Published Science

Lipedema is a condition characterized by swelling and enlargement of the lower limbs due to abnormal deposition of subcutaneous fat. Lipedema is an under-recognized condition, often misdiagnosed as lymphedema or dismissed as simple obesity. We present a series of pedigrees and propose that lipedema is a genetic condition with either X-linked dominant inheritance or more likely, autosomal dominant inheritance with sex limitation. Lipedema appears to be a condition almost exclusively affecting females, presumably estrogen-requiring as it usually manifests at puberty. Lipedema is an entity distinct from obesity, but may be wrongly diagnosed as primary obesity, due to clinical overlap. The phenotype suggests a condition distinct from obesity and associated with pain, tenderness, and easy bruising in affected areas. © 2010 Wiley-Liss, Inc.

Purpose: The ketogenic diet has well-established short- and long-term outcomes for children with intractable epilepsy, but only for those actively receiving it. However, no information exists about its long-term effects years after it has been discontinued. Methods: Living subjects were identified who were treated at the Johns Hopkins Hospital with the ketogenic diet from November 1993 to December 2008 for ≥1 month, and had discontinued it ≥6 months prior to this study. Of 530 patients who were eligible, 254 were successfully contacted by phone or e-mail with a survey and request for laboratory studies. Results: Questionnaires were completed by 101 patients, with a median current age of 13 years (range 2–26 years). Median time since discontinuing the ketogenic diet was 6 years (range 0.8–14 years). Few (8%) still preferred to eat high fat foods. In comparison to the 52% responder rate (>50% seizure reduction) at ketogenic diet discontinuation, 79% were now similarly improved (p = 0.0001). Ninety-six percent would recommend the ketogenic diet to others, yet only 54% would have started it before trying anticonvulsants. Lipids were normal (mean total cholesterol 158 mg/dl), despite most being abnormal while on the ketogenic diet. The mean Z scores for those younger than age 18 years were −1.28 for height and −0.79 for weight. In those 18 years of age or older, the mean body mass index (BMI) was 22.2. Discussion: This is the first study to report on the long-term effects of the ketogenic diet after discontinuation. The majority of subjects are currently doing well with regard to health and seizure control.

BACKGROUND: Data on the long-term association between low-carbohydrate diets and mortality are sparse.$\backslash$n$\backslash$nOBJECTIVE: To examine the association of low-carbohydrate diets with mortality during 26 years of follow-up in women and 20 years in men.$\backslash$n$\backslash$nDESIGN: Prospective cohort study of women and men who were followed from 1980 (women) or 1986 (men) until 2006. Low-carbohydrate diets, either animal-based (emphasizing animal sources of fat and protein) or vegetable-based (emphasizing vegetable sources of fat and protein), were computed from several validated food-frequency questionnaires assessed during follow-up.$\backslash$n$\backslash$nSETTING: Nurses' Health Study and Health Professionals' Follow-up Study.$\backslash$n$\backslash$nPARTICIPANTS: 85 168 women (aged 34 to 59 years at baseline) and 44 548 men (aged 40 to 75 years at baseline) without heart disease, cancer, or diabetes.$\backslash$n$\backslash$nMEASUREMENTS: Investigators documented 12 555 deaths (2458 cardiovascular-related and 5780 cancer-related) in women and 8678 deaths (2746 cardiovascular-related and 2960 cancer-related) in men.$\backslash$n$\backslash$nRESULTS: The overall low-carbohydrate score was associated with a modest increase in overall mortality in a pooled analysis (hazard ratio [HR] comparing extreme deciles, 1.12 [95% CI, 1.01 to 1.24]; P for trend = 0.136). The animal low-carbohydrate score was associated with higher all-cause mortality (pooled HR comparing extreme deciles, 1.23 [CI, 1.11 to 1.37]; P for trend = 0.051), cardiovascular mortality (corresponding HR, 1.14 [CI, 1.01 to 1.29]; P for trend = 0.029), and cancer mortality (corresponding HR, 1.28 [CI, 1.02 to 1.60]; P for trend = 0.089). In contrast, a higher vegetable low-carbohydrate score was associated with lower all-cause mortality (HR, 0.80 [CI, 0.75 to 0.85]; P for trend \textless/= 0.001) and cardiovascular mortality (HR, 0.77 [CI, 0.68 to 0.87]; P for trend \textless 0.001).$\backslash$n$\backslash$nLIMITATIONS: Diet and lifestyle characteristics were assessed with some degree of error. Sensitivity analyses indicated that results were probably not substantively affected by residual confounding or an unmeasured confounder. Participants were not a representative sample of the U.S. population.$\backslash$n$\backslash$nCONCLUSION: A low-carbohydrate diet based on animal sources was associated with higher all-cause mortality in both men and women, whereas a vegetable-based low-carbohydrate diet was associated with lower all-cause and cardiovascular disease mortality rates.$\backslash$n$\backslash$nPRIMARY FUNDING SOURCE: National Institutes of Health.

CONCLUSIONS: A diet rich in fiber and PUFAs is correlated with a reduced risk of MS in subjects at high cardiovascular risk. Copyright 2010 S. Karger AG, Basel.

By the beginning of the twentieth century, meat eating was a regular part of daily life in the Western world. Whilst the extra protein in this diet had a beneficial effect on growth and resilience to certain diseases, excessive amounts were found to promote cancer, heart disease and obesity. When it comes to meat this is often what we talk about today: its implications for us, our planet and our health. However, few seem to agree on what these implications are. This collection of ten historical essays explores some of the complex relations between meat and human health in twentieth-century North America and Europe. Its subjects include the relations between the meat and the pharmaceutical industries, the slaughterhouse and the rise of endocrinology, the therapeutic benefits of meat extracts and the short-lived fate of liver ice-cream in the treatment of pernicious anaemia. Other articles examine responses to BSE and bovine tuberculosis, cancer and meat consumption, DES in cattle, American-style meat in Mexico and Nazi attitudes towards meat eating. Together these papers highlight a complicated array of often contradictory attitudes towards meat and human health.

The Myc oncoprotein family comprises transcription factors that control multiple cellular functions and are widely involved in oncogenesis. Here we report the identification of Myc-nick, a cytoplasmic form of Myc generated by calpain-dependent proteolysis at lysine 298 of full-length Myc. Myc-nick retains conserved Myc box regions but lacks nuclear localization signals and the bHLHZ domain essential for heterodimerization with Max and DNA binding. Myc-nick induces α-tubulin acetylation and altered cell morphology by recruiting histone acetyltransferase GCN5 to microtubules. During muscle differentiation, while the levels of full-length Myc diminish, Myc-nick and acetylated α-tubulin levels are increased. Ectopic expression of Myc-nick accelerates myoblast fusion, triggers the expression of myogenic markers, and permits Myc-deficient fibroblasts to transdifferentiate in response to MyoD. We propose that the cleavage of Myc by calpain abrogates the transcriptional inhibition of differentiation by full-length Myc and generates Myc-nick, a driver of cytoplasmic reorganization and differentiation. © 2010 Elsevier Inc.

Nuclear magnetic resonance (NMR)-based metabonomics was applied to investigate the effects of pre-slaughter exercise stress on the plasma metabolite profile at time of slaughter. The study included a total of 40 slaughter pigs, which were exposed to one of the following treatments: No pre-slaughter stress (control treatment), pre-slaughter exercise on a treadmill and subsequently 0, 1, or 3 h rest prior to slaughter. NMR-based metabonomics revealed a clear difference in the plasma metabolite profile at time of slaughter between control pigs and pigs exercised without rest, which mainly could be ascribed to increased plasma lactate due to exercise. A resting period of 1 or 3 h prior to slaughter reversed the stress-induced perturbations in the plasma metabolite profile. The plasma metabolite profile at time of slaughter was highly correlated with muscle temperature 1 min post-mortem, and a correlation to WHC was also demonstrated. Lactate was found to be the metabolite of importance for the association between the plasma metabolome and pH, temperature and WHC. © 2009 Elsevier Ltd. All rights reserved.

Omega-3 fatty acids are essential fatty acids that must be consumed in the diet. Adequate consumption of omega-3 fatty acids is vitally important during pregnancy as they are critical building blocks of fetal brain and retina. Omega-3 fatty acids may also play a role in determining the length of gestation and in preventing perinatal depression. The most biologically active forms of omega-3 fatty acids are docosahexaenoic acid and eicosapentaenoic acid, which are primarily derived from marine sources such as seafood and algae. Recent surveys, however, indicate that pregnant women in the United States and in other countries eat little fish and therefore do not consume enough omega-3 fatty acids, primarily due to concern about the adverse effects of mercury and other contaminants on the developing fetus. This review discusses the benefits of omega-3 fatty acid consumption during pregnancy and provides guidelines for obstetricians advising patients.

Aboriginal rock paintings of policemen near Laura and their ‘ethnographic interpretation’ were reported by Percy Trezise (1985:74, 1993) but are otherwise unstudied. This research integrates formal analysis of an assemblage of police and associated depictions with cultural, historical and archaeological evidence to shed light on Indigenous society and identity in the frontier period (c.1873-1890s). In drawing on Aboriginal testimony the study connects with local webs of meaning. Stylistic analysis reveals the police motif as an innovative, specialised category within Quinkan style. Signs of cognitive structure include visual, material and contextual attributes (e.g. shape, colour and form, paint recipes, graphic associations, positions and locations). Stylistic coherence suggests that radically new contexts of production (war, social and demographic transformations) did not disrupt the ancestral knowledge systems and unique worldviews which lie at the heart of visual culture at Laura. Unlike most colonial texts, the depictions record Indigenous identity in the contexts of local agency and colonialism.

BACKGROUND/AIMS: Graves' disease (GD) is the most common cause of thyrotoxicosis in children and adolescents. Caused by immunologic stimulation of the thyroid-stimulating hormone receptor, lasting remission occurs in only a minority of pediatric patients with GD, including children treated with antithyroid drugs (ATDs) for many years. Thus the majority of pediatric patients with GD will need thyroidectomy or treatment with radioactive iodine (RAI; (131)I). RESULTS: When ATDs are used in children, only methimazole should be used. Propylthiouracil is associated with an unacceptable risk of severe liver injury in children and should never be used as first-line therapy. If remission (defined as normal thyroid function off ATDs) is not achieved after 1 or 2 years of ATD therapy, (131)I or surgery may be considered, with the choice influenced by the age of the individual. When (131)I is used, administered doses should be >150 μCi/g of thyroid tissue. When surgery is performed, near total or total thyroidectomy is recommended. CONCLUSION: Choosing a treatment approach for childhood GD is often a difficult and highly personal decision. Discussion of the advantages and risks of each therapeutic option is essential to help the patient and family select a treatment option.

Attention deficit hyperactivity disorder (ADHD) is a most common psychiatric disorder in the childhood. The exact pathomechanisms related to ADHD core symptoms--hyperactivity, impulsivity and inattention--are still unclear. The developmental dysfunction of cortical-striatal-thalamic-cortical network combined with the dysregulation of catecholamine neurotransmitters could be responsible for symptoms of the disorder. Magnetic resonance spectroscopy is a method which allows a partial view on molecular mechanisms of biochemical and metabolic processes in human brain by in vivo measurement. We address the hypothesis of a potential pathomechanisms associated with ADHD symptoms which is based on the studies concerning magnetic resonance spectroscopy method and ADHD.

Context The prevalence of obesity increased in the United States between 1976-1980 and 1988-1994 and again between 1988-1994 and 1999-2000. Objective To examine trends in obesity from 1999 through 2008 and the current prevalence of obesity and overweight for 2007-2008. Design, Setting, and Participants Analysis of height and weight measurements from 5555 adult men and women aged 20 years or older obtained in 2007-2008 as part of the National Health and Nutrition Examination Survey (NHANES), a nationally representative sample of the US population. Data from the NHANES obtained in 2007-2008 were compared with results obtained from 1999 through 2006. Main Outcome Measure Estimates of the prevalence of overweight and obesity in adults. Overweight was defined as a body mass index (BMI) of 25.0 to 29.9. Obesity was defined as a BMI of 30.0 or higher. Results In 2007-2008, the age-adjusted prevalence of obesity was 33.8% (95% confidence interval [CI], 31.6%-36.0%) overall, 32.2% (95% CI, 29.5%-35.0%) among men, and 35.5% (95% CI, 33.2%-37.7%) among women. The corresponding prevalence estimates for overweight and obesity combined (BMI ≥25) were 68.0% (95% CI, 66.3%-69.8%), 72.3% (95% CI, 70.4%-74.1%), and 64.1% (95% CI, 61.3%-66.9%). Obesity prevalence varied by age group and by racial and ethnic group for both men and women. Over the 10-year period, obesity showed no significant trend among women (adjusted odds ratio [AOR] for 2007-2008 vs 1999-2000, 1.12 [95% CI, 0.89-1.32]). For men, there was a significant linear trend (AOR for 2007-2008 vs 1999-2000, 1.32 [95% CI, 1.12-1.58]); however, the 3 most recent data points did not differ significantly from each other. Conclusions In 2007-2008, the prevalence of obesity was 32.2% among adult men and 35.5% among adult women. The increases in the prevalence of obesity previously observed do not appear to be continuing at the same rate over the past 10 years, particularly for women and possibly for men. Conclusions Published online January 13, 2010 (doi:10.1001/jama.2009.2014). The National Health and Nutrition Examination Survey (NHANES) provides the opportunity to track trends in the prevalence of obesity in the United States by collecting data on height and weight measurements. Data from 1988-1994 showed that the prevalence of obesity in adults had increased by approximately 8 percentage points in the United States since 1976-1980, after being relatively stable over the period 1960-1980.1,2 Analyses of data from 1999-2000 showed further increases in obesity for both men and women and in all age groups.3 The increases in obesity from 1976-1980 to 1988-1994 were statistically significant in all sex and age groups. The increases in obesity from 1988-1994 to 1999-2000 were statistically significant in all sex and age groups except men aged 40 to 59 years. Analyses of data from 2001-2002 and 2003-2004 suggested increasing trends since 1999-2000 among men but not among women.4,5 Comparisons between 2003-2004 and 2005-2006 showed no significant changes but had limited statistical power.6 Herein we report the results from the latest NHANES data from 2007-2008 regarding population trends in obesity and compare the results over the 10-year period from 1999 through 2008.

BACKGROUND: Evidence suggests that excess mortality among African-American cancer patients is explained in part by the healthcare setting. The objective of this study was to compare mortality among African-American and Caucasian cancer patients and to evaluate the influence of attendance at a National Cancer Institute (NCI)-designated comprehensive or clinical cancer center. METHODS: The authors conducted a retrospective cohort analysis of Medicare beneficiaries with an incident diagnosis of lung, breast, colorectal, or prostate cancer between 1998 and 2002 who were identified from Surveillance, Epidemiology, and End Results data. Multivariate logistic regression models were used to assess the impact of NCI cancer center attendance and race on all-cause and cancer-specific mortality at 1 year and 3 years after diagnosis. RESULTS: The likelihood of 1-year and 3-year all-cause and cancer-specific mortality was higher for African Americans than for Caucasians in crude and adjusted models (cancer-specific adjusted: Caucasian referent, 1-year odds ratio [OR], 1.13; 95% confidence interval [CI], 1.07-1.19; 3-year OR, 1.23; 95% CI, 1.17-1.30). By cancer site, cancer-specific mortality was higher among African Americans at 1 year for breast and colorectal cancers and for all cancers at 3 years. NCI cancer center attendance was associated with significantly lower odds of mortality for African Americans (1-year OR, 0.63; 95% CI, 0.56-0.76; 3-year OR, 0.71; 95% CI, 0.62-0.81). With Caucasians as the referent group, the excess mortality risk among African Americans no longer was observed for all-cause or cancer-specific mortality risk among patients who attended NCI cancer centers (cancer-specific mortality:1-year OR, 0.95; 95% CI, 0.76-1.19; 3-year OR, 1.00; 95% CI, 0.82-1.21). CONCLUSIONS: African-American Medicare beneficiaries with lung, breast, colorectal, and prostate cancers had higher mortality compared with their Caucasian counterparts; however, there were no significant differences in mortality by race among those who attended NCI cancer centers. The results of this study suggested that place of service may explain some of the cancer mortality excess observed in African Americans. Cancer 2010;116:2698–706. VC 2010 American Cancer Society.

Background The lymphatic system plays critical roles in tissue fluid homoeostasis, immune defence and metabolic maintenance. Lymphatic vessels transport lymph, proteins, immune cells and digested lipids, allowing fluid and proteins to be returned to the blood stream, lipids to be stored and metabolized and antigens to be sampled in lymph nodes. Lymphatic drainage is mainly driven by rhythmic constrictions intrinsic to the vessels and critically modulated by fluid pressure and inflammatory mediators. Aim To collect and discuss the compelling available information linking the lymphatic system, adiposity and inflammation. Methods A literature search was performed through PubMed focusing on lymphatic system, inflammation, immune cells and fat transport and function in the context of IBD. Results Evidence collected allows us to propose the following working model. Compromised lymph drainage, reported in IBD, leads to oedema, lymphangiogenesis, impaired immune cell trafficking and lymph leakage. Lymph factor(s) stimulate adipose tissue to proliferate and produce cytokines, which affect immune cell functions and exacerbate inflammation. Conclusions Understanding the lymphatic system’s role in immune cell trafficking and immune responses, contribution to fat transport, distribution, metabolism and implication in the pathogenesis of chronic intestinal inflammation may provide the basis for new therapeutic strategies and improved quality-of-life.

Although the phenomenon of β-hydroxybutyric acid (BHBA) impact on satiety and thermogenesis has been described in the past decades, the underlying molecular mechanisms involved remain unresolved. Other metabolites such as glucose, fatty or branched chain amino acids are known to activate the AMP kinase pathway leading to an increase of anorexic and a decrease of orexigenic neuropeptides in the hypothalamus, one of the central regulators of energy homeostasis. Since BHBA is utilized as an energy source by the brain particularly in suckling newborns and under starving conditions, it is supposed to be a further central signal and energy providing substrate involved in the regulation of food intake. Moreover, BHBA might present a therapeutic approach for treating neuronal diseases because of its neuroprotective properties. Therefore, the purpose of this review is to summarize the known central effects of BHBA and to point out the importance of the identification of cellular pathways triggered in response to BHBA. © 2010 Elsevier Ltd.

Disruption of autophagy–a key homeostatic process in which cytosolic components are degraded and recycled through lysosomes–can cause neurodegeneration in tissue culture and in vivo. Upregulation of this pathway may be neuroprotective, and much effort is being invested in developing drugs that cross the blood brain barrier and increase neuronal autophagy. One well-recognized way of inducing autophagy is by food restriction, which upregulates autophagy in many organs including the liver; but current dogma holds that the brain escapes this effect, perhaps because it is a metabolically privileged site. Here, we have re-evaluated this tenet using a novel approach that allows us to detect, enumerate and characterize autophagosomes in vivo. We first validate the approach by showing that it allows the identification and characterization of autophagosomes in the livers of food-restricted mice. We use the method to identify constitutive autophagosomes in cortical neurons and Purkinje cells, and we show that short-term fasting leads to a dramatic upregulation in neuronal autophagy. The increased neuronal autophagy is revealed by changes in autophagosome abundance and characteristics, and by diminished neuronal mTOR activity in vivo, demonstrated by a reduction in levels of phosphorylated S6 ribosomal protein in Purkinje cells. The increased abundance of autophagosomes in Purkinje cells was confirmed using transmission electron microscopy. Our data lead us to speculate that sporadic fasting might represent a simple, safe and inexpensive means to promote this potentially therapeutic neuronal response.

Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss. Elevations in these mediators have been found to occur in healthy, rigorously screened individuals undergoing experimental vigils of more than 24 h, and have also been seen in response to various durations of sleep restricted to between 25 and 50% of a normal 8 h sleep amount. While these altered profiles represent small changes, such sub-clinical shifts in basal inflammatory cytokines are known to be associated with the future development of metabolic syndrome disease in healthy, asymptomatic individuals. Although the mechanism of this altered inflammatory status in humans undergoing experimental sleep loss is unknown, it is likely that autonomic activation and metabolic changes play key roles. © 2010 Published by Elsevier Ltd.

The c-myc protooncogene encodes a transcription factor (Myc) with oncogenic potential. Myc and its dimerization partner Max are bHLH-Zip DNA binding proteins controlling fundamental cellular processes. Deregulation of c-myc leads to tumorigenesis and is a hallmark of many human cancers. We have identified and extensively characterized ancestral forms of myc and max genes from the early diploblastic cnidarian Hydra, the most primitive metazoan organism employed so far for the structural, functional, and evolutionary analysis of these genes. Hydra myc is specifically activated in all stem cells and nematoblast nests which represent the rapidly proliferating cell types of the interstitial stem cell system and in proliferating gland cells. In terminally differentiated nerve cells, nematocytes, or epithelial cells, myc expression is not detectable by in situ hybridization. Hydra max exhibits a similar expression pattern in interstitial cell clusters. The ancestral Hydra Myc and Max proteins display the principal design of their vertebrate derivatives, with the highest degree of sequence identities confined to the bHLH-Zip domains. Furthermore, the 314-amino acid Hydra Myc protein contains basic forms of the essential Myc boxes I through III. A recombinant Hydra Myc/Max complex binds to the consensus DNA sequence CACGTG with high affinity. Hybrid proteins composed of segments from the retroviral v-Myc oncoprotein and the Hydra Myc protein display oncogenic potential in cell transformation assays. Our results suggest that the principal functions of the Myc master regulator arose very early in metazoan evolution, allowing their dissection in a simple model organism showing regenerative ability but no senescence.

Stone tools are the most durable and common type of archaeological remain and one of the most important sources of information about behaviors of early hominins. Stone Tools and the Evolution of Human Cognition develops methods for examining questions of cognition, demonstrating the progression of mental capabilities from early hominins to modern humans through the archaeological record. Dating as far back as 2.5-2.7 million years ago, stone tools were used in cutting up animals, woodworking, and preparing vegetable matter. Today, lithic remains give archaeologists insight into the forethought, planning, and enhanced working memory of our early ancestors. Contributors focus on multiple ways in which archaeologists can investigate the relationship between tools and the evolving human mind-including joint attention, pattern recognition, memory usage, and the emergence of language. Offering a wide range of approaches and diversity of place and time, the chapters address issues such as skill, social learning, technique, language, and cognition based on lithic technology. Stone Tools and the Evolution of Human Cognition will be of interest to Paleolithic archaeologists and paleoanthropologists interested in stone tool technology and cognitive evolution.

Abstract Contemporary research has shown that a high number of alcohol-dependent and other drug-dependent individuals have a sweet preference, specifically for foods with a high sucrose concentration. Moreover, both human and animal studies have demonstrated that in some brains the consumption of sugar-rich foods or drinks primes the release of euphoric endorphins and dopamine within the nucleus accumbens, in a manner similar to some drugs of abuse. The neurobiological pathways of drug and “sugar addiction” involve similar neural receptors. neurotransmitters, and hedonic regions in the brain. Craving, tolerance, withdrawal and sensitization have been documented in both human and animal studies. In addition, there appears to be cross sensitization between sugar addiction and narcotic dependence in some individuals. It has also been observed that the biological children of alcoholic parents, particularly alcoholic fathers, are at greater risk to have a strong sweet preference. and this may manifest in some with an eating disorder. In the last two decades research has noted that specific genes may underlie the sweet preference in alcohol- and drug-dependent individuals, as well as in biological children of paternal alcoholics. There also appears to be some common genetic markers between alcohol dependence, bulimia, and obesity, such as the A1 allele gene and the dopamine 2 receptor gene.

The early history of nutrient research leads back to the turn of the 19 th century and the milieu of chemically interested physicians. William Prout, a physician in London, is supposed to be the first who developed a concept of nutrients or alimentary substances as he called them. The paper introduces Prout’s life, states his work and contributions to the development of chemistry and concentrates on Prout’s use of chemical analysis as a way of understanding human digestion. It will be shown in detail how he came to introduce the term “alimentary substance”. The aim of the paper is to show from the point of view of the history of knowledge that nutrients are not so much the building blocks of our food but merely experimental laboratory entities. Hence, as technologically produced objects of knowledge they cannot be considered independently from the style of research, theory or apparatus, which brought them into life.

Although numerous studies examine diabetes self-care, few regard ecological framework correlates such as community and institutional level factors as fundamental for understanding diabetes management for Latinos. This article addresses the dearth of research that exists regarding social contextual forces and diabetes management for Latinos. Given the scarcity of research on this topic, studies of non-Latino groups were reviewed to illustrate the importance of community and institutional influences on diabetes care. Consideration of fundamental correlates within the ecological framework may better discern the underlying rationale for inadequate diabetes self-management for individuals who live in impoverished communities.

Increased intake of marine long-chain n-3 PUFA (n-3 LCPUFA) may decrease the risk of CVD and reduce mortality by lowering serum TAG and blood pressure (BP). Furthermore, n-3 LCPUFA may affect novel CVD risk markers related to inflammation and vascular function. The objective of the present study was to examine the effect of farmed trout on novel and traditional CVD risk markers in healthy men, and to evaluate whether this was affected by the aquacultural feed regime. We performed a parallel, 8-week intervention study in which sixty-eight healthy male volunteers were randomised to consume either a daily meal with 150 g farmed trout raised on either marine or vegetable-based feed, or a reference meal containing 150 g chicken. Twenty-four hour BP, pulse wave velocity, augmentation index, fatty acid composition of erythrocyte (RBC), and concentrations of TAG, HDL-cholesterol, LDL-cholesterol, glucose, insulin, C-reactive protein (CRP) and other markers of inflammation were measured at weeks 0 and 8. RBC content of total n-3 LCPUFA, both EPA and DHA, was significantly higher among men consuming trout raised on marine feed compared with men consuming the vegetable-fed trout or chicken. The three intervention groups did not differ significantly with respect to any of the other outcome variables, although there were trends towards associations between the changes in RBC n-3 LCPUFA and those in BP and CRP. In the present study, we conclude that we could not confirm the fish oil-induced reduction in CVD risk markers after daily consumption of trout with high or low n-3 LCPUFA content. However, trout raised on vegetable-based feed had less pronounced impact on RBC n-3 LCPUFA status.

OBJECTIVES: Decreased quality of life in diabetes is associated with poor health outcomes. Far-infrared sauna treatments improve the quality of life for those with chronic pain, chronic fatigue syndrome, depression, and congestive heart failure. The objective of this study is to determine whether far-infrared saunas have a beneficial effect on quality of life in those with type II diabetes.$\backslash$n$\backslash$nDESIGN: This was a sequential, longitudinal, interrupted time series design study.$\backslash$n$\backslash$nSETTING/LOCATION: The setting was Fraser Lake BC, a rural village in central British Columbia, Canada.$\backslash$n$\backslash$nSUBJECTS: All patients of the Fraser Lake Community Health Center with type II diabetes were invited to participate in this study.$\backslash$n$\backslash$nINTERVENTIONS: The study consisted of 20-minute, 3 times weekly infrared sauna sessions, over a period of 3 months.$\backslash$n$\backslash$nOUTCOME MEASURES: To assess quality of life, subjects completed the 36-item Short-form Health Survey Version 2 (SF-36v2) questionnaire as well as "Zero-to-Ten" Visual Analogue Scales. Baseline study parameters were measured within 1 week prior to commencing sauna sessions. Postintervention measurements were collected between 1 and 3 days after the last sauna session.$\backslash$n$\backslash$nRESULTS: Physical health, general health, and social functioning indices of the SF-36v2 improved. Visual Analogue Scales for stress and fatigue improved.$\backslash$n$\backslash$nCONCLUSIONS: Far-infrared sauna use maybe associated with improved quality of life in people with type II diabetes mellitus. Uptake of infrared saunas use is greater than the uptake of other lifestyle interventions.

INTRODUCTION: Vegetarian diets can be healthy when they are well balanced and if a variety of foods is consumed. However, elimination of animal products from the diet (vegan diets) decreases the intake of some essential nutrients and may influence the bone metabolism. This is especially important in childhood and adolescence, when growth and bone turnover are most intensive. The aim of the study was to assess the effect of vegan diet on bone density (BMD) density and serum concentrations of bone metabolism markers. MATERIAL AND METHODS: We examined a family on vegan diet which consisted of parents and two children. Dietary constituents were analysed using a nutritional program. Total and regional BMD were measured by dual-energy X-ray absorptiometry. Concentrations of calcium and phosphate in serum obtained from fasting patients were determined by colorimetric methods, 25-hydroxyvitamin D by the chemiluminescence method and bone turnover markers by specific enzyme immunoassays. RESULTS: In studied vegans, the dietary intake of phosphate was adequate while calcium and vitamin D were below the recommended range. Concentrations of calcium, phosphate and bone turnover markers in the serum of all subjects were within the physiological range, but 25-hydroxyvitamin D level was low. Age-matched Z-score total BMD was between -0.6 and 0.3 in adults, however in children it was lower (-0.9 and -1.0). Z-score BMD lumbar spine (L2-L4) was between -0.9 to -1.9 in parents and -1.5 to -1.7 in children. CONCLUSIONS: Our results suggest that an inadequate dietary intake of calcium and vitamin D may impair the bone turnover rate and cause a decrease in bone mineral density in vegans. The parameters of bone density and bone metabolism should be monitored in vegans, especially children, in order to prevent bone abnormalities.

INTRODUCTION: Vegetarian diets can be healthy when they are well balanced and if a variety of foods is consumed. However, elimination of animal products from the diet (vegan diets) decreases the intake of some essential nutrients and may influence the bone metabolism. This is especially important in childhood and adolescence, when growth and bone turnover are most intensive. The aim of the study was to assess the effect of vegan diet on bone density (BMD) density and serum concentrations of bone metabolism markers. MATERIAL AND METHODS: We examined a family on vegan diet which consisted of parents and two children. Dietary constituents were analysed using a nutritional program. Total and regional BMD were measured by dual-energy X-ray absorptiometry. Concentrations of calcium and phosphate in serum obtained from fasting patients were determined by colorimetric methods, 25-hydroxyvitamin D by the chemiluminescence method and bone turnover markers by specific enzyme immunoassays. RESULTS: In studied vegans, the dietary intake of phosphate was adequate while calcium and vitamin D were below the recommended range. Concentrations of calcium, phosphate and bone turnover markers in the serum of all subjects were within the physiological range, but 25-hydroxyvitamin D level was low. Age-matched Z-score total BMD was between -0.6 and 0.3 in adults, however in children it was lower (-0.9 and -1.0). Z-score BMD lumbar spine (L2-L4) was between -0.9 to -1.9 in parents and -1.5 to -1.7 in children. CONCLUSIONS: Our results suggest that an inadequate dietary intake of calcium and vitamin D may impair the bone turnover rate and cause a decrease in bone mineral density in vegans. The parameters of bone density and bone metabolism should be monitored in vegans, especially children, in order to prevent bone abnormalities.

Soyfoods have long been prized among vegetarians for both their high protein content and versatility. Soybeans differ markedly in macronutrient content from other legumes, being much higher in fat and protein, and lower in carbohydrate. In recent years however, soyfoods and specific soybean constituents, especially isoflavones, have been the subject of an impressive amount of research. Nearly 2,000 soy-related papers are published annually. This research has focused primarily on the benefits that soyfoods may provide independent of their nutrient content. There is particular interest in the role that soyfoods have in reducing risk of heart disease, osteoporosis and certain forms of cancer. However, the estrogen-like effects of isoflavones observed in animal studies have also raised concerns about potential harmful effects of soyfood consumption. This review addresses questions related to soy and chronic disease risk, provides recommendations for optimal intakes, and discusses potential contraindications. As reviewed, the evidence indicates that, with the exception of those individuals allergic to soy protein, soyfoods can play a beneficial role in the diets of vegetarians. Concerns about adverse effects are not supported by the clinical or epidemiologic literature. Based on the soy intake associated with health benefits in the epidemiologic studies and the benefits noted in clinical trials, optimal adult soy intake would appear to be between two and four servings per day.

Neurotrophic factors are critical regulators of the formation and plasticity of neuronal networks. Brain-derived neurotrophic factor (BD-NF) is abundant in the brain and periphery, and is found in both human serum and plasma. Animal studies have demonstrated that stress reduces BDNF expression or activity in the hippocampus and that this reduction can be prevented by treatment with antidepressant drugs. A similar change in BDNF activity occurs in the brain of patients with major depression disorder (MDD). Recently, clinical studies have indicated that serum or plasma BDNF levels are decreased in untreated MDD patients. Antidepressant treatment for at least four weeks can restore the decreased BDNF function up to the normal value. Therefore, MDD is associated with impaired neuronal plasticity. Suicidal behavior can be a consequence of severe impaired neuronal plasticity in the brain. Antidepressant treatment promotes increased BDNF activity as well as several forms of neuronal plasticity, including neurogenesis, synaptogenesis and neuronal maturation. BDNF could also play an important role in the modulation of neuronal networks. Such a neuronal plastic change can positively influence mood or recover depressed mood. These alterations of BDNF levels or neuronal plasticity in MDD patients before and after antidepressant treatment can be measured through the examination of serum or plasma BDNF concentrations. BDNF levels can therefore be useful markers for clinical response or improvement of depressive symptoms, but they are not diagnostic markers of major depression. ? 2010 Korean Neuropsychiatric Association.

In this study, we investigated the feasibility of using a novel volatile organic compound (VOC)-based metabolic profiling approach with a newly devised chemometrics methodology which combined rapid multivariate analysis on total ion currents with in-depth peak deconvolution on selected regions to characterise the spoilage progress of pork. We also tested if such approach possessed enough discriminatory information to differentiate natural spoiled pork from pork contaminated with Salmonella typhimurium, a food poisoning pathogen commonly recovered from pork products. Spoilage was monitored in this study over a 72-h period at 0-, 24-, 48- and 72-h time points after the artificial contamination with the salmonellae. At each time point, the VOCs from six individual pork chops were collected for spoiled vs. contaminated meat. Analysis of the VOCs was performed by gas chromatography/mass spectrometry (GC/MS). The data generated by GC/MS analysis were initially subjected to multivariate analysis using principal component analysis (PCA) and multi-block PCA. The loading plots were then used to identify regions in the chromatograms which appeared important to the separation shown in the PCA/multi-block PCA scores plot. Peak deconvolution was then performed only on those regions using a modified hierarchical multivariate curve resolution procedure for curve resolution to generate a concentration profiles matrix C and the corresponding pure spectra matrix S. Following this, the pure mass spectra (S) of the peaks in those region were exported to NIST 02 mass library for chemical identification. A clear separation between the two types of samples was observed from the PCA models, and after deconvolution and univariate analysis using N-way ANOVA, a total of 16 significant metabolites were identified which showed difference between natural spoiled pork and those contaminated with S. typhimurium. © 2010 Springer-Verlag.

A well-balanced vegetarian diet can provide for the needs of children and adolescents. However, appropriate caloric intake should be ensured and growth monitored. Particular attention should be paid to adequate protein intake and sources of essential fatty acids, iron, zinc, calcium, and vitamins B12 and D. Supplementation may be required in cases of strict vegetarian diets with no intake of any animal products. Pregnant and nursing mothers should also be appropriately advised to ensure that the nutritional needs of the fetus and infant are adequately met. Recommendations are provided. Adolescents on restricted vegetarian or other such diets should be screened for eating disorders.

Background: We previously reported that Waon therapy upregulates endothelial nitric oxide synthase protein, and augments ischemia-induced angiogenesis in mice with hindlimb ischemia, and it improves limb ischemia in patients with peripheral arterial disease (PAD). The aim of this study was to investigate the underlying mechanism of Waon therapy for the treatment of patients with PAD, and to determine whether Waon therapy can mobilize blood-derived progenitor cells. Methods: 21 consecutive PAD patients received standard medications, and were randomly divided into control (n=10) and Waon therapy groups (n=11). The Waon therapy group received Waon therapy daily for 6 weeks. The control group continued conventional therapy for 6 weeks. Leg pain was scored using a visual analogue scale. The ankle-brachial pressure index (ABPI) and the 6-min walking distance were measured at baseline and 6 weeks after therapy. Frequency of circulating CD34+ progenitor cell numbers was measured by quantitative real-time polymerase chain reaction, and the serum nitrate and nitrite levels were also measured at baseline and 6 weeks after therapy. Results: The leg pain score, ABPI and the 6-min walking distance improved significantly after 6 weeks in the Waon therapy group, but not in the control group. Frequency of circulating CD34+ cells increased after 6 weeks of Waon therapy [2.0±1.2 (×10-4) at baseline to 3.9±1.9 (×10-4), p=0.015], while it remained unchanged in the control group [1.8±1.8 (×10-4) at baseline to 1.2±0.9 (×10-4)]. Serum nitrate and nitrite levels increased significantly after Waon therapy (29.6±17.6 to 36.0±17.7μmol/ml, p\textless0.05), but not in the control group (34.4±9.4 to 38.3±8.8μmol/ml). Conclusion: Waon therapy mobilized circulating endothelial progenitor cells and improved limb ischemia in patients with PAD. Waon therapy is a highly promising therapy for patients with PAD. © 2010 Japanese College of Cardiology.

"Building upon his critical work in Good Calories, Bad Calories and presenting fresh evidence for his claim, Gary Taubes revisits the urgent question of what’s making us fat—and how we can change. He reveals the bad nutritional science of the last century—none more damaging or misguided than the “calories-in, calories-out” model of why we get fat—and the good science that has been ignored. He also answers the most persistent questions: Why are some people thin and others fat? What roles do exercise and genetics play in our weight? What foods should we eat, and what foods should we avoid? Persuasive, straightforward, and practical, Why We Get Fat is an essential guide to nutrition and weight management."

Attention-Deficit Hyperactivity Disorder (ADHD) is the most prevalent neurodevelopmental disorder among children. There are 3 subtypes of ADHD: (1) with prevalent inattentive symptoms (2) with prevalent hyperactive-impulsive symptoms and (3) the combined subtype. It typically manifests itself before age 7 years and occurs more frequently in boys than in girls. It is diagnosed when the hyperactivity, impulsiveness and inattention last long, appear at least in two environments and their intensity impairs the functioning of the child. The etiology of ADHD is not well-known but recent studies have shown that genetic factors are of big importance. Also several environmental influences that raise the risk for ADHD development have been identified. Recently, it has been postulated that the reduced activity of the dopaminergic and noradrenergic systems play a crucial role in ADHD pathogenesis. It is evidenced by the fact that drugs intensifying the noradrenergic and dopaminergic transmission are the most successful for ADHD treatment. At present, it has been also postulated that the disturbances in endocrine and immune systems are involved in the ADHD pathogenesis. Interconnections between functions of these systems and function of neurotransmitters are better recognized now and show that disturbances in their cooperation can be involved in some psychiatric disorders. In the case of ADHD, most data are related to disturbances in the activity of the hypothalamus-pituitary-adrenal (HPA) axis activity. In particular, the lower level of cortisol in children with ADHD, especially in the hyperactive-impulsive type ADHD, the disturbance in the circadian rhythm of this steroid and the lack of its inhibition by the dexamethasone have been documented. Many clinical data indicate that in children with ADHD, the psychological stress evokes a weaker activation of the HPA axis than in the control group. Epidemiological and preclinical investigations have shown that the disturbance in the HPA axis in ADHD can result from an excessive exposure to glucocorticoids in the fetal and early postnatal periods. Glucocorticoid administration in this period of life can provoke permanent changes in the level of brain glucocorticoid receptors and, in consequence, dysregulation of HPA axis activity, disturbances in biosynthesis of the neurotransmitters and their receptors and changes in the intracellular pathways. Glucocorticoids are known to intensify the dopaminergic system activity, so the decrease in their expression in ADHD can cause the hypofunction of this system. Since the attention and motor activity disorders often occur in children with generalized resistance to thyroid hormones, their role in ADHD pathogenesis was evaluated. However, most of the studies indicated that the levels of triiodothyronine (T3), thyroxine (T4), the free thyroxine, and the thyroid stimulating hormone (TSH) did not change in ADHD. Preclinical data concerning the role of androgens in the ADHD pathogenesis suggest that the elevated testosterone level can diminish the brain blood flow in the frontal cortex, via lowering of the level of estrogen receptor-alpha and the vascular endothelial growth factor (VEGF), and in consequence disturb processes of the memory. The association between ADHD and the polymorphism of the gene coding for androgen receptor, which leads to its higher expression has been found, however, the issue of the androgen participation in the ADHD pathogenesis is still poorly recognized. Frequent co-occurrence of ADHD and allergic diseases and correlation between ADHD and streptococcus-mediated neuropsychiatric disorders suggest the participation of the immune system in the ADHD pathogenesis. Also experimental data from an animal model of ADHD showed changes in the expression in at least several essential genes for the immune system function. However, on the other hand, the lack of the association between asthma and immunoglobulin E- dependent athopic reaction and the lack of the elevated anti-ganglia antibodies in ADHD speaks against the implication of autoimmunity in ADHD pathogenesis. Since psychostimulants, the most therapeutically efficient drugs in ADHD, not only increase the level of the dopamine and norepinephrines but also increase the activity of the HPA axis and reduce the concentration of androgens, it cannot be excluded that their beneficial effect can partly issue from a normalizing action on hormonal levels. However, currently available clinical and experimental data do not permit precise estimation of the role of endocrine and immune systems in the pathogenesis of ADHD and in therapeutic action of psychostimulants.

Background There is a growing trend towards the use of alternative forms of treatment for attention deficit hyperactivity disorder (adhd), such as the food supplements omega-3 and omega-6 fatty acids. AIM: To study biochemical aspects, important hypotheses regarding the role of these fatty acids in brain development, the mode of operation and research results concerning the effectiveness of treating adhd with these supplements. METHOD: A Medline search was performed using the Mesh-term 'fatty acids' and the search terms 'omega-3 and omega-6 fatty acids' and 'attention deficit hyperactivity disorder'. results Some rct's (randomised controlled trails) involving children with adhd didn't show any improvement after treatment with omega-3 and omega-6 fatty acids. Some other rct's, however, did show a reduction in adhd symptoms and learning difficulties, but the children concerned had not been officially diagnosed with adhd. A recent rct showed a substantial reduction in adhd symptoms in children with the inattentive type of adhd and in children with adhd and comorbid problems. CONCLUSION: There are indications that there is a theoretical rationale for the effectiveness of fatty acids in the treatment of adhd; research is ongoing. At the moment, however, treatment of adhd with omega-3 and omega-6 fatty acids is not recommended because it does not qualify as being evidence-based.

Mediterranean diet, especially rich in virgin olive oil, is associated with higher levels of plasma antioxidant capacity. Plasma TAC is related to a reduction in body weight after 3 years of intervention in a high cardiovascular risk population with a Mediterranean-style diet rich in virgin olive oi …