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His research interests include diabetes mellitus effective 20 mg simvastatin, control of glycogen metabolism buy 40mg simvastatin fast delivery, and glycogen synthase and phosphorylase systems purchase genuine simvastatin on line. Previously best purchase for simvastatin, he was chair and a professor of the Depart- ment of Biostatistics and Epidemiology at the School of Public Health and Health Sciences at the University of Massachusetts at Amherst. Pastides is a consultant to the World Health Organization’s Program in Environ- mental Health and is a fellow of the American College of Epidemiology. He was a Fulbright Senior Research Fellow and visiting professor at the University of Athens Medical School in Greece from 1987 to 1988. Pastides has been a principal investigator or coinvestigator on over 30 externally-funded research grants, results of which have been published in numerous peer-reviewed journals. He is the recipient of several prestigious awards such as the Borden Award in Nutrition of the Canadian Society for Nutritional Sciences, the Sandoz Award of the Clinical Research Society of Toronto, the Agnes Higgins Award of the March of Dimes, the Osborne Mendel Award of the American Society for Nutrition Sciences, and the Nutrition Award of the American Academy of Pediatrics. Pencharz has served on the grant review boards for the Medical Research Council, the National Institutes of Health, the U. His research expertise is protein, amino acid, and energy metabolism in neonates and young adults, especially in patients suffering from cystic fibrosis. Luke’s– Roosevelt Hospital Center, and a professor of medicine at the College of Physicians and Surgeons, Columbia University. His research interests are in the hormonal control of carbohydrate metabolism, diabetes mellitus, obesity, and food intake regulation. Pi-Sunyer is a past president of the American Diabetes Association, the American Society for Clinical Nutri- tion, and the North American Association for the Study of Obesity. Pi-Sunyer is editor-in- chief of Obesity Research and associate editor of the International Journal of Obesity. Rand’s general expertise is in statistical modeling and application of statistics to biomedical problems. He was the recipient of several honors and awards and has served on many journal editorial boards. Reeds served as a permanent member of the Nutrition Study Section, National Institutes of Health and the International Review Panel, United Kingdom Agricultural and Food Research Council. Reeds’ research expertise was protein metabolism and amino acid requirements, specifically the regula- tion of growth and protein deposition by diet and other environmental variables such as stress and infection. Rimm is project director of a National Heart, Lung, and Blood Institute- and National Cancer Institute-funded prospective study of diet and chronic disease among men, as well as the principal investigator of a National Institute on Alcoholism and Alcohol Abuse study. Memberships include the Executive Committee of the Epidemiology and Prevention Council of the American Heart Asso- ciation and the Society for Epidemiologic Research. He has authored over 150 papers with a main research focus on the associations between diet and other lifestyle characteristics and the risk of obesity, diabetes, and cardiovascular disease. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University. She is also a professor of nutrition in the School of Nutrition Science and Policy at Tufts and a professor of psychiatry and a scientific staff member in the Department of Pediatrics at Tufts University Medical School. Her research focus is infant and adult obesity, infant nutrient requirements, breastfeeding, and nutri- tion and aging. She chairs national meetings on dietary prevention of obesity and sits on international committees for evaluation of nutritional requirements. He has more than 100 scientific publications on food safety and risk assessment and has lectured nationally and internationally on these subjects. Rodricks is the author of Calculated Risks, a nontechnical introduction to toxicology and risk assessment. Her laboratory is actively involved in research on dietary fiber, phytoestrogens from flax and soy, and whole grains. Slavin has published more than 100 reviewed research articles and has given hundreds of nutrition semi- nars for professional and lay audiences. She is a science communicator for the Institute of Food Technologists and a member of numerous scientific societies, including the America Dietetic Association, the American Soci- ety for Nutritional Sciences, and the American Association for Cancer Research. She is a frequent source for the media on topics ranging from functional foods to sports nutrition. Her research interests are human nutrition, dietary fiber, nutrient bioavailability, sports nutrition, carbo- hydrate metabolism, and the role of diet in cancer prevention. He has served on the editorial board of the Journal of Nutrition, as program manager of the U. His research interests are dietary fiber and cholesterol and bile acid metabolism. Her special- ties within these areas are in social and economic determinates of health and nutrition, population-level indicators of risk, evaluation of public poli- cies in response to food insecurity, and the statistical analysis of dietary intake data at the individual and population levels. Tarasuk has served on several committees and advisory groups including the Nutrition Expert Advisory Group of the Canadian Community Health Survey, the External Advisory Panel for Food Directorate Review of Policies on the Addition of Vitamins and Minerals to Foods, the Expert Scientific Workshop to Evalu- ate the Integrated National Food and Nutrition Survey, the Advisory Baseline Study Group for the Canada Prenatal Nutrition Program, and the Nutrition Expert Group for the National Population Health Survey. Previously, he was Vice President for Corporate Research at Baxter-International and associate dean of the School of Medicine at West Virginia University. He has held professorships in the departments of pharmacology and toxicology in sev- eral medical schools including Iowa, Virginia, and West Virginia. He has authored over 12 textbooks and research monographs and has published over 350 scientific articles in the areas of endocrine pharmacology and reproductive toxicology. He is the recipient of several national awards including the Merit Award from the Society of Toxicology, Certificate of Scientific Services from the U. Environmental Protection Agency, and Distinguished Lecturer in Medical Sciences from the American Medical Association. Thomas serves as a specialty editor for Toxicology and Applied Pharmacology and is on the editorial board of Food and Chemical Toxicology. She is the current chair of the American Heart Association’s Committee on Atherosclerosis, Hypertension and Obesity in Youth. Lehman Award from the Society of Toxicology in 1982, the Ambassador in Toxicology Award from the Mid-Atlantic Chapter of the Society of Toxicology in 2001, and the Enhancement of Animal Welfare Award from the Society of Toxicology in 2002. Williams has served on numerous editorial boards and currently is a member of the boards of Archives of Toxicology, European Journal of Cancer Prevention, and Drug and Chemical Toxicology. He has also served on numerous working groups and committees of the National Research Council, U. Environmental Protection Agency, International Agency for Research on Cancer, and World Health Organization. His research focuses in mecha- nisms of chemical genotoxicity and carcinogenicity. See also individual nutrients 1240-1243 defined, 84, 973 energy metabolism, 33, 54, 108, 116, 289 insufficient evidence of, 102-103, 970- extrapolation of data to infants and 971 children, 25, 26-27, 34, 46, 47, 284 nutrient–nutrient interactions, 85, 95 fat (dietary), 459-460, 769, 809, 1234- Aerobics Center Longitudinal Study, 912 1237, 1240-1243 African Americans fiber, 354, 358, 366, 387-389, 396, 398, breast cancer, 379 788, 809, 1234-1237, 1240-1243 energy expenditure, 145-146, 179 glucose metabolism, 285-289, 388, 784- fiber, 379 785 pubertal development, 33 high fat, low carbohydrate diets, 792-810 Age/aging. See also Physical activity 732, 795 amino acid supplements, 702, 706 Arabinose, 345 endurance training, 660 Arachidonic acid, 425, 426, 433-434, 435, energy balance, 221-223, 452 438, 439, 440, 442, 443, 444, 446-447, high-carbohydrate diet, 452 453-454, 455-456, 465, 469, 472, 476, high-fat diet, 452 478, 824, 838 lipoprotein profile, 61 Arginase, 605 low fat, high carbohydrate diet, 773 Arginine (dispensable), 591, 593, 594, 597, protein, 660-661 605, 608, 697-700, 709, 712, 717, 724, resistance training, 660 736, 994-995 runners, 61, 773 Arginine glutamate, 714 skeletal health, 66 Arginionsuccinic acid synthetase, 697, 700 Autoimmune diseases, 487 Arizona Wheat-bran Fiber Trial, 374 Arteriosclerosis, 130, 842 Asians, obese, 352 B Asparagine (dispensable), 591, 593, 594, 700 Balance studies. See also Thermic effect of food Gastric emptying additives, 90, 350, 366, 391 amino acids, 615 energy density of food and, 795 allergies, 692 amino acid composition, 683-686, 689- fat, 438 690 fiber and, 4, 63, 65, 339, 348, 360, 370, 379, 382, 383 energy-dense, nutrient-poor, 302, 312, 794-796 Gastrointestinal distress, fiber intake and, palatability, 425, 795, 808, 809 394-395, 396-397, 398 Gastrointestinal health plant- vs. See monounsaturated fatty acid intake and, also Guar gum 817-818 physical exercise and, 60, 61 polyunsaturated fatty acids and, 820, H 821, 822-823, 826, 828, 830-831 protective effect, 560 Hawaiian natives, 798 saturated fatty acids and, 483 Hazard identification. See also individual sugar intake and, 298-301, 302 nutrients trans fatty acids and, 495-503 animal data, 94-95, 96, 696, 697-698, transport, 543, 544 701-702, 707-708, 711-712, 713-714, Health Canada, 349, 481, 883, 979 721-722, 724, 725-726, 727, 729, 730- Health Professionals Follow-Up Study, 321, 732, 734-735 363, 364, 368, 371-372, 375-376, 377, asthma, 716-717 387, 562, 563, 827 behavior, 295-296 Healthy People 2000, 882 cancer, 319-321 Heart disease. See also Cardiovascular causality, 94, 96, 102 disease; Coronary heart disease Chinese restaurant syndrome, 715-716 carbohydrate intake and, 59 components of, 87, 94-98 fiber intake and, 59-60 data sources, 96-97 physical activity and, 60-61 defined, 87, 975 protein intake and, 60 dental caries, 296-297 Heat of combustion, 108, 109 developmental studies, 708-710 Height. See also Balance studies intervention studies, 794-796, 798-799, advantages, 91, 98 803-807 amino acids, 608-699, 702-703, 705-706, metabolic syndrome, 802-808 712, 714-715, 720, 722-723, 724-725, and micronutrient inadequacy or excess, 726, 727, 729, 730, 731-733, 735 808-809, 816 controlled, 40 obesity risk, 792-797, 814 dose–response assessment, 98 saturated fatty acid intakes, 799-802 feeding trials, 40-41 sugar inadequacy, 809 limitations of, 40-41, 94 High-fiber diets, 297, 374, 378-379, 383, Hunger, 117, 313, 732, 795, 796 788, 839 Hydrogenated fat, 427-428, 436, 455, 456, High fructose corn syrup, 294, 295 479, 495, 498-504, 836 High glycemic index diets, 302 5-Hydroxyindoleacetic acid, 732 Hippuric acid, 604 Hydroxylysine, 593 Histidine (indispensable), 589, 591, 592, 3-Hydroxy-3-methylglutaryl coenzyme A, 545 593, 597, 604, 662, 663-665, 666, 668, Hydroxyproline, 592-593, 728-729 672-675, 678-682, 686, 687, 689, 709, Hyperactivity, 295 712, 720-723, 736, 1004-1005 Hyperammonemia, 699, 714, 718 Homocysteine, 302, 726 Hypercalciuria, 694, 841 Homovanillic acid, 735 Hyperchloremic acidosis, 698 Honolulu Heart Program, 562 Hypercholesteremia, 276, 352, 355, 356, Human chorionic somatomammotropin, 189 358, 359, 366, 367, 494, 495, 721, Human milk. See also 611, 630, 669, 982 specific indicators, nutrients, and life hyperammonemic, 699 stages language development, 447 methodological considerations, 43 malnutrition, 165, 167, 608-609 risk reduction-based methodological considerations, 44-46 Infants, 0-12 months. See also Diabetes design features, 43 mellitus diabetes mellitus (type 2), 381-382, 785, Insulin Resistance Atherosclerosis Study, 786-787, 806-807, 832-833 803 of dietary patterns, 43 Insulin response. See also Hyperinsulinemia fiber and disease prevention, 344, 351, age/aging and, 62 365-368, 374-377, 378-379, 381-382, amino acids, 696, 701, 705, 710 383-384 and cancer, 320 glucose response, 381-382, 803-807 to carbohydrate intake, 268, 269, 273, high fat, low carbohydrate diets, 794- 274, 275, 277, 303, 320, 437 796, 798-799, 803-807 and diabetes, type 2, 63, 275, 303, 306- hyperlipidemia prevention, 365-368 307, 308-312, 784-785 hypertension prevention, 365-368 epidemiological studies, 380-381 insulin response to fat intake, 803-807 to fat, 62, 303, 430, 437, 438, 484-485, low n-9 monounsaturated fatty acid 802-808 diets, 817-818 fiber intake and, 60, 63, 297, 306-307, meta-analyses, 58, 777, 798 339, 351, 353, 355-356, 360, 380-382, methodological issues, 43, 376-377 388 obesity, 311, 773-776, 794-796, 797 to glucose metabolism, 268, 273, 274 polyunsaturated fatty acids, 821, 828, glycemic index of foods and, 63, 269, 830-831, 832-833 306-307, 308-312, 322 satiety and weight maintenance, 383-384 hazard identification, 303, 306-307 timing of, 376 intervention studies, 381-382 Intestinal absorption. See also Basal metabolic rate; 661, 663-665, 666, 668, 669-670, 671- Glucose metabolism; Lipids and lipid 682, 685, 686, 687, 689, 692, 723-725, metabolism; individual nutrients 736, 1010-1011 cellular uptake of nutrients, 273 eiconasanoid, 55 glycogen synthesis and utilization, 274 M insulin, 275 intracellular utilization of sugars, 273- Macronutrients. See also Carbohydrate; Fat; 274 Protein physical activity and, 138 brain requirements, 771 splanchnic, 600, 717 defined, 108 Methionine (indispensable), 589, 591, 593, imbalances and chronic diseases, 771 594, 597, 608, 614, 663-665, 666, 668, integrated planning of intakes, 936-966 672-675, 677, 678, 679-682, 685, 686, Magnesium, 394, 789, 790-791, 813, 838, 687, 689, 711, 723, 725-726, 736, 1204-1211, 1214-1221, 1224-1225 1012-1013 Malabsorption syndrome, 30 Methodological issues. See also Data and Malnutrition, 167, 437, 595, 608-610, 704, database issues; Indicators of 839. See also Protein Nuclear peroxisome proliferator activating amino acid utilization through receptors, 425 nonprotein pathways, 607-608, 684 Nurses’ Health Study, 306-307, 363, 368, balance, 275, 279, 287, 594, 611, 694, 376, 377, 387, 563, 827-828, 842 718 Nutrient intakes. See also 357-360, 365, 366, 371, 374-375, 388, individual nutrients 398-399, 693-694 adverse effects, 970-971 Puberty/pubertal development amino acids, 737-738 age at onset, 33, 983 approach to setting, 968 developmental changes, 177 body composition and size, 225, 240 growth spurt, 142 carbohydrates, 323-324 racial/ethnic differences, 33 cholesterol, 574-575, 578 Purine nucleotide cycle, 604, 605 chronic disease relationships to intakes, Pyrimidine nucleotides, 620 970 Pyruvate, 604, 605 data and database issues, 969-971 energy, 225, 240, 323-324 fat (total), 324, 505, 514 R fiber, 399-400 major information gaps and, 18, 44, 969- Race/ethnicity. See also Special Risk characterization, 86, 89, 90, 976 considerations Risk management, 87, 89, 104, 976 identification of, 97-98 Septicemia, 609, 705 Serine (dispensable), 591, 593, 594, 597, S 604, 608, 711, 719, 729-730, 736, 1018-1019 Satiety, 65, 313, 348, 382-384, 388, 794, 795, Serotonin, 608, 706, 731, 732, 916 796, 843 Seven Countries Study, 562, 817, 826, 827 Saturated fatty acids.

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Lymph nodes may re- Indolent lymphomas have a predicted median survival duce in size spontaneously making it difficult to dis- time of 5–10 years purchase genuine simvastatin. B symp- ◦ sponsive to chemotherapy but have a predicted median toms (fever >38 C generic simvastatin 10mg mastercard, drenching night sweats order generic simvastatin online, weight survival 2–5 years purchase simvastatin 10mg. On Paraproteinaemias examination there is lymphadenopathy and hep- atosplenomegaly. The cells are trophic to the skin particularly the hands and feet, and result Age in plaques and lumps of associated with generalised Most commonly diagnosed 60–65 years. Gas- trointestinallymphomaisparticularlycommoninthe Pathophysiology MiddleEastandisalsoseeninassociationwithcoeliac There is expansion of a single clone of plasma cells that disease. Cleavage of these immunoglobulins tribution according to the Ann Arbor system, which result in the production of Fab and Fc fragments; the Fab is suffixed by B if B symptoms are present (see fragment is termed the Bence-Jones protein and is found Table 12. Investigations There is also production of osteoclast stimulation fac- Thediagnosisismadebylymphnodebiopsy,cytogenetic tor causing lytic bone lesions, bone pain and hypercal- studies of lymphoma cells may give prognostic informa- caemia. Chapter 12: Paraproteinaemias 491 Clinical features Age r Marrow infiltration results in anaemia, thrombocy- Onset most commonly aged 60 years. Spinal cord compression occurs in approx- imately 10–20% of patients at some time during Pathophysiology the course of disease. Hypercalcaemia causes thirst, The abnormal proliferation of lymphoplasmacytoid polyuria, constipation and abdominal pain. Investigations The diagnosis of myeloma is made if there are: Clinical features r Bone marrow aspirate has at least 10–15% plasma Hyperviscosity presents as weakness, tiredness, confu- cells. Patients also often have peripheral lymphadenopa- Other investigations include: thy. Chemotherapy with single alkylating agents improves r Protein electrophoresis shows an IgM parapro- prognosis. Recently, thalidomide has been demonstrated to produce a significant response Management in 30% of patients whose disease progressed following Chemotherapy produces a variable response. Supportive care includes blood transfu- pheresis is used for symptomatic hyperviscosity. Unlike multiple myeloma there are preserved levels of 492 Chapter 12: Haematology and clinical immunology normal immunoglobulins, no lytic bone lesions and no Age renal failure. Investigations Sex Electropheresis of serum protein demonstrates a raised X linked; males only affected. Aetiology Mutations on the X chromosome including deletions, Management frame shifts and insertions. One third of cases are new Aproportionofpatients will go on to develop multi- mutations. Clinical features Type 1 and 2 causes mild disease with bleeding following Investigations injury, menorrhagia and epistaxis. Type 3 causes spon- r Activated partial thromboplastin time is raised, but taneous bleeding from early life. Clinical features Investigations Similar to haemophilia A with mild deficiency causing r Coagulation studies reveal prolonged clotting times only bleeding post surgery and trauma. Activated partial thromboplastin time is raised, but correctablewith50%normalserum(i. Patients re- quire supportive care and normally are managed in in- Management tensive care units. Definition Deficiency of vitamin K, a fat-soluble vitamin, leads to a Disseminated intravascular bleeding tendency. Deficiency occurs in obstructive jaundice and cer- widespread generation of fibrin within blood vessels and tain malabsorption syndromes. Aetiology Causes include Gram −ve and meningococcal sep- Pathophysiology ticaemia, disseminated malignant disease, haemolytic Vitamin K is a co factor in the synthesis of clotting fac- transfusion reactions, trauma, burns, surgery and P. Vitamin K is also involved in Pathophysiology producing proteins required for bone calcification. Widespread activation of intrinsic, extrinsic pathways and platelet aggregation causes consumption of platelets Clinical features and clotting factors (a consumptive coagulopathy) re- Patients present with bruising, mucosal bleeding and sulting in a severe bleeding risk. Red cells are fragmented during Investigations passage through occluded vessels causing a micro angio- The prothrombin time and the partial thromboplastin pathic haemolytic picture. Chapter 12: Bleeding disorders 495 Management ceptors within the spleen) shorten the course of the con- Vitamin K (phytomenadione) can be given as iv. If given orally in malabsorption syndromes it must be performed to exclude leukaemia. Pre- vious response to intravenous immunoglobulin is sug- Acute immune thrombocytopenia gestive of a favourable outcome of splenectomy. Chronic idiopathic thrombocytopenia purpura Age Definition More common in childhood, peak onset 2–10 years. The cause is largely not understood but it may arise 1–4 weeks after a viral infection. Clinical problems only ders such as systemic lupus erythematosus and thyroid become apparent when the platelet count falls below disease. Clinical features Clinical features Children present with petechiae and superficial bruis- Patients present with easy bruising, purpura, epistaxis ing, however in severe cases mucosal bleeds occur such and menorrhagia. Investigations Full blood count and blood film identify the low platelet Investigations count, a bone marrow aspirate demonstrates normal or Full blood count shows the level of platelets. Intravenous immunoglobulin works by blocking Management the Fc receptors in the spleen. Steroids and intra- but is useful in severe bleeding and predicts the poten- venous immunoglobulin (acts by saturating the Fc re- tial success of splenectomy. Other drugs used include 496 Chapter 12: Haematology and clinical immunology azathioprine, vincristine and danzol. Platelet transfu- Clinical features sions are only used in life threatening haemorrhage. Dilation of small arteries and capillaries result in charac- teristic small red spots that blanch on pressure (telang- iectasia) in the skin and mucous membranes particularly Thrombotic thrombocytopenia the nose and gastrointestinal tract. Patients suffer from purpura recurrent epistaxis and chronic gastrointestinal bleeds. Thrombotic disorders Thrombophilia Transfusion medicine Definition Thrombophilia is a group of disorders resulting in an Transfusion medicine increased risk of thrombosis. This failure in the normal control of the coagulation r The patient’s red cells are incubated with commercial cascade results in a thrombotic tendency. Inher- agglutination patterns are read to check the blood itance of a single mutation for any of these conditions group. Antibody screening Forclinical features and management of venous throm- The patient’s serum is also tested for atypical red cell an- boembolism see page 81. Any IgM antibodies present will automatically agglutinate the donor red cells suspended Anti-phospholipid syndrome in saline (see Fig. Cross matching Vascular causes of bleeding Agroup matched blood unit (antigen matched if patient See also Henoch Schonlein Purpura (see page 381). A full cross match consists of incubating the patient’s serum with the donor red cells and then Hereditary haemorrhagic performing a direct agglutination and indirect Coomb’s telangiectasia test as above. In an emergency, if the patient has no atyp- Definition ical antibodies a rapid cross match can be performed by Rare autosomal dominant vascular disorder resulting in briefly incubating the patient’s serum with the donor telangiectasia and recurrent bleeding. There is intravascular haemolysis and coagu- immunological complications and other problems (see lation. Duffy, Kell, Kidd) by previous transfusion or preg- r Hyperkalaemia from degeneration of red cells within nancy. Patient may develop anaemia and jaundice stored blood particularly if there is associated renal about a week after the transfusion. The trans- r Acute respiratory distress syndrome may occur due fusion should be slowed or stopped and an antihis- to hypovolaemia, poor tissue perfusion or if patients tamine given (e. Patients typically develop flushing, Clinical immunology tachycardia, fever and rigors towards the end of trans- fusion. Patients develop vasodilation, hypoten- There are five basic types of hypersensitivity reactions sion, bronchoconstriction and laryngeal constric- (see Table 12. Anyfuture transfusions should be with washed red Type I hypersensitivity (allergy) cells, autologous blood or blood from IgA deficient On the first encounter with an antigen IgE antibodies donors. These bind to a receptor on the surface of If atransfusion reaction is suspected any ongoing trans- mastcells. The remaining blood unit and is cross-linking of IgE on the mast cells which triggers a sample of the patient’s blood should be sent to the lab- them to degranulate releasing histamine and other pre- oratory for repeat cross match. The clinical reaction is characterised by vasodilation, bronchoconstriction, and localised tissue Transfusionequivalenttoreplacingtheentirecirculating oedema (see also anaphylaxis page 499).

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In these children order simvastatin amex, the ketoacid concentration was in the range of 2 to 3 mmol/L (i buy cheap simvastatin online. Long-term data in Westernized popula- tions safe simvastatin 40mg, which could determine the minimal amount of carbohydrate com- patible with metabolic requirements and for optimization of health buy simvastatin with mastercard, are not available. This amount of glucose should be sufficient to supply the brain with fuel in the absence of a rise in circulating aceto- acetate and β-hydroxybutyrate concentrations greater than that observed in an individual after an overnight fast (see “Evidence Considered for Estimating the Average Requirement for Carbohydrate”). This assumes the consumption of an energy-sufficient diet containing an Acceptable Macronutrient Distribution Range of carbohydrate intake (approximately 45 to 65 percent of energy) (see Chapter 11). Data on glucose consumption by the brain for various age groups using information from Dobbing and Sands (1973) and Dekaban and Sadowsky (1978) were also used, which corre- lated weight of the brain with body weight. The average rate of brain glucose utilization in the postabsorptive state of adults based on several studies is approximately 33 µmol/100 g of brain/min (5. Based on these data, the brain’s requirement for carbohydrate is in the range of approximately 117 to 142 g/d (Gottstein and Held, 1979; Reinmuth et al. Regardless of age and the associated change in brain mass, the glucose utilization rate/100 g of brain tissue remains rather constant, at least up to age 73 years (Reinmuth et al. In 351 men (aged 21 to 39 years), the average brain weight at autopsy was reported to be 1. There was excellent correlation between body weight and height and brain weight in adults of all ages. Therefore, the overall dietary carbohydrate requirement in the presence of an energy-adequate diet would be approximately 87 (117 – 30) to 112 (142 – 30) g/d. This amount of carbohydrate is similar to that reported to be required for the prevention of ketosis (50 to 100 g) (Bell et al. The carbohydrate requirement is modestly greater than the potential glucose that can be derived from an amount of ingested protein required for nitrogen balance in people ingesting a carbohydrate-free diet (Azar and Bloom, 1963). This amount of carbohydrate will not provide sufficient fuel for those cells that are dependent on anaerobic glycolysis for their energy supply (e. That is, the cyclic interconversion of glucose with lactate or alanine occurs without a net loss of carbon. The amount of dietary protein required approaches the theoretical maximal rate of gluconeogenesis from amino acids in the liver (135 g of glucose/24 h) (Brosnan, 1999). This amount should be sufficient to fuel central nervous system cells without having to rely on a partial replacement of glucose by ketoacids. Although the latter are used by the brain in a concentration-dependent fashion (Sokoloff, 1973), their utilization only becomes quantitatively significant when the supply of glucose is considerably reduced and their circulating concentra- tion has increased several-fold over that present after an overnight fast. Never- theless, it should be recognized that the brain can still receive enough glucose from the metabolism of the glycerol component of fat and from the gluconeogenic amino acids in protein when a very low carbohydrate diet is consumed. It is well known that the overall rate of energy metabolism decreases with aging (Roberts, 2000a). In adults 70 years of age or older, the glucose oxidation rate was only about 10 percent less than in young adults between 19 and 29 years of age (Robert et al. This decrease is similar to that reported from autopsy data in Japan (mean 1,422 to 1,336 g) (Yamaura et al. Whether glucose oxidation changes out of proportion to brain mass remains a controversial issue (Gottstein and Held, 1979; Leenders et al. In any case, the decrease in brain glucose oxidation rate is not likely to be substantially less. There is no evidence to indicate that a certain amount of carbohydrate should be provided as starch or sugars. However, most individuals do not choose to eat a diet in which sugars exceed approximately 30 percent of energy (Nuttall and Gannon, 1981). This increased fuel requirement is due to the establish- ment of the placental–fetal unit and an increased energy supply for growth and development of the fetus. It is also necessary for the maternal adapta- tion to the pregnant state and for moving about the increased mass of the pregnant woman. This increased need for metabolic fuel often includes an increased maternal storage of fat early in pregnancy, as well as suffi- cient energy to sustain the growth of the fetus during the last trimester of pregnancy (Knopp et al. In spite of the recognized need for increased energy-yielding substrates imposed by pregnancy, the magnitude of need, as well as how much of the increased requirement needs to be met from exogenous sources, remains incompletely understood and is highly variable (Tables 5-23 through 5-27). There is general agreement that the additional food energy requirement is relatively small. Several doubly labeled water studies indicate a progres- sive increase in total energy expenditure over the 36 weeks of pregnancy (Forsum et al. The mean difference in energy expenditure between week 0 and 36 in the studies was approximately 460 kcal/d and is proportional to body weight. The fetus does not utilize significant amounts of free fatty acids (Rudolf and Sherwin, 1983). As part of the adaptation to pregnancy, there is a decrease in maternal blood glucose concentration, a development of insulin resistance, and a tendency to develop ketosis (Burt and Davidson, 1974; Cousins et al. A higher mean respiratory quotient for both the basal metabolic rate and total 24-hour energy expenditure has also been reported in pregnant women when compared to the postpartum period. The increased glucose utilization rate persists after fasting, indicating an increased endogenous production rate as well (Assel et al. Thus, irrespective of whether there is an increase in total energy expenditure, these data indicate an increase in glucose utilization. Earlier, it was reported that the glucose turnover in the overnight fasted state based on maternal weight gain remains unchanged from that in the nonpregnant state (Cowett et al. The fetus reportedly uses approximately 8 ml O2/kg/min or 56 kcal/ kg/d (Sparks et al. The transfer of glucose from the mother to the fetus has been estimated to be 17 to 26 g/d in late gestation (Hay, 1994). If this is the case, then glucose can only account for approximately 51 percent of the total oxidizable substrate transferred to the fetus at this stage of gestation. The mean newborn infant brain weight is reported to be approximately 380 g (Dekaban and Sadowsky, 1978). Assuming the glucose consumption rate is the same for infants and adults (approximately 33 µmol/100 g of brain/min or 8. This is greater than the total amount of glucose transferred daily from the mother to the fetus. Data obtained in newborns indicate that glucose oxidation can only account for approximately 70 percent of the brain’s estimated fuel require- ment (Denne and Kalhan, 1986). In addition, an increase in circulating ketoacids is common in pregnant women (Homko et al. Taken together, these data suggest that ketoacids may be utilized by the fetal brain in utero. If nonglucose sources (largely ketoacids) supply 30 percent of the fuel requirement of the fetal brain, then the brain glucose utilization rate would be 23 g/d (32. These data also indicate that the fetal brain utilizes essentially all of the glucose derived from the mother. There is no evidence to indicate that a certain portion of the carbohydrate must be consumed as starch or sugars. The lactose content of human milk is approximately 74 g/L; this concentration changes very little during the nursing period. Therefore, the amount of precursors necessary for lactose synthesis must increase. Lactose is synthe- sized from glucose and as a consequence, an increased supply of glucose must be obtained from ingested carbohydrate or from an increased supply of amino acids in order to prevent utilization of the lactating woman’s endogenous proteins. However, the amount of fat that can be oxidized daily greatly limits the contribution of glycerol to glucose production and thus lactose formation. For extended periods of power output exceeding this level, the dependence on carbohydrate as a fuel increases rapidly to near total dependence (Miller and Wolfe, 1999). Therefore, for such individuals there must be a corre- sponding increase in carbohydrate derived directly from carbohydrate- containing foods. Additional consumption of dietary protein may assist in meeting the need through gluconeogenesis, but it is unlikely to be con- sumed in amounts necessary to meet the individual’s need. A requirement for such individuals cannot be determined since the requirement for carbohydrate will depend on the particular energy expenditure for some defined period of time (Brooks and Mercier, 1994). They are composed of various proportions of glucose (dextrose), maltose, trisaccharides, and higher molecular-weight products including some starch itself. These syrups are also derived from cornstarch through the conversion of a portion of the glucose present in starch into fructose.

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