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Dong H.V.,Institute of Human Nutrition | Shiau S.,Gertrude rgievsky Center | Yin M.T.,Columbia University
AIDS | Year: 2014

Objective: There is growing evidence that fracture risk is increased in individuals with HIV and/or hepatitis C virus (HCV) infection. We systematically reviewed the literature to determine whether prevalence of osteoporosis and incidence of fracture is increased in HIV/HCV-coinfected individuals. Design: A systematic review and meta-analysis. Methods: A search was performed of Medline, Scopus and the Cochrane Library databases, as well as of abstracts from annual retroviral, liver and bone meetings (up to 2013) for studies with bone mineral density (BMD) or bone fracture data for HIV/ HCV-coinfected individuals. Osteoporosis odds ratios (ORs) and fracture incidence rate ratios (IRRs) were estimated from studies with data on HIV-monoinfected or HIV/HCVuninfected comparison groups. Results: Of 15 included studies, nine reported BMD data and six reported fracture data. For HIV/HCV-coinfected, the estimated osteoporosis prevalence was 22% [95% confidence interval (95% CI) 12-31] and the crude OR for osteoporosis compared with HIV-monoinfected was 1.63 (95% CI 1.27-2.11). The pooled IRR of overall fracture risk for HIV/HCV-coinfected individuals was 1.77 (95% CI 1.44-2.18) compared with HIV-monoinfected and 2.95 (95% CI 2.17-4.01) compared with uninfected individuals. In addition to HIV/HCV-coinfection, older age, lower BMI, smoking, alcohol and substance use were significant predictors of osteoporosis and fractures across studies. Conclusion: HIV/HCV coinfection is associated with a greater risk of osteoporosis and fracture than HIV monoinfection; fracture risk is even greater than uninfected controls. These data suggest that HIV/HCV-coinfected individuals should be targeted for fracture prevention through risk factor modification at all ages and DXA screening at age 50. © 2014 Wolters Kluwer Health.


Spurgeon D.J.,UK Center for Ecology and Hydrology | Jones O.A.H.,University of Cambridge | Jones O.A.H.,Durham University | Dorne J.-L.C.M.,Unit on Contaminants in the Food Chain | And 4 more authors.
Science of the Total Environment | Year: 2010

Environmental mixtures of chemicals constitute a prevalent issue in ecotoxicology and the development of new methods to reduce the uncertainties associated with their ecological risk assessment is a critical research need. Historically, a number of models have been explored to predict the potential combined effects of chemicals on species. These models, especially concentration addition and the independent action, have been applied to a number of mixtures. While often providing a good prediction of joint effect, there are cases where these models can have limitations: notably in cases where there are interactions for which they fail to adequately predict joint effects. To support the better mechanistic understanding of interactions in mixture toxicology a framework to support experimental studies to investigate the basis of observed interactions is proposed. The conceptual framework is derived from the extension of a three stage scheme which has previously been applied to understand chemical bioavailability. The framework considers that interactions in mixtures result from processes related to 1) the speciation, binding and transport of chemicals in the exposure medium (external exposure); 2) the adsorption, distribution, metabolism and excretion of chemicals within the organisms (toxicokinetics); 3) associations governing the binding and toxicity of the chemical(s) at the target site (toxicodynamics). The current state of the art in (eco)toxicology in relation to investigation of the mechanisms of interactions between chemicals is discussed with particular emphasis towards the multi-disciplinary tools and techniques within environmental chemistry; toxicology; biochemistry and systems biology that can be used to address such effects. © 2010 Elsevier B.V.


News Article | November 16, 2016
Site: www.sciencedaily.com

Columbia University Medical Center (CUMC) researchers have demonstrated that vision loss associated with a form of retinitis pigmentosa (RP) can be slowed dramatically by reprogramming the metabolism of photoreceptors, or light sensors, in the retina. The study, conducted in mice, represents a novel approach to the treatment of RP, in which the therapy aims to correct downstream metabolic aberrations of the disease rather than the underlying genetic defect. The findings were published online in the Journal of Clinical Investigation. "Although gene therapy has shown promise in RP, it is complicated by the fact that defects in 67 genes have been linked to the disorder, and each genetic defect would require a different therapy," said study leader Stephen H. Tsang, MD, PhD, the László Z. Bitó Associate Professor of Ophthalmology, Pathology and Cell Biology, and the Institute of Human Nutrition. "Our study shows that precision metabolic reprogramming can improve the survival and function of affected rods and cones in at least one type of RP. Since many, if not most, forms of the disorder have the same metabolic error, precision reprogramming could conceivably be applied to a wide range of RP patients." RP, an inherited form of vision loss, is caused by genetic defects that lead to the breakdown and loss of rods, the photoreceptors in the retina that enable peripheral and night vision. Over time, the deterioration of rods compromises the function of cones, the color-sensing photoreceptors. People with RP start to experience vision loss in childhood, and many are blind by the time they reach adulthood. Currently, there is no cure or effective treatment for RP, which affects about 1 in 4,000 people worldwide. Rods are among the most metabolically active cells in the body. They are particularly active during periods of darkness, when they burn glucose to release energy. In an earlier paper, Dr. Tsang and his colleagues theorized that rods deteriorate in RP, in part, because they lose the daytime's ability to use glucose to rebuild the rods' outer segment (the light-absorbing portion of the photoreceptor). "We hypothesized that diseased rods could be rescued by reprogramming sugar metabolism," said Dr. Tsang. Dr. Tsang tested this hypothesis in mice with a mutation in the Pde6 gene that disrupts rod metabolism, leading to an RP-like disorder. The mice were treated so that their rods could not express Sirt6, a gene that inhibits sugar metabolism. Examination of photoreceptors with electroretinography showed that the mice had significantly greater measures of rod and cone health than untreated controls. Overall, the metabolomes (all of the metabolites found in an organism) of the treated mice had accumulated the molecules needed to build the outer segment. In addition, both rods and cones survived longer in the treated mice than in the controls. While the treatment significantly prolonged survival of the diseased rods and cones, it did not prevent their eventual death. "Our next challenge is to figure out how to extend the therapeutic effect of Sirt6 inhibition," said Dr. Tsang. "Although the treatment that was used in the mice cannot be applied directly to humans, several known Sirt6 inhibitors could be evaluated for clinical use," according to Vinit B. Mahajan, MD, PhD, a contributing researcher from the University of Iowa. The inhibitors include enzyme blockers called thiomyristoyl peptides, a common plant pigment known as quercetin, and vitexin, a substance derived from the English Hawthorn tree. Dr. Tsang noted, "Further studies are needed to explore the exciting possibility that precision metabolic reprogramming may be used to treat other forms of RP and retinal degeneration."


News Article | November 2, 2016
Site: www.eurekalert.org

According to a new nutritional study conducted by the German Institute of Human Nutrition (DIfE) on individuals with type 2 diabetes, high-protein diets reduced liver fat by up to 48 percent within six weeks. It did not matter whether the diet was mainly based on plant or animal protein. The team of scientists led by Mariya Markova, Olga Pivovarova, Silke Hornemann and Andreas F. H. Pfeiffer of DIfE, a partner of the German Center for Diabetes Research (DZD), has now published its findings in the journal Gastroenterology (Markova et al. 2016; DOI: http://dx. ). Nonalcoholic fatty liver disease is the most common chronic liver disease in Europe and the U.S. "When left untreated, fatty liver is an important step progress to type 2 diabetes and can develop into liver cirrhosis, which can have life-threatening effects," said endocrinologist Andreas F. H. Pfeiffer of DIfE, who led the study. "Since the number of affected persons is increasing, it is therefore more important than ever to work together with our partners to develop effective dietary strategies that prevent the disease," he added. Various studies throughout the world have already investigated the effects of high-protein diets on human metabolism. In many of these studies, scientists have observed beneficial effects on body weight, liver fat content, blood lipid levels, long-term blood glucose levels and muscle mass retention. However, some studies have also concluded that high protein intake can reduce insulin activity and affect renal function. Since both positive as well as negative effects have been observed, the researchers at DIfE posed the question whether the protein source was decisive for the respective effect. Therefore, in the current study, they investigated the effects of two high-protein diets* on the metabolism of 37 female and male subjects between the ages of 49 and 78 years suffering from type 2 diabetes and, in most cases, from fatty liver. The two diets differed only in the protein sources, which were either mainly plant or animal origin. To ensure that the weight of the participants remained stable during the entire study and that any weight loss could not influence the result, the scientists individually adjusted the energy content of the diet to each individual. The scientists randomized which of the two diet forms each participant should follow. The main source for the plant protein group were foods such as noodles or bread that were enriched with pea protein and were especially prepared by the company IGV Institut für Getreideverarbeitung GmbH. The animal protein group consumed lean milk products as well as white meat and fish as protein sources. "As our results show, all study participants benefited from the high-protein diet, whether based on plant or animal protein. Negative effects on renal function or glucose metabolism were not observed," said first author Markova. "Liver fat content decreased significantly, in half of the study participants by more than 50 percent. In conjunction with this, we observed favorable changes in the liver and lipid metabolism, improved insulin sensitivity of the participants and in addition a significant reduction in the hormone fibroblast growth factor 21 in the blood," added Olga Pivovarova, who along with Mariya Markova and Silke Hornemann coordinated the current study. The function of the hormone released by the liver into the blood has not yet been adequately clarified and thus the results are not easy to interpret, according to the scientist. However, previous studies have shown that the hormone affects different organs and adipose tissue. Especially in overweight people, high concentrations are found in the blood. According to Silke Hornemann, a physician involved in the study, other studies as well as their own studies suggest that the hormone concentration also depends on the type and quantity of the consumed macronutrients. "Larger and longer studies are needed to better understand the metabolic mechanisms underlying the observation, to study the long-term effects, and to see whether also younger patients would benefit from the change in diet," said Pfeiffer. "The favorable effects we observed in the study may also be age-dependent, because the study participants were on average older than sixty years of age. If no renal disease is present, sufficient protein supply plays an important role particularly in this age group. For example, a decrease in muscle mass is often associated with age," Pfeiffer added. Further research is still needed to elucidate the hormonal regulation mechanisms involved. In conclusion, however, it can be said that from the observations and taking into account environmentally relevant aspects, consumers should preferably rely on plant foods for their protein source. In both diets, the respective protein content contributed 30 percent to the energy supply. The proportion of carbohydrate intake amounted to 40 percent, and fats amounted to 30 percent of the energy supply. In addition, the nutritionists advised both groups to maintain an equal intake of saturated, mono- and polyunsaturated fatty acids. Prior to the change in diet of the study participants the protein content of their diet contributed an average of 17 percent to the energy supply, the carbohydrate content 42 percent and fat content 41 percent. Foods such as lean meat, fish, eggs and low-fat dairy products are very rich in protein, as are legumes (e.g. peas, beans, lentils), nuts and almonds. According to the German Nutrient Database (Bundeslebensmittelschlüssel), 100 grams of roast turkey breast contain 25.2 grams of protein, and 100 grams of dried green peas contain 22.9 grams. The German Society of Nutrition (DGE) recommends for adults a daily intake of 0.8 grams of protein per kilogram of body weight. That means for a body weight of 60 kilograms, for example, 48 grams of protein per day. (Source: DGE). The German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE) is a member of the Leibniz Association. It investigates the causes of diet-related diseases in order to develop new strategies for prevention and therapy and to provide dietary recommendations. Its research focus includes the causes and consequences of the metabolic syndrome, which is a combination of obesity, high blood pressure, insulin resistance and lipid metabolism disorder, as well as the role of diet in healthy aging and the biological basis of food choices and eating habits. In addition, the DIfE is a partner of the German Center for Diabetes Research (DZD), which has been funded since 2009 by the BMBF. More information on the DZD can be found at http://www. The Leibniz Association is the umbrella organization for 88 independent research institutions whose spectrum encompasses the natural, engineering and environmental sciences, economics and the spatial and social sciences as well as the humanities. Leibniz Institutes address issues of social, economic and ecological relevance. They conduct knowledge-driven and applied basic research, also in the overarching Leibniz research networks, as well as constitute or maintain scientific infrastructures and provide research-based services. The Leibniz Association sets priorities in knowledge transfer, in particular with the Leibniz research museums. It provides advice and information for policymakers, academia, business and industry and the general public. Leibniz Institutes collaborate intensively with universities - e.g. in the form of "Leibniz Science Campi" as well as with industry and other partners in Germany and abroad. They are subject to a transparent and independent review procedure. Due to their importance for Germany as a whole, they are funded jointly by the federal and state governments. Leibniz Institutes employ some 18,100 individuals, including 9,200 scientists. The overall budget of the institutes amounts to more than EUR 1.6 billion. More information can be found at http://www. . Dr. Gisela Olias Coordinator for Press and Public Relations German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE) phone: +49 (0)33200 88-2278/-2335 e-mail: olias@dife.de or presse@dife.de http://www.


News Article | November 14, 2016
Site: www.eurekalert.org

NEW YORK NY (November 14, 2016)--Columbia University Medical Center (CUMC) researchers have demonstrated that vision loss associated with a form of retinitis pigmentosa (RP) can be slowed dramatically by reprogramming the metabolism of photoreceptors, or light sensors, in the retina. The study, conducted in mice, represents a novel approach to the treatment of RP, in which the therapy aims to correct downstream metabolic aberrations of the disease rather than the underlying genetic defect. The findings were published online today in the Journal of Clinical Investigation. "Although gene therapy has shown promise in RP, it is complicated by the fact that defects in 67 genes have been linked to the disorder, and each genetic defect would require a different therapy," said study leader Stephen H. Tsang, MD, PhD, the László Z. Bitó Associate Professor of Ophthalmology, Pathology and Cell Biology, and the Institute of Human Nutrition. "Our study shows that precision metabolic reprogramming can improve the survival and function of affected rods and cones in at least one type of RP. Since many, if not most, forms of the disorder have the same metabolic error, precision reprogramming could conceivably be applied to a wide range of RP patients." RP, an inherited form of vision loss, is caused by genetic defects that lead to the breakdown and loss of rods, the photoreceptors in the retina that enable peripheral and night vision. Over time, the deterioration of rods compromises the function of cones, the color-sensing photoreceptors. People with RP start to experience vision loss in childhood, and many are blind by the time they reach adulthood. Currently, there is no cure or effective treatment for RP, which affects about 1 in 4,000 people worldwide. Rods are among the most metabolically active cells in the body. They are particularly active during periods of darkness, when they burn glucose to release energy. In an earlier paper, Dr. Tsang and his colleagues theorized that rods deteriorate in RP, in part, because they lose the daytime's ability to use glucose to rebuild the rods' outer segment (the light-absorbing portion of the photoreceptor). "We hypothesized that diseased rods could be rescued by reprogramming sugar metabolism," said Dr. Tsang. Dr. Tsang tested this hypothesis in mice with a mutation in the Pde6 gene that disrupts rod metabolism, leading to an RP-like disorder. The mice were treated so that their rods could not express Sirt6, a gene that inhibits sugar metabolism. Examination of photoreceptors with electroretinography showed that the mice had significantly greater measures of rod and cone health than untreated controls. Overall, the metabolomes (all of the metabolites found in an organism) of the treated mice had accumulated the molecules needed to build the outer segment. In addition, both rods and cones survived longer in the treated mice than in the controls. While the treatment significantly prolonged survival of the diseased rods and cones, it did not prevent their eventual death. "Our next challenge is to figure out how to extend the therapeutic effect of Sirt6 inhibition," said Dr. Tsang. "Although the treatment that was used in the mice cannot be applied directly to humans, several known Sirt6 inhibitors could be evaluated for clinical use," according to Vinit B. Mahajan, MD, PhD, a contributing researcher from the University of Iowa. The inhibitors include enzyme blockers called thiomyristoyl peptides, a common plant pigment known as quercetin, and vitexin, a substance derived from the English Hawthorn tree. Dr. Tsang noted, "Further studies are needed to explore the exciting possibility that precision metabolic reprogramming may be used to treat other forms of RP and retinal degeneration." The study is titled, "Reprogramming Sirtuin-6 Attenuates Retinal Degeneration." The other contributors are: Lijuan Zhang (CUMC, the Edward S Harkness Eye Institute, and the Shanxi Eye Hospital, affiliated with Shanxi Medical University, Xinghualing, Taiyuan, Shanxi, China), Jianhai Du (University of Washington, Seattle, WA), Sally Justus (CUMC and the Edward S Harkness Eye Institute), Chun-Wei Hsu (CUMC and the Edward S Harkness Eye Institute), Luis Bonet-Ponce (National Institutes of Health, Bethesda, MD), Wen-Hsuan Wu (CUMC and the Edward S Harkness Eye Institute), Yi-Ting Tsai (CUMC and the Edward S Harkness Eye Institute), Wei-Pu Wu (CUMC and the Edward S Harkness Eye Institute), Yading Jia (Shanxi Eye Hospital), Jimmy K. Duong (CUMC), Chyuan-Sheng Lin (CUMC), Shuang Wang (CUMC), and James B. Hurley (University of Washington). The study was supported by grants from the National Institutes of Health (5P30EY019007, R01EY018213, R01EY024698, 1R01EY026682, and R21AG050437), The National Cancer Institute Core (5P30CA013696), the Research to Prevent Blindness (RPB) Physician-Scientist Award, unrestricted funds from RPB, the Tistou and Charlotte Kerstan Foundation, the Schneeweiss Stem Cell Fund, New York State (C029572), the Foundation Fighting Blindness New York Regional Research Center Grant (C-NY05-0705-0312), Jonas Family Fund, and the Gebroe Family Foundation. The authors declare no conflicts of interest. Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. The campus that Columbia University Medical Center shares with its hospital partner, NewYork-Presbyterian, is now called the Columbia University Irving Medical Center. For more information, visit cumc.columbia.edu or columbiadoctors.org.


Wolgemuth D.J.,150 St Nicholas Avenue | Wolgemuth D.J.,Institute of Human Nutrition | Wolgemuth D.J.,Columbia University | Roberts S.S.,150 St Nicholas Avenue
Philosophical Transactions of the Royal Society B: Biological Sciences | Year: 2010

Key components of the cell cycle machinery are the regulatory subunits, the cyclins, and their catalytic partners the cyclin-dependent kinases. Regulating the cell cycle in the male germ line cells represents unique challenges for this machinery given the constant renewal of gametes throughout the reproductive lifespan and the induction of the unique process of meiosis, a highly specialized kind of cell division. With challenges come opportunities to the critical eye, recognizing that understanding these specialized modes of regulation will provide considerable insight into both normal differentiation as well as disease conditions, including infertility and oncogenesis. © 2010 The Royal Society.


PubMed | Institute of Human Nutrition, Herbert Irving Comprehensive Cancer Center, The Hospital for Sick Kids, Moffitt Cancer Center and 2 more.
Type: Journal Article | Journal: The American journal of clinical nutrition | Year: 2016

Obesity is a worldwide epidemic in children and adolescents. Adult cohort studies have reported an association between higher body mass index (BMI) and increased leukemia-related mortality; whether a similar effect exists in childhood leukemia remains controversial.We conducted a meta-analysis to determine whether a higher BMI at diagnosis of pediatric acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML) is associated with worse event-free survival (EFS), overall survival (OS), and cumulative incidence of relapse (CIR).We searched 4 electronic databases from inception through March 2015 without language restriction and included studies in pediatric ALL or AML (0-21 y of age) reporting BMI as a predictor of survival or relapse. Higher BMI, defined as obese (95%) or overweight/obese (85%), was compared with lower BMI [nonoverweight/obese (<85%)]. Summary risk estimates for EFS, OS, and CIR (ALL only) were calculated with random- or fixed-effects models according to tests for between-study heterogeneity.Of 4690 reports identified, 107 full-text articles were evaluated, with 2 additional articles identified via review of citations; 11 articles were eligible for inclusion in this meta-analysis. In ALL, we observed poorer EFS in children with a higher BMI (RR: 1.35; 95% CI: 1.20, 1.51) than in those at a lower BMI. A higher BMI was associated with significantly increased mortality (RR: 1.31; 95% CI: 1.09, 1.58) and a statistically nonsignificant trend toward greater risk of relapse (RR: 1.17; 95% CI: 0.99, 1.38) compared with a lower BMI. In AML, a higher BMI was significantly associated with poorer EFS and OS (RR: 1.36; 95% CI: 1.16, 1.60 and RR: 1.56; 95% CI: 1.32, 1.86, respectively) than was a lower BMI.Higher BMI at diagnosis is associated with poorer survival in children with pediatric ALL or AML.


PubMed | University of Tübingen, Institute of Human Nutrition, Tianjin Medical University, University of Washington and 4 more.
Type: Journal Article | Journal: Human molecular genetics | Year: 2016

Inactivating mutations of the TSC1/TSC2 complex (TSC1/2) cause tuberous sclerosis (TSC), a hereditary syndrome with neurological symptoms and benign hamartoma tumours in the brain. Since TSC effectors are largely unknown in the human brain, TSC patient cortical tubers were used to uncover hyperphosphorylation unique to TSC primary astrocytes, the cell type affected in the brain. We found abnormal hyperphosphorylation of catenin delta-1 S268, which was reversible by mTOR-specific inhibitors. In contrast, in three metastatic astrocytoma cell lines, S268 was under phosphorylated, suggesting S268 phosphorylation controls metastasis. TSC astrocytes appeared epithelial (i.e. tightly adherent, less motile, and epithelial (E)-cadherin positive), whereas wild-type astrocytes were mesenchymal (i.e. E-cadherin negative and highly motile). Despite their epithelial phenotype, TSC astrocytes outgrew contact inhibition, and monolayers sporadically generated tuberous foci, a phenotype blocked by the mTOR inhibitor, Torin1. Also, mTOR-regulated phosphokinase C epsilon (PKCe) activity induced phosphorylation of catenin delta-1 S268, which in turn mediated cell-cell adhesion in astrocytes. The mTOR-dependent, epithelial phenotype of TSC astrocytes suggests TSC1/2 and mTOR tune the phosphorylation level of catenin delta-1 by controlling PKCe activity, thereby regulating the mesenchymal-epithelial-transition (MET). Thus, some forms of TSC could be treated with PKCe inhibitors, while metastasis of astrocytomas might be blocked by PKCe stimulators.


Saunders J.,Institute of Human Nutrition | Saunders J.,University of Southampton | Smith T.,University of Southampton | Stroud M.,University of Southampton
Medicine | Year: 2011

The term malnutrition is used to describe a deficiency, excess or imbalance of a wide range of nutrients, resulting in measurable adverse effects on body composition, function and clinical outcome.1 As such it can refer to individuals who are either over- or under-nourished although it is frequently used synonymously with undernutrition, as is the case in this article. Although it is well known that malnutrition is common in the developing world, the fact that significant malnourishment occurs in UK society and health settings is not widely appreciated. Malnutrition occurs for psychosocial reasons and as a consequence of disease. It has direct effects on clinical outcomes and is associated with massive healthcare expenditure. Recognition and treatment can have a significant impact on patient care and can reduce costs. Failure to diagnose and manage carries medico-legal risks. It is the responsibility of all doctors to recognize the fundamental importance of proper nutritional care to good clinical practice.2 The focus of this article is predominantly concerned with malnutrition and its consequences in the UK. © 2010 Elsevier Ltd. All rights reserved.


News Article | January 22, 2016
Site: www.biosciencetechnology.com

Sleeping through the night and reaching deep, slow-wave sleep may be tied to how much sugar, fiber and saturated fat you eat, says new research from the American Academy of Sleep Medicine. The findings were published in January in the Journal of Clinical Sleep Medicine. For the randomized study, 13 women and 13 men, with an average age of 35, participated in a five night sleep lab.  Participants laid in bed between the hours of 10 p.m. and 7 a.m., and slept for an average of seven hours and 35 minutes.  Sleep data, such as brain waves, oxygen levels, and heart rate was recorded. On night three, after three days of eating fixed meals, the data was analyzed, and again on night five, after one day of participants eating as they pleased. There were a number of findings that connected lower saturated fat and sugar intake with better quality sleep.  Those who ate a higher percentage of energy from saturated fat had less slow-wave sleep, while those that had more fiber spent longer in deep-sleep stages. Higher sugar consumption was associated with waking up more often from sleep. “Our main finding was that diet quality influenced sleep quality,” principal investigator Marie-Pierre St-Onge, Ph.D., assistant professor in the department of medicine and Institute of Human Nutrition at Columbia University Medical Center said in a prepared statement.  “It was most surprising that a single day of greater fat intake and lower fiber could influence sleep.” The ability to fall asleep faster after eating high protein, low saturated fat meals, which were designed by a nutritionist, was observed in participants, compared to eating self-selected meals.  On average participants took 29 minutes to fall asleep after eating meals of their choosing, compared to 17 minutes after eating controlled meals. “The finding that diet can influence sleep has tremendous health implications, given the increasing recognition of the role of sleep in the development of chronic disorders such as hypertension, diabetes and cardiovascular disease,” St-Onge said. More studies are needed to assess the link between diet and sleep quality, the researchers said.

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