysis. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) for all-cause mortality, CVD mortality and CVD incidence were calculated using the random-effects model with inverse-variance weighting.$\backslash$n$\backslash$nRESULTS: We included 17 studies for a systematic review, followed by a meta-analysis using pertinent data. Of the 272,216 people in 4 cohort studies using the low-carbohydrate score, 15,981 (5.9%) cases of death from all-cause were reported. The risk of all-cause mortality among those with high low-carbohydrate score was significantly elevated: the pooled RR (95% CI) was 1.31 (1.07-1.59). A total of 3,214 (1.3%) cases of CVD death among 249,272 subjects in 3 cohort studies and 5,081 (2.3%) incident CVD cases among 220,691 people in different 4 cohort studies were reported. The risks of CVD mortality and incidence were not statistically increased: the pooled RRs (95% CIs) were 1.10 (0.98-1.24) and 0.98 (0.78-1.24), respectively. Analyses using low-carbohydrate/high-protein score yielded similar results.$\backslash$n$\backslash$nCONCLUSION: Low-carbohydrate diets were associated with a significantly higher risk of all-cause mortality and they were not significantly associated with a risk of CVD mortality and incidence. However, this analysis is based on limited observational studies and large-scale trials on the complex interactions between low-carbohydrate diets and long-term outcomes are needed.

Meditation refers to a family of practices that may share many similarities, but can have differences in underlying methods and goals. Religious and spiritual associations are common but are not requisite for meditation practice and it should be recognized that the basis of many if not all practices is the training of the brain and body, a process that appears to have profound effects on both structure and function. In recent decades there has been interest regarding the effects of these ancient practices on the cardiovascular system, as meditation has intuitive appeal for benefit in this area. Though there is a relative shortage of quality data, available evidence suggests that meditation may exert beneficial effects on autonomic tone, autonomic reflexes, and decrease blood pressure acutely and after long term practice. In addition, meditation has the potential to positively influence the cardiovascular system through the mind-heart connection and the anti-inflammatory reflex. There is limited but promising data to suggest that meditation based interventions can have beneficial effects on patients with established cardiovascular disease. More high quality and unbiased studies of meditation practices on relevant endpoints in cardiovascular disease are needed, including the effects of such practices on inflammation, baseline heart rate variability, arrhythmias, myocardial infarction, and cardiovascular mortality. © 2013 Elsevier Ireland Ltd. All rights reserved.

PURPOSE OF REVIEW: The purpose of this review is to highlight recent studies on mammalian sirtuins that coordinately regulate cellular metabolic homeostasis upon fasting and to summarize the beneficial effects of fasting on carcinogenesis and cancer therapy.$\backslash$n$\backslash$nRECENT FINDINGS: Recent studies have demonstrated that fasting may protect normal cells and mice from the metabolic conditions that are harmful as well as decrease the incidence of carcinogenesis. Fasting could also slow the tumor growth and augment the efficacy of certain systemic agents/chemotherapy drugs in various cancers. The mechanism behind this proposed idea may be due to, at least in some part, the metabolic regulation by Sirtuin family proteins whose functions are involved in specific aspects of longevity, stress response and metabolism. Sirtuins, particularly SIRT1 and SIRT3, can be activated by fasting and further exhibit their effects in insulin response, antioxidant defense, and glycolysis. Therefore, sirtuins may have anticancer effects by shifting metabolism to a less proliferative cell phenotype as well as less prone to oxidative stress attack.$\backslash$n$\backslash$nSUMMARY: The in-depth understanding of the essential role of sirtuins in fasting process may have significant implications in developing a new metabolic diagram of cancer prevention or treatment.

Traditional methods for assessing dietary exposure can be unreliable, with under reporting one of the main problems. In an attempt to overcome such problems there is increasing interest in identifying biomarkers of dietary intake to provide a more accurate measurement. Metabolomics is an analytical technique that aims to identify and quantify small metabolites. Recently, there has been an increased interest in the application of metabolomics coupled with statistical analysis for the identification of dietary biomarkers, with a number of putative biomarkers identified. This minireview focuses on metabolomics based approaches and highlights some of the key successes.

Mitochondrial disease is a heterogeneous group of multisystemic diseases that develop consequent to mutations in nuclear or mitochondrial DNA. The prevalence of inherited mitochondrial disease has been estimated to be greater than 1 in 5,000 births; however, the diagnosis and treatment of this disease are not taught in most adult-cardiology curricula. Because mitochondrial diseases often occur as a syndrome with resultant multiorgan dysfunction, they might not immediately appear to be specific to the cardiovascular system. Mitochondrial cardiomyopathy can be described as a myocardial condition characterized by abnormal heart-muscle structure, function, or both, secondary to genetic defects involving the mitochondrial respiratory chain, in the absence of concomitant coronary artery disease, hypertension, valvular disease, or congenital heart disease. The typical cardiac manifestations of mitochondrial disease-hypertrophic and dilated cardiomyopathy, arrhythmias, left ventricular myocardial noncompaction, and heart failure-can worsen acutely during a metabolic crisis. The optimal management of mitochondrial disease necessitates the involvement of a multidisciplinary team, careful evaluations of patients, and the anticipation of iatrogenic and noniatrogenic complications. In this review, we describe the complex pathophysiology of mitochondrial disease and its clinical features. We focus on current practice in the diagnosis and treatment of patients with mitochondrial cardiomyopathy, including optimal therapeutic management and longterm monitoring. We hope that this information will serve as a guide for practicing cardiologists who treat patients thus affected. © 2013 by the Texas Heart ® Institute, Houston.

"American eating changed dramatically in the early twentieth century. As food production became more industrialized, nutritionists, home economists, and so-called racial scientists were all pointing Americans toward a newly scientific approach to diet. Food faddists were rewriting the most basic rules surrounding eating, while reformers were working to reshape the diets of immigrants and the poor. And by the time of World War I, the country's first international aid program was bringing moral advice about food conservation into kitchens around the country. In this book the author argues that the twentieth-century food revolution was fueled by a powerful conviction that Americans had a moral obligation to use self-discipline and reason, rather than taste and tradition, in choosing what to eat. She weaves together cultural history and the history of science to bring readers into the strange and complex world of the American Progressive Era. The era's emphasis on science and self-control left a profound mark on American eating, one that remains today in everything from the ubiquity of science-based dietary advice to the tenacious idealization of thinness"--Provided by publisher.

Advanced glycation end-products (AGEs) are a heterogeneous group of compounds formed by the Maillard chemical process of non-enzymatic glycation of free amino groups of proteins, lipids and nucleic acids. This chemical modification of biomolecules is triggered by endogeneous hyperglycaemic or oxidative stress-related processes. Additionally, AGEs can derive from exogenous, mostly diet-related, sources. Considering that AGE accumulation in tissues correlates with ageing and is a hallmark in several age-related diseases it is not surprising that the role of AGEs in ageing and pathology has become increasingly evident. The receptor for AGEs (RAGE) is a single transmembrane protein being expressed in a wide variety of human cells. RAGE binds a broad repertoire of extracellular ligands and mediates responses to stress conditions by activating multiple signal transduction pathways being mostly responsible for acute and/or chronic inflammation. RAGE activation has been implicated in ageing as well as in a number of age-related diseases, including atherosclerosis, neurodegeneration, arthritis, stoke, diabetes and cancer. Here we present a synopsis of findings that relate to AGEs-reported implication in cell signalling pathways and ageing, as well as in pathology. Potential implications and opportunities for translational research and the development of new therapies are also discussed. © 2013 Informa UK, Ltd.

Albatross Bay, near Weipa on western Cape York Peninsula, is well known for the large number of anthropogenic late Holocene shell mound sites that occur in the region. Recent research on shell mound formation and use both here and elsewhere across northern Australia has focused upon the extent to which mound formation may have been tied to intensive use of periodically available gluts of the intertidal bivalve Anadara granosa. This paper explores whether such a model applies in the Albatross Bay region, drawing on data available from 477 shell matrix sites recorded in this region. Data on site size, morphology, composition, substrate type, proximity to contemporary shorelines and shell mound chronology support a model of Aboriginal people episodically and strategically targeting a highly variable niche estuarine resource base rather than intensively focusing on one species. It is proposed that these production strategies were characterised by a high degree of flexibility in terms of resource focus, at times involving a considerable emphasis on A. granosa, but also incorporating other estuarine resources, and that the level or intensity of production was able to be scaled up or down in line with resource availability and abundance. This production system was based upon nuanced knowledge of annual and intra-annual ecosystem dynamics along with social organisation and communication networks that facilitated a high degree of flexibility around the strategic exploitation of variable estuarine resource bases.

Carnivores, such as the dolphin and the domestic cat, have numerous adaptations that befit consumption of diets with high protein and fat content, with little carbohydrate content. Consequently, nutrient metabolism in carnivorous species differs substantially from that of non-carnivores. Important metabolic pathways known to differ between carnivores and non-carnivores are implicated in the development of diabetes and insulin resistance in non-carnivores: (1) the hepatic glucokinase (GCK) pathway is absent in healthy carnivores yet GCK deficiency may result in diabetes in rodents and humans, (2) healthy dolphins and cats are prone to periods of fasting hyperglycemia and exhibit insulin resistance, both of which are risk factors for diabetes in non-carnivores. Similarly, carnivores develop naturally occurring diseases such as hemochromatosis, fatty liver, obesity, and diabetes that have strong parallels with the same disorders in humans. Understanding how evolution, environment, diet, and domestication may play a role with nutrient metabolism in the dolphin and cat may also be relevant to human diabetes.

Ulcerative colitis (UC) is an inflammation-associated disease of the colon and rectum. The onset and progress of the disease are directly influenced by the nature of the intestinal microflora, the intestinal barrier function, and the immunological responses of the host. The epithelial invasion of pathogenic bacteria due to excess contact and/or barrier dysfunction is related to inflammation mediated by intestinal immune responses. Although the etiology of UC is not clearly understood, recent studies have shown a rising incidence of UC worldwide, and this phenomenon is more prominent in Asian countries and in Asian immigrants in Western countries. The increased prevalence of UC also contributes to an increased risk of developing colorectal cancer. Environmental factors, including changes in dietary habits, have been suggested as major risk factors of UC. A systematic review showed a negative association between UC risk and vegetable intake, whereas total fat, omega-6 fatty acids and meat intake were positively associated with an increased risk of UC. Individual dietary factors and energy balance have been suggested as having important roles in inducing changes in the microbial population and intestinal barrier integrity and in regulating inflammatory immune responses, directly or indirectly. Excess energy intake is now known to increase pathogenic microbial populations. Likewise, the application of appropriate probiotics may reverse the pathogenic progression of the disease. In the meantime, dietary anti-inflammatory compounds, including omega-3 fatty acids and other phytochemicals, may directly suppress inflammatory responses in the course of UC development. In this review, the increased prevalence of UC and its management are interpreted from the standpoint of nutritional modulation to regulate the intestinal microflora population, intestinal epithelium permeability, and inflammatory responses. © 2013 Baishideng. All rights reserved.

The objective of this article is to present to physicians an update on plant-based diets. Concerns about the rising cost of health care are being voiced nationwide, even as unhealthy lifestyles are contributing to the spread of obesity, diabetes, and cardiovascular disease. For these reasons, physicians looking for cost-effective interventions to improve health outcomes are becoming more involved in helping their patients adopt healthier lifestyles. Healthy eating may be best achieved with a plant-based diet, which we define as a regimen that encourages whole, plant-based foods and discourages meats, dairy products, and eggs as well as all refined and processed foods. We present a case study as an example of the potential health benefits of such a diet. Research shows that plant-based diets are cost-effective, low-risk interventions that may lower body mass index, blood pressure, HbA1C, and cholesterol levels. They may also reduce the number of medications needed to treat chronic diseases and lower ischemic heart disease mortality rates. Physicians should consider recommending a plant-based diet to all their patients, especially those with high blood pressure, diabetes, cardiovascular disease, or obesity.

Popularized by Michael Pollan in his best-selling In Defense of Food, Gyorgy Scrinis' concept of nutritionism refers to the reductive understanding of nutrients as the key indicators of healthy food?an approach to food that now dominates nutrition science, dietary advice, and food marketing. Scrinis argues that this ideology of nutritionism has narrowed and in some cases distorted our appreciation of food quality, such that even highly processed foods may be perceived as healthful depending on their content of "good" or "bad" nutrients. Through an engaging investigation into such issues as the butter versus margarine debate, the battle between low-fat, low-carb, and other weight-loss diets, and the food industry's strategic promotion of nutritionally enhanced foods, Scrinis builds a revealing history of the scientific, social, and economic factors driving our modern fascination with nutrition.

Abdominal elephantiasis is a rare entity. Abdominal elephantiasis is an uncommon, but deformative and progressive cutaneous disease caused by chronic lymphedema and recurrent streptococcal or Staphylococcus infections of the abdominal wall. We present 3 cases of patients with morbid obesity who presented to our hospital with abdominal wall swelling, thickening, erythema, and pain. The abdominal wall and legs were edematous, with cobblestone-like, thickened, hyperpigmented, and fissured plaques on the abdomen. Two patients had localised areas of skin erythema, tenderness, and increased warmth. There was purulent drainage from the abdominal wall in one patient. They were managed with antibiotics with some initial improvement. Meticulous skin care and local keratolytic treatment for the lesions were initiated with limited success due to their late presentation. All three patients refused surgical therapy. Conclusion. Early diagnosis is important for the treatment of abdominal elephantiasis and prevention of complications.

Oxidation of meat occurs under postmortem conditions and is inevitable. This oxidation includes the biochemical changes in meat leading to changes in color pigments and lipids. As a consequence, color deteriorates, and undesirable flavors and rancidity develop in meat thereby impacting on consumer appeal and satisfaction. Across carcasses, there is variation in the rate at which muscle undergoes chemical reactions under postmortem conditions that reflect inherent variation at the biochemical level. It is expected that this underlying biochemical variation will be reflected in living muscle through oxidative processes. The oxidative process of muscle tissues will vary according to an animal's immunity status, temperament, and ability to cope with stress, with all these affected by nutrition, genetics, management practices, and environmental conditions (hot and cold seasons). Identification of biomarkers that indicate the oxidative status levels of animals or muscle tissues in vivo could provide insight as to how the muscle will respond to the anoxic conditions that produce undesirable results in meat. This review outlines the potential use of 1 group of biomarkers, the isoprostanes, in the context of complex biochemical reactions relating to oxidative processes that take place in the biological systems of live animals (in vivo) and subsequently in meat (in vitro). © 2013 Institute of Food Technologists®.

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.

Receptor for Advanced Glycation End-products (RAGE) is a multi-ligand receptor ubiquitous present on epithelial, neuronal, vascular and inflammatory cells, usually expressed at low levels in homeostasis and to increased degrees at sites of stress or injury. The aim of the present study was to evaluate sRAGE plasma levels in patients with Acute Coronary Syndrome (ACS) and to assess its diagnostic efficacy in identification of patients with acute events. Plasma levels of sRAGE were determined in 860 patients with Coronary Artery Disease (CAD): 530 patients presented stable angina and 330 were observed during acute ischemic event (147 with unstable angina and 183 with myocardial infarction). sRAGE plasma levels were significantly lower in patients with ACS than in patients with stable angina: [median 584 pg/mL (IQR: 266–851 pg/mL) in MI patients, median 769 pg/mL (IQR: 394–987 pg/mL) in patients with unstable angina, median 834 pg/mL (IQR 630–1005 pg/mL) in patients with stable angina; P

Navigation and environmental perception precede most actions in mobile organisms. Navigation is based upon the fundamental assumption of a ubiquitous Preference for the Nearest of otherwise equivalent navigational goals (PfN). However, the magnitude and triggers for PfN are unknown and there is no clear evidence that PfN exists. I tested for PfN in human participants on a retrieval task. Results of these experiments provide the first evidence for PfN. Further, these data quantify the three primary PfN triggers and provide an experimental structure for using PfN as a behavioral metric across domains. Surprisingly, PfN exists at a high, but not universal, magnitude. Further, PfN derives most from the absolute distance to the farthest of multiple goals (d(f)), with little influence of the distance to the nearest goal (d(n)). These data provide previously unavailable quantification of behavioral motivation across species and may provide a measurable index of selection. These methods hold particular import for behavioral modification because proximity is a powerful determinant of decision outcomes across most behaviors.

Basic and translational (or preclinical) prostate cancer research has traditionally been conducted with a limited repertoire of immortalized cell lines, which have homogeneous phenotypes and have adapted to long-term tissue culture. Primary cell culture provides a model system that allows a broader spectrum of cell types from a greater number of patients to be studied, in the absence of artificially induced genetic mutations. Nevertheless, primary prostate epithelial cell culture can be technically challenging, even for laboratories experienced in immortalized cell culture. Therefore, we provide methods to isolate and culture primary epithelial cells directly from human prostate tissue. Initially, we describe the isolation of bulk epithelial cells from benign or tumor tissues. These cells have a predominantly basal/intermediate phenotype and co-express cytokeratin 8/18 and high molecular weight cytokeratins. Since prostatic stem cells play a major role in disease progression and are considered to be a therapeutic target, we also describe a prospective approach to specifically isolate prostatic basal cells that include both stem and transit-amplifying basal populations, which can be studied independently or subsequently differentiated to supply luminal cells. This approach allows the study of stem cells for the development of new therapeutics for prostate cancer.

"The classic expose; on the dangers of sugar, with a new introduction by Robert H. Lustig, the bestselling author of Fat Chance Scientist John Yudkin was the first to sound the alarm about the excess of sugar in the diet of modern Americans. His classic expose, Pure, White, and Deadly, clearly and engagingly describes how sugar is damaging our bodies, why we eat so much of it, and what we can do to stop. He explores the ins and out of sugar, from the different types-is brown sugar really better than white?-to how it is hidden inside our everyday foods, and how it is damaging our health. In 1972, Yudkin was mostly ignored by the health industry and media, but the events of the last forty years have proven him spectacularly right. Yudkin's insights are even more important and relevant now, with today's record levels of obesity, than when they were first published. Brought up-to-date by childhood obesity expert Dr. Robert H. Lustig, this emphatic treatise on the hidden dangers of sugar is essential reading for anyone concerned about their health, the health of their children, and the wellbeing of modern society."

Review of the RAGE receptor as strongly up-regulated in different types of leukocytes upon stimulation, and mediating the transition from start to persistent inflammation.

RAGE (receptor for advanced glycation end products) is a multi-ligand receptor that belongs to the immunoglobulin superfamily of transmembrane proteins. RAGE binds AGEs (advanced glycation end products), HMGB1 (high-mobility group box-1; also designated as amphoterin), members of the S100 protein family, glycosaminoglycans and amyloid β peptides. Recent studies using tools of structural biology have started to unravel common molecular patterns in the diverse set of ligands recognized by RAGE. The distal Ig domain (V1 domain) of RAGE has a positively charged patch, the geometry of which fits to anionic surfaces displayed at least in a proportion of RAGE ligands. Association of RAGE to itself, to HSPGs (heparan sulfate proteoglycans), and to Toll-like receptors in the cell membrane plays a key role in cell signaling initiated by RAGE ligation. Ligation of RAGE activates cell signaling pathways that regulate migration of several cell types. Furthermore, RAGE ligation has profound effects on the transcriptional profile of cells. RAGE signaling has been mainly studied as a pathogenetic factor of several diseases, where acute or chronic inflammation plays a role. Recent studies have suggested a physiological role for RAGE in normal lung function and in neuronal signaling.

Cardiovascular disease is not exclusive to the modern era. In The Lancet today, Randall C Thompson and colleagues show in the HORUS study—the largest set of mummies to date—that atherosclerosis was common in ancient people of varying lifestyle, geographical location, and over different time periods. Probable or definite atherosclerosis was noted in 47 (37%) of the 137 mummies imaged by whole body CT scan. Ultra-processed foods had not touched their ancient lips—and by contrast with earlier work, the study included individuals from hunter-gatherer communities. Although the findings should not detract from important efforts towards a healthy diet and lifestyle, the study highlights that there is still more to understand about cardiovascular disease risk.$\backslash$nOne of the most important risk factors for cardiovascular disease is hypertension. To mark World Health Day (WHD) on April 7, WHO has released a new report: A Global Brief on Hypertension. High blood pressure is defined as systolic blood pressure equal to or above 140 mm Hg and diastolic pressure above 90 mm Hg. The Global Burden of Diseases Study 2010 (GBD 2010) reported that high blood pressure is the leading risk factor for global disease burden, and is estimated to cause 9·4 million deaths every year—more than half of the estimated 17 million deaths a year caused by total cardiovascular disease. In 2012, the World Health Assembly set a global goal of a 25% reduction of premature deaths from non-communicable diseases (NCDs) by 2025 (the 25 by 25 goal). Among the set of voluntary targets is a 25% relative reduction in the prevalence of raised blood pressure. The new WHO report outlines crucial components for any country initiative to address hypertension, which include integrated primary care programmes, the provision of basic diagnosis and medicines, and the reduction of risk factors in the population—such as dietary salt consumption, smoking, and physical inactivity.$\backslash$nTo succeed in reducing hypertension worldwide, efforts should be targeted where they are most needed. The LancetSeries on NCDs reported that hypertension and other compounding risk factors for NCDs, such as tobacco and obesity, are increasingly concentrated in low-income and middle-income countries. 80% of deaths due to cardiovascular disease occur in countries and poor communities where health systems are weak. The African region has the highest prevalence of hypertension among adults older than 25 years. In China, more than 50% of the disease burden is expected to be from cardiovascular disease by 2050. Prompt management of high blood pressure can reduce the risk of complications—such as the development of atherosclerotic plaques, ischaemic heart disease, stroke, renal disease, and retinopathy. However, in the early stages, high blood pressure does not usually cause noticeable symptoms, and patients are left undiagnosed, or might not have access to treatment. Treatment of the complications of hypertension, such as cardiac bypass surgery and renal dialysis, are expensive, and can rapidly deplete family and national budgets. Cardiovascular disease, including hypertension, now accounts for nearly half of the estimated US$500 billion annual lost economic output associated with NCDs in low-income and middle-income countries.\backslashnStrong leadership and a multi-sectorial approach are crucial to successfully address these challenges. One promising new leadership entity was welcomed earlier this week into the NCD fray. Public Health England (PHE), a new executive agency of the UK Department of Health, is described in a World Report this week. Duncan Selbie, the new Chief Executive, is also profiled in this issue. One of PHE's key priorities is to reduce preventable deaths from disorders such as heart disease, stroke, cancer, and diabetes. Although there is hope that the new system will more effectively address the social determinants of health by combining multi-sectorial functions in one agency, it remains to be seen how successful PHE will be in supporting and inspiring local government.\backslashnModification of behavioural risk factors and medical treatment of people at high risk for cardiovascular disease continue to be the best way forward—both to reduce the burden of high blood pressure, and to make progress towards the 25 by 25 goal. But WHD 2013 must be more than a fleeting moment for hypertension. In the context of the dismal progress on the post-2015 development agenda—where health is not yet mentioned—WHD 2013 should be the catalyst for a committed scale-up of resources directed towards addressing the world's most important risk factor for preventable mortality. Only then will NCDs have a reasonable chance of being relegated to ancient history.\backslashn