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Zinc, Magnesium, Selenium and Depression: A Review of the Evidence, Potential Mechanisms and Implications.
Wang, J, Um, P, Dickerman, BA, Liu, J
Nutrients. 2018;10(5)
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Adequate micronutrient consumption and mental health are of major public health importance. Recent findings suggest micronutrient deficiencies may play a role in the development and progression of depression, yet the findings remain unclear. The aim of this review is to present the recent evidence on the association between several micronutrients and depression and discuss the potential mechanisms and clinical implications. Based on the current literature, evidence shows an association between both zinc and magnesium deficiency and the risk of depression, with stronger evidence supporting zinc. Studies on selenium are limited or inconclusive. According to these findings, the authors support the importance of adequate micronutrient consumption for promoting mental health. They suggest future research should investigate the safety and efficacy of micronutrient supplementation as an adjunct treatment for depression to better inform current prevention and treatment strategies.
Abstract
Micronutrient deficiency and depression are major global health problems. Here, we first review recent empirical evidence of the association between several micronutrients—zinc, magnesium, selenium—and depression. We then present potential mechanisms of action and discuss the clinical implications for each micronutrient. Collectively, empirical evidence most strongly supports a positive association between zinc deficiency and the risk of depression and an inverse association between zinc supplementation and depressive symptoms. Less evidence is available regarding the relationship between magnesium and selenium deficiency and depression, and studies have been inconclusive. Potential mechanisms of action involve the HPA axis, glutamate homeostasis and inflammatory pathways. Findings support the importance of adequate consumption of micronutrients in the promotion of mental health, and the most common dietary sources for zinc and other micronutrients are provided. Future research is needed to prospectively investigate the association between micronutrient levels and depression as well as the safety and efficacy of micronutrient supplementation as an adjunct treatment for depression.
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Metabolic and Microbiota Measures as Peripheral Biomarkers in Major Depressive Disorder.
Horne, R, Foster, JA
Frontiers in psychiatry. 2018;9:513
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Though the connection between the gut microbiome, physical health and mental health is becoming more established, there remains a lack of understanding around the underlying cause of major depressive disorder (MDD). There is a need to identify biomarkers in MDD in order to help identify individual differences and improve treatment outcomes. The aim of this review is to investigate the link between metabolic biomarkers and the gut microbiota in individuals experiencing MDD. The current literature points to two potential biomarkers, leptin and ghrelin, which play a role in both metabolic disease and depression. Based on these findings, the authors conclude these biomarkers may help researchers and clinicians establish subgroups in depressed individuals in order to better predict treatment responses and develop more targeted therapies.
Abstract
Advances in understanding the role of the microbiome in physical and mental health are at the forefront of medical research and hold potential to have a direct impact on precision medicine approaches. In the past 7 years, we have studied the role of microbiota-brain communication on behavior in mouse models using germ-free mice, mice exposed to antibiotics, and healthy specific pathogen free mice. Through our work and that of others, we have seen an amazing increase in our knowledge of how bacteria signal to the brain and the implications this has for psychiatry. Gut microbiota composition and function are influenced both by genetics, age, sex, diet, life experiences, and many other factors of psychiatric and bodily disorders and thus may act as potential biomarkers of the gut-brain axis that could be used in psychiatry and co-morbid conditions. There is a particular need in major depressive disorder and other mental illness to identify biomarkers that can stratify patients into more homogeneous groups to provide better treatment and for development of new therapeutic approaches. Peripheral outcome measures of host-microbe bidirectional communication have significant translational value as biomarkers. Enabling stratification of clinical populations, based on individual biological differences, to predict treatment response to pharmacological and non-pharmacological interventions. Here we consider the links between co-morbid metabolic syndrome and depression, focusing on biomarkers including leptin and ghrelin in combination with assessing gut microbiota composition, as a potential tool to help identify individual differences in depressed population.
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Guts and Gall: Bile Acids in Regulation of Intestinal Epithelial Function in Health and Disease.
Hegyi, P, Maléth, J, Walters, JR, Hofmann, AF, Keely, SJ
Physiological reviews. 2018;98(4):1983-2023
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Bile acids are bioactive bacterial metabolites which recent research shows may be helpful in protecting the epithelial cells which line the entire surface of the gastrointestinal tract. Many conditions such as inflammatory bowel disease, chronic diarrhoea, pancreatitis, reflux esophagitis, and cancer are influenced by the integrity of the intestinal lining and/or disruption of epithelial transport; the movement of digestive enzymes, nutrients, electrolytes, and fluids. Bile acids are now being further studied as a new target for therapies to help these conditions. Typically, bile acids help with the digestion of fats. These acids are created in the liver and stored in the gall bladder and transported throughout the small and large intestines where they support the cells in the intestinal lining. This is the same lining which acts as a barrier to external pathogens and toxins. All the conditions above appear to show alterations in bile acid activity indicating a role for therapeutic targeting of bile acids in intestinal disease. This may include dietary manipulation, probiotics and fecal transfers to support bile acid production and function.
Abstract
Epithelial cells line the entire surface of the gastrointestinal tract and its accessory organs where they primarily function in transporting digestive enzymes, nutrients, electrolytes, and fluid to and from the luminal contents. At the same time, epithelial cells are responsible for forming a physical and biochemical barrier that prevents the entry into the body of harmful agents, such as bacteria and their toxins. Dysregulation of epithelial transport and barrier function is associated with the pathogenesis of a number of conditions throughout the intestine, such as inflammatory bowel disease, chronic diarrhea, pancreatitis, reflux esophagitis, and cancer. Driven by discovery of specific receptors on intestinal epithelial cells, new insights into mechanisms that control their synthesis and enterohepatic circulation, and a growing appreciation of their roles as bioactive bacterial metabolites, bile acids are currently receiving a great deal of interest as critical regulators of epithelial function in health and disease. This review aims to summarize recent advances in this field and to highlight how bile acids are now emerging as exciting new targets for disease intervention.
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Effects of caffeine intake on muscle strength and power: a systematic review and meta-analysis.
Grgic, J, Trexler, ET, Lazinica, B, Pedisic, Z
Journal of the International Society of Sports Nutrition. 2018;15:11
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The possible physical performance enhancing (or 'ergogenic) effects of caffeine have been extensively studied since the early 1900s. Recent focus has shifted to its impact on anaerobic physical performance outcomes such as muscular strength, endurance and jumping tasks that require power. Although it has been found to enhance muscle endurance, less is known about its impact on strength and power. This is the first meta-analysis on caffeine and muscle power, and includes 20 studies - ten on muscle strength outcomes and ten on muscle power. The analysis found that caffeine significantly improves muscle strength (SMD = 0.20; 95% confidence interval [CI]: 0.03, 0.36; p = 0.023) but only for upper and not lower body strength. These results were found for men but more robust studies are needed to examine the impact for women (although the limited research suggests there may be a positive impact). This is in contrast to a previous meta-analysis that found no impact of caffeine on muscle strength (Polito, Souza, Casonatto & Farinatti, 2016). It was also found to significantly improve muscle power (SMD = 0.17; 95% CI: 0.00, 0.34; p = 0.047). Although the pooled effect of caffeine on performance outcomes was small to medium, even small improvements can make a big difference competitively. Future research is needed to identify the best dosage and form of caffeine to maximise its performance enhancing effects. Additionally, more robust research is needed to reduce bias, and studies including women. It is important to recognise that individual physical performance changes as a result of caffeine are variable, so these findings must be applied on a case-by-case basis. * Polito MD, Souza DB, Casonatto J, Farinatti P. Acute effect of caffeine consumption on isotonic muscular strength and endurance: a systematic review and meta-analysis. Sci Sports. 2016;31:119–28.
Abstract
BACKGROUND Caffeine is commonly used as an ergogenic aid. Literature about the effects of caffeine ingestion on muscle strength and power is equivocal. The aim of this systematic review and meta-analysis was to summarize results from individual studies on the effects of caffeine intake on muscle strength and power. METHODS A search through eight databases was performed to find studies on the effects of caffeine on: (i) maximal muscle strength measured using 1 repetition maximum tests; and (ii) muscle power assessed by tests of vertical jump. Meta-analyses of standardized mean differences (SMD) between placebo and caffeine trials from individual studies were conducted using the random effects model. RESULTS Ten studies on the strength outcome and ten studies on the power outcome met the inclusion criteria for the meta-analyses. Caffeine ingestion improved both strength (SMD = 0.20; 95% confidence interval [CI]: 0.03, 0.36; p = 0.023) and power (SMD = 0.17; 95% CI: 0.00, 0.34; p = 0.047). A subgroup analysis indicated that caffeine significantly improves upper (SMD = 0.21; 95% CI: 0.02, 0.39; p = 0.026) but not lower body strength (SMD = 0.15; 95% CI: -0.05, 0.34; p = 0.147). CONCLUSION The meta-analyses showed significant ergogenic effects of caffeine ingestion on maximal muscle strength of upper body and muscle power. Future studies should more rigorously control the effectiveness of blinding. Due to the paucity of evidence, additional findings are needed in the female population and using different forms of caffeine, such as gum and gel.
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Intestinal microbiome-gut-brain axis and irritable bowel syndrome.
Moser, G, Fournier, C, Peter, J
Wiener medizinische Wochenschrift (1946). 2018;168(3-4):62-66
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The gut-brain-microbiota axis connects the nervous system with the metabolic, hormonal and immune functions of the intestines. Irritable bowel syndrome (IBS) is a functional gut disorder that commonly presents with psychological co-morbidities, and while animal studies show strong associations between stress and gut microbiota, studies in humans are rare. This review assesses the current literature on intestinal microbiome and its association with stress, anxiety and depression in patients with IBS. Based on existing studies, the authors found the gut microbiota forms a crucial link between the intestine and nervous system. Therapies targeted at both modulating the gut microbiome and psychological interventions are recommended. The authors conclude further randomised clinical trials are needed to better understand which therapies work best for patients with IBS.
Abstract
Psychological comorbidity is highly present in irritable bowel syndrome (IBS). Recent research points to a role of intestinal microbiota in visceral hypersensitivity, anxiety, and depression. Increased disease reactivity to psychological stress has been described too. A few clinical studies have attempted to identify features of dysbiosis in IBS. While animal studies revealed strong associations between stress and gut microbiota, studies in humans are rare. This review covers the most important studies on intestinal microbial correlates of psychological and clinical features in IBS, including stress, anxiety, and depression.
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Nutritional Ketosis for Weight Management and Reversal of Metabolic Syndrome.
Gershuni, VM, Yan, SL, Medici, V
Current nutrition reports. 2018;7(3):97-106
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The five main components of Metabolic Syndrome — obesity, fasting blood sugar, high triglycerides (TGs), low HDL cholesterol, and hypertension — are all improved by carbohydrate restriction which reduces insulin secretion. Ketones are water-soluble molecules produced by the liver from fatty acids when blood glucose and liver glycogen stores are depleted, for example through fasting, low carbohydrate intake or intense exercise. Nutritional ketosis through a very low carbohydrate ketogenic diet (VLCKD) results in lower insulin levels which can lead to a shift in metabolism towards the use of fat stores for energy. A “well-formulated” ketogenic diet is described as composed of 5–10% carbohydrates (<20–50g/day), adequate protein (1–1.5g/kg/day), and fat until satiated, with blood ketone levels of 0.5 to 3 mg/dL. Nutritional ketosis is different from diabetic ketoacidosis which can affect type 1 diabetics and which is a medical emergency. A number of meta-analyses of randomised controlled trials have shown that VLCKD are better than low fat diets with respects to weight loss, lipid profiles, glucose metabolism, blood pressure and inflammatory markers. The authors review the literature and mechanisms of action.
Abstract
PURPOSE OF REVIEW The goal of this paper is to review current literature on nutritional ketosis within the context of weight management and metabolic syndrome, namely, insulin resistance, lipid profile, cardiovascular disease risk, and development of non-alcoholic fatty liver disease. We provide background on the mechanism of ketogenesis and describe nutritional ketosis. RECENT FINDINGS Nutritional ketosis has been found to improve metabolic and inflammatory markers, including lipids, HbA1c, high-sensitivity CRP, fasting insulin and glucose levels, and aid in weight management. We discuss these findings and elaborate on potential mechanisms of ketones for promoting weight loss, decreasing hunger, and increasing satiety. Humans have evolved with the capacity for metabolic flexibility and the ability to use ketones for fuel. During states of low dietary carbohydrate intake, insulin levels remain low and ketogenesis takes place. These conditions promote breakdown of excess fat stores, sparing of lean muscle, and improvement in insulin sensitivity.
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Adiponectin-leptin ratio: A promising index to estimate adipose tissue dysfunction. Relation with obesity-associated cardiometabolic risk.
Frühbeck, G, Catalán, V, Rodríguez, A, Gómez-Ambrosi, J
Adipocyte. 2018;7(1):57-62
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Obesity is medically defined as a condition of abnormal or excessive fat accumulation in adipose tissue, of sufficient extent to produce adverse health consequences. Presently, adipose tissue has emerged as an extremely active endocrine organ, based on its ability to secrete a plethora of biologically active adipokines [a class of cytokine mediators that are predominantly secreted by adipose cells] such as leptin and adiponectin. Furthermore, obesity is characterized by an increase in circulating leptin concentrations, in parallel to a decrease in blood levels of adiponectin. Thus, the adiponectin/leptin ratio has been suggested as a marker of adipose tissue dysfunction. A dysfunctional adipose tissue, evidenced by a lower adiponectin/ leptin ratio, is a clear contributor to the low-grade chronic inflammation associated with metabolic syndrome. Authors conclude that this ratio is highly and negatively correlated with markers of low-grade chronic inflammation emerging as a useful estimator of obesity- and metabolic syndrome- associated cardiometabolic risk.
Abstract
Obesity is currently the most extended metabolic disturbance worldwide favoring the development of cardiometabolic alterations such as type 2 diabetes, hypertension, and dyslipidemia. Obesity and the metabolic syndrome (MS) are characterized by an increase in circulating leptin concentrations, in parallel to a decrease in blood levels of adiponectin. Consequently, the adiponectin/leptin ratio has been suggested as a maker of adipose tissue dysfunction. This emerging biomarker correlates with insulin resistance better than adiponectin or leptin alone, or even HOMA and is decreased with increasing number of metabolic risk factors having been proposed as a predictive marker for the MS. Moreover, the adiponectin/leptin ratio is negatively correlated with markers of low-grade chronic inflammation. In this sense, an increase in this ratio has been related with reduced atherosclerosis risk as well as with a decreased risk of some types of cancer in epidemiological studies. In this commentary we propose new cutoffs to estimate obesity- and MS-associated cardiometabolic risk according to the adiponectin/leptin ratio and discuss different therapeutic strategies to increase this promising biomarker of metabolic risk.
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Etiology of Metabolic Syndrome and Dietary Intervention.
Xu, H, Li, X, Adams, H, Kubena, K, Guo, S
International journal of molecular sciences. 2018;20(1)
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Metabolic syndrome (MetS) is a complex disease characterised by high blood sugar, raised blood pressure, dyslipidemia and obesity. It is a major contributing factor to chronic disease such as type 2 diabetes and cardiovascular disease. The aim of this study is to review the cause of MetS, understand how it progresses to chronic disease and analyse the efficacy of clinical interventions in reducing this progression. According to the existing research, this study found insulin sensitivity to be a critical aspect of the pathogenesis in MetS. Effective intervention strategies should be aimed at increasing insulin sensitivity. Based on this information, the authors conclude health practitioners should help patients manage energy balance and reduce overall inflammatory markers to best control the progression of MetS.
Abstract
The growing prevalence of metabolic syndrome (MetS) in the U.S. and even worldwide is becoming a serious health problem and economic burden. MetS has become a crucial risk factor for the development of type 2 diabetes mellitus (T2D) and cardiovascular diseases (CVD). The rising rates of CVD and diabetes, which are the two leading causes of death, simultaneously exist. To prevent the progression of MetS to diabetes and CVD, we have to understand how MetS occurs and how it progresses. Too many causative factors interact with each other, making the investigation and treatment of metabolic syndrome a very complex issue. Recently, a number of studies were conducted to investigate mechanisms and interventions of MetS, from different aspects. In this review, the proposed and demonstrated mechanisms of MetS pathogenesis are discussed and summarized. More importantly, different interventions are discussed, so that health practitioners can have a better understanding of the most recent research progress and have available references for their daily practice.
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Fructose metabolism and metabolic disease.
Hannou, SA, Haslam, DE, McKeown, NM, Herman, MA
The Journal of clinical investigation. 2018;128(2):545-555
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Sugar consumption is thought to be a contributing factor in the increase in diabetes and obesity and the associated risk of cardiovascular disease worldwide. Sucrose (table sugar) and high fructose corn syrup contain almost equal amounts of fructose and glucose and are commonly added to processed foods. Whilst long-term studies are lacking, some short-term intervention studies show that fructose can impair lipid metabolism and insulin sensitivity in humans. This article reviews the biochemistry and molecular genetics of fructose metabolism as well as potential mechanisms by which excessive fructose consumption contributes to cardiometabolic disease. Fructose absorption in the human intestine is saturable, and there is a large range in capacity to absorb fructose between individuals, and unabsorbed fructose may contribute to gastrointestinal symptoms including pain and bloating. Fructose concentrations in the blood can increase 10-fold after consumption, but are rapidly cleared, mostly by the liver, where it provides substrate for metabolic processes, but may also be involved in signalling functions. Fructose may enhance glucose uptake by the liver and storage as glycogen and lipids. It may also increase production of uric acid which is implicated with gout. Excessive fructose consumption affects lipid metabolism and may contribute to fat accumulation in the liver and increase circulating triglycerides, a risk factor for heart disease. In animal models it also induces increased insulin levels. Fructose is one of the sweetest sugars which may affect appetite and overeating. It may also induce addiction-like behaviours such as binging and dependence in part by stimulating dopaminergic pathways. It also appears to induce leptin resistance which further increases food intake and obesity.
Abstract
Increased sugar consumption is increasingly considered to be a contributor to the worldwide epidemics of obesity and diabetes and their associated cardiometabolic risks. As a result of its unique metabolic properties, the fructose component of sugar may be particularly harmful. Diets high in fructose can rapidly produce all of the key features of the metabolic syndrome. Here we review the biology of fructose metabolism as well as potential mechanisms by which excessive fructose consumption may contribute to cardiometabolic disease.
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Effectiveness and safety of carbohydrate counting in the management of adult patients with type 1 diabetes mellitus: a systematic review and meta-analysis.
Vaz, EC, Porfírio, GJM, Nunes, HRC, Nunes-Nogueira, VDS
Archives of endocrinology and metabolism. 2018;62(3):337-345
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Glycaemic control of patients with diabetes mellitus is important because it impacts the development of diabetic complications. Carbohydrate counting is a meal planning tool that allows for great variation and flexibility in food choices among individuals with diabetes mellitus. The aim of the study was to evaluate the effectiveness and safety of carbohydrate counting in the treatment of adult patients with type 1 diabetes mellitus using a systematic literature review. The study included randomised controlled trials with at least 3 months of follow-up, and evaluation of outcomes in which patients were randomly divided into two groups. The meta-analysis showed that the final haemoglobin A1c (HbA1c) - a test that shows the average blood glucose levels for the last two to three months - was significantly lower in the carbohydrate counting group than in the control group. Authors conclude that the meta-analysis showed evidence favouring the use of carbohydrate counting in the management of adult patients with type 1 diabetes mellitus. However, this benefit was limited to the final HbA1c.
Abstract
OBJECTIVE This study aimed to evaluate the effectiveness and safety of carbohydrate counting (CHOC) in the treatment of adult patients with type 1 diabetes mellitus (DM1). MATERIALS AND METHODS We performed a systematic review of randomized studies that compared CHOC with general dietary advice in adult patients with DM1. The primary outcomes were changes in glycated hemoglobin (HbA1c), quality of life, and episodes of severe hypoglycemia. We searched the following electronic databases: Embase, PubMed, Lilacs, and the Cochrane Central Register of Controlled Trials. The quality of evidence was analyzed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE). RESULTS A total of 3,190 articles were identified, and two reviewers independently screened the titles and abstracts. From the 15 potentially eligible studies, five were included, and 10 were excluded because of the lack of randomization or different control/intervention groups. Meta-analysis showed that the final HbA1c was significantly lower in the CHOC group than in the control group (mean difference, random, 95% CI: -0.49 (-0.85, -0.13), p = 0.006). The meta-analysis of severe hypoglycemia and quality of life did not show any significant differences between the groups. According to the GRADE, the quality of evidence for severe hypoglycemia, quality of life, and change in HbA1c was low, very low, and moderate, respectively. CONCLUSION The meta-analysis showed evidence favoring the use of CHOC in the management of DM1. However, this benefit was limited to final HbA1c, which was significantly lower in the CHOC than in the control group.