Yes, you can loose as much as 8 Kilograms (1. In short, you will need to QUIT all other foods like MILKs, Fizzy Drinks, Wheat, Pizzas, Breads & Rice. Strictly avoid all vegetables, fruits & juices while you follow this PROTEIN only diet. Our focus should be only Meat consumption base diet, to get maximum benefits. I would recommend: Breakfast; 4- 6 boiled egg whites (no yolks) with at- least 1. Steaks are preferred or Cooked food recipes (no vegetables, rice or grains allowed). Eat your MEAT MEALS in little quantities after every few hours, lets say 2. Drink lots of water. Consume as many Egg whites as you can in a day (1. You can preferably eat cheese as much you like (upto 2. NO Juices, NO Vegetables, NO other food items during the 2 week long schedule. Workout (exercise) at least 2. I can guarantee that once you WILL loose at least 4 KILOGRAMS of weight in just 7 days. Their are NO Side effects or Bad effects if this is practiced for no longer than 2 weeks in single go. Important: However, i will NEVER recommend anyone to follow this diet schedule for Longer than 2 weeks, because your BODY needs everything, from Proteins to Nutrients to Cholesterol to Vitamins. Restricting yourself to PROTEIN only diet for a LONG period of over a month, could make you weaker from inside and can cause hormonal imbalance, thus keeping in limits is the best thing. This PROTEIN diet can be considered safe if practiced after 2 months period gap. 1 Week Diet Plan To Lose 10kgs In TwoThe HCG Weight Loss Diet System How to lose weight fast with HCG. Lose 10KGs a month with the HCG Diet System which is an affordable slimming plan that offers. How to Lose 5 Kilograms in One Week. Losing any significant amount of weight in one week may seem impossible, but it is actually quite doable. This wikiHow will show.
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The degree of asymptomatic hyperuricemia and the risk of gout. A retrospective analysis of a large cohort. Clin Rheumatol. 3. The Gout Diet. While there isn’t a regimented gout diet, anyone who is diagnosed with gout should follow a healthy, balanced diet. Avoid High Purine Foods. General practice geriatric medicine gynaecology infectious disease haematology: musculoskeletal medicine neurology obstetrics oncology ophthalmology paediatrics. Evidence Based Practice. PhD and reviewed by the American College of Rheumatology. Gout Family Practice Notebook. The diet must reduce. Fortunately gout prevention can soon spread to other joint gout family practice notebook. Gout (Podagra) Dr. Weyrich's Naturopathic Functional Medicine Notebook > Schedule a Consultation with Dr. Family history. Polynesian. Treatment- failure gout: a moving target. Arthritis Rheum. 5. Bluestone R, Waisman J, Klinenberg JR. The gouty kidney. Semin Arthritis Rheum. Ben Salem C, Slim R, Fathallah N, Hmouda H. Drug- induced hyperuricaemia and gout. Rheumatology (Oxford). Bleyer AJ, Hart TC. Genetic factors associated with gout and hyperuricemia. Adv Chronic Kidney Dis. Reginato AM, Mount DB, Yang I, Choi HK. The genetics of hyperuricaemia and gout. Nat Rev Rheumatol. Nature versus nurture in gout: a twin study. Liu- Bryan R, Scott P, Sydlaske A, et al. Innate immunity conferred by Toll- like receptors 2 and 4 and myeloid differentiation factor 8. Arthritis Rheum. 5. Nagase M, Baker DG, Schumacher HR Jr. Immunoglobulin G coating on crystals and ceramics enhances polymorphonuclear cell superoxide production: correlation with immunoglobulin G adsorbed. J Rheumatol. 1. 6(7): 9. Ortiz- Bravo E, Sieck MS, Schumacher HR Jr. Changes in the proteins coating monosodium urate crystals during active and subsiding inflammation. Immunogold studies of synovial fluid from patients with gout and of fluid obtained using the rat subcutaneous air pouch model. Arthritis Rheum. 3. Akahoshi T, Murakami Y, Kitasato H. Recent advances in crystal- induced acute inflammation. Curr Opin Rheumatol. Mechanisms of uric acid crystal- mediated autoinflammation. Immunol Rev. 2. 33(1): 2. Terkeltaub RA. What stops a gouty attack? J Rheumatol. Yagnik DR, Evans BJ, Florey O, et al. Macrophage release of transforming growth factor beta. Arthritis Rheum. 5. Recent developments in crystal- induced inflammation pathogenesis and management. Curr Rheumatol Rep. Richette P, Bardin T. Jan 2. 3. 3. 75(9. Singh JA, Reddy SG, Kundukulam J. Risk factors for gout and prevention: a systematic review of the literature. Curr Opin Rheumatol. Mc. Adams- Demarco MA, Maynard JW, Coresh J, Baer AN. Anemia and the onset of gout in a population- based cohort of adults: Atherosclerosis Risk in Communities study. Arthritis Res Ther. Aug 2. 0. Fructose- rich beverages and risk of gout in women. Nov 2. 4. 3. 04(2. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. Genome- wide search for genes affecting serum uric acid levels: the Framingham Heart Study. Dehghan A, K. Association of three genetic loci with uric acid concentration and risk of gout: a genome- wide association study. Genome- wide association study identifies genes for biomarkers of cardiovascular disease: serum urate and dyslipidemia. Am J Hum Genet. 8. Meta- analysis of 2. Population heterogeneity in the genetic control of serum urate. Semin Nephrol. 3. Vitart V, Rudan I, Hayward C, Gray NK, Floyd J, Palmer CN, et al. SLC2. A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout. Campion EW, Glynn RJ, De. Labry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Hall AP, Barry PE, Dawber TR, Mc. Namara PM. Epidemiology of gout and hyperuricemia. A long- term population study. Lin HY, Rocher LL, Mc. Quillan MA, Schmaltz S, Palella TD, Fox IH. Cyclosporine- induced hyperuricemia and gout. N Engl J Med. 3. 21(5): 2. Rho YH, Zhu Y, Zhang Y, Reginato AM, Choi HK. Risk factors for pseudogout in the general population. Rheumatology (Oxford). Pseudogout attack induced during etidronate disodium therapy. Mod Rheumatol. 1. Taggarshe D, Ng CH, Molokwu C, Singh S. Acute pseudogout following contrast angiography. Clin Rheumatol. 2. Ciancio G, Bortoluzzi A, Govoni M. Epidemiology of gout and chondrocalcinosis. Jan 1. 9. 6. 3(4): 2. Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: The National Health and Nutrition Examination Survey 2. Arthritis Rheum. 6. Kim KY, Ralph Schumacher H, Hunsche E, Wertheimer AI, Kong SX. A literature review of the epidemiology and treatment of acute gout. Terkeltaub RA. Gout: Recent advances and emerging therapies. Rheumatic Disease Clinics Update. Garg R, Sayles HR, Yu F, Michaud K, Singh J, Saag KG, et al. Gout- related health care utilization in US emergency departments, 2. Arthritis Care Res (Hoboken). Miao Z, Li C, Chen Y, Zhao S, Wang Y, Wang Z, et al. Dietary and lifestyle changes associated with high prevalence of hyperuricemia and gout in the Shandong coastal cities of Eastern China. J Rheumatol. 3. 5(9): 1. Cea Soriano L, Rothenbacher D, Choi HK, Garc. Contemporary epidemiology of gout in the UK general population. Arthritis Res Ther. Epidemiology of gout and hyperuricaemia in Italy during the years 2. Ann Rheum Dis. 7. Reed D, Labarthe D, Stallones R. Epidemiologic studies of serum uric acid levels among Micronesians. Arthritis Rheum. 1. Jul- Aug. 1. 5(4): 3. Gout in Maoris. Semin Arthritis Rheum. Choi HK, De Vera MA, Krishnan E. Gout and the risk of type 2 diabetes among men with a high cardiovascular risk profile. Rheumatology (Oxford). Olaniyi- Leyimu BY. Consider gout in patients with risk factors, regardless of age. Am Fam Physician. Jul 1. 5. Fravel MA, Ernst ME. Management of gout in the older adult. Am J Geriatr Pharmacother. Singh H, Torralba KD. Therapeutic challenges in the management of gout in the elderly. Simmonds HA, Mc. Bride MB, Hatfield PJ, Graham R, Mc. Caskey J, Jackson M. Polynesian women are also at risk for hyperuricaemia and gout because of a genetic defect in renal urate handling. Br J Rheumatol. 3. Hochberg MC, Thomas J, Thomas DJ, Mead L, Levine DM, Klag MJ. Racial differences in the incidence of gout. The role of hypertension. Arthritis Rheum. 3. Mody GM, Naidoo PD. Gout in South African blacks. Ann Rheum Dis. 4. Outcome evaluations in gout. J Rheumatol. 3. 4(6): 1. Becker MA, Mac. Donald PA, Hunt BJ, Lademacher C, Joseph- Ridge N. Determinants of the clinical outcomes of gout during the first year of urate- lowering therapy. Nucleosides Nucleotides Nucleic Acids. Changing trends of mortality in gout. Semin Arthritis Rheum. Forman JP, Choi H, Curhan GC. Uric acid and insulin sensitivity and risk of incident hypertension. Arch Intern Med. 2. Jan 2. 6. 1. 69(2): 1. Gout and mortality. Clin Exp Rheumatol. Sep- Oct. 2. 6(5 Suppl 5. S1. 15- 9. Lottmann K, Chen X, Sch. Association between gout and all- cause as well as cardiovascular mortality: a systematic review. Curr Rheumatol Rep. The role of uric acid in pediatric hypertension. Krishnan E, Svendsen K, Neaton JD, et al. Long- term cardiovascular mortality among middle- aged men with gout. Arch Intern Med. 2. May 2. 6. 1. 68(1. Kuo CF, See LC, Luo SF, Ko YS, Lin YS, Hwang JS, et al. Gout: an independent risk factor for all- cause and cardiovascular mortality. Rheumatology (Oxford). Gout Tied to Higher Risk of Heart Attack and Stroke. Medscape Medical News. Available at http: //www. Accessed: November 4, 2. Seminog OO, Goldacre MJ. Gout as a risk factor for myocardial infarction and stroke in England: evidence from record linkage studies. Rheumatology (Oxford). Sep 1. 7. Gout Linked to Increased Vascular Disease Risk. Medscape Medical News. Available at http: //www. Accessed: September 8, 2. Clarson LE, Hider SL, Belcher J, Heneghan C, Roddy E, Mallen CD. Increased risk of vascular disease associated with gout: a retrospective, matched cohort study in the UK Clinical Practice Research Datalink. Ann Rheum Dis. 2. Aug 2. 7. Chen JH, Lan JL, Cheng CF, Liang WM, Lin HY, Tsay GJ, et al. Effect of Urate- lowering Therapy on the Risk of Cardiovascular Disease and All- cause Mortality in Patients with Gout: A Case- matched Cohort Study. J Rheumatol. 4. 2 (9): 1. Solomon DH, Liu CC, Kuo IH, Zak A, Kim SC. Effects of colchicine on risk of cardiovascular events and mortality among patients with gout: a cohort study using electronic medical records linked with Medicare claims. Ann Rheum Dis. 7. Cervical myelopathy induced by pseudogout in ligamentum flavum and retro- odontoid mass: a case report. Spinal Cord. 4. 4(1. Puig JG, Michan AD, Jimenez ML, et al. Female gout. Clinical spectrum and uric acid metabolism. Arch Intern Med. 1. Meyers OL, Monteagudo FS. Gout in females: an analysis of 9. Clin Exp Rheumatol. Apr- Jun. Macfarlane DG, Dieppe PA. Diuretic- induced gout in elderly women. Br J Rheumatol. 2. Kramer HM, Curhan G. The association between gout and nephrolithiasis: the National Health and Nutrition Examination Survey III, 1. Am J Kidney Dis. 4. Marchini GS, Sarkissian C, Tian D, Gebreselassie S, Monga M. Gout, stone composition and urinary stone risk: a matched case comparative study. Taniguchi Y, Yoshida M, Tamaki T. Posterior interosseous nerve syndrome due to pseudogout. J Hand Surg Br. 2. Dalbeth N, Schauer C, Macdonald P, Perez- Ruiz F, Schumacher HR, Hamburger S, et al. Methods of tophus assessment in clinical trials of chronic gout: a systematic literature review and pictorial reference guide. Ann Rheum Dis. 7. Stocker SL, Graham GG, Mc. Lachlan AJ, Williams KM, Day RO. Pharmacokinetic and pharmacodynamic interaction between allopurinol and probenecid in patients with gout. 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Unit One Part 2: naming and functional groups gjr-–- Migration of Chemical Compounds from Packaging Polymers during Microwave, Conventional Heat Treatment, and Storage - Bhunia - 2. Comprehensive Reviews in Food Science and Food Safety. Original Article. Authors. Kanishka Bhunia,Dept. Sablani,Corresponding author. Dept. Chemical compounds that are incorporated within polymeric packaging materials to improve functionality, may interact with food components during processing or storage and migrate into the food. Once these compounds reach a specified limit, food quality and safety may be jeopardized. Possible chemical migrants include plasticizers, antioxidants, thermal stabilizers, slip compounds, and monomers. Chemical migration from food packaging is affected by a number of parameters including the nature and complexity of food, the contact time and temperature of the system, the type of packaging contact layer, and the properties of the migrants. Researchers study the migration of food- packaging compounds by exposing food or food- simulating liquids to conventional and microwave heating and storage conditions, primarily through chromatographic or spectroscopic methods; from these data, they develop kinetic and risk assessment models. This review provides a comprehensive overview of the migration of chemical compounds into food or food simulants exposed to various heat treatments and storage conditions, as well as a discussion of regulatory issues. Introduction. Food Packaging is a rapidly evolving field. Besides keeping foods safe from contamination and retaining the nutritional properties and sensory characteristics of foods, packaging provides additional features that are important to consumers. These include resealability, tamper evidence, and the display of product information, as well as reuse or recycling features. The use of both flexible and rigid polymeric packaging is growing rapidly, and is driven by new developments in bio- plastics, and the desire to reduce the bulk and weight of metal and glass containers. Polymer packaging incorporated with chemical compounds is commonly referred to as plastics. Incorporation of low- molecular- weight chemical compounds improves functional properties of plastics. However, the potential influence these substances on product safety and quality remains in question when amount of these migrating compounds in food exceed their specified limits. The term “migration” refers to the diffusion of substances from a zone of higher concentration (the food- contact layer) to one of a lower concentration (usually the food surface). This process is often influenced by food- packaging interactions (Arvatoyannis and Bosnea 2. Diffusion of chemical substances from polymers is a very complex process, and is dependent on several parameters, such as concentration of substances in packaging film and food, nature of the foods, temperature, and the time period over which duration of contact occurs. About the Cover: The rhodium(III)-catalyzed, redox-neutral coupling reaction of N-acyl ketimines, generated in situ from 3-hydroxyisoindolinones, with various. During the process of diffusion, these compounds enter into another matrix (such as film or food), which changes their concentration in both the packaging and food. Although chemical compound migration is mainly a diffusion- controlled process, it is equally important to consider the mechanism of convection and chemical reactions. The degree of solvent stirring, polymer- solvent partition coefficients, swelling of solvents, and concentration- dependent diffusivity play a key role in the diffusion process (Reid and others 1. For example, in a liquid, viscous, or solid food, diffusivity may change since the interface between plastics and food material would be different in each of these cases. The migration process can be divided into 4 major steps: diffusion of chemical compounds through the polymers, desorption of the diffused molecules from the polymer surface, sorption of the compounds at the plastic–food interface, and desorption of the compounds in the food (Ferrara and others 2. The mass diffusion process is usually governed by Fick's law. The steady state diffusion process indicates no change in concentration over the time (. NA is the steady state flux; Cp is the concentration of migrant in the polymer; Dp is the diffusion coefficient of migrant in polymer. For practical purposes, diffusion and partition coefficients are assumed to be constant. In polymers such as polyethylene (PE) and polypropylene (PP) with low glass transition temperatures (Tg), it can be assumed that migration of substances made from these materials obey Fick's laws (Brandsch and others 2. The partition coefficient (kp) that determines the migration at the polymer- solvent boundary can be written as: Cs is the migrant concentration in food/food simulant/solvent phase. The lower the k. P value, the more the migrant is absorbed into the food from the polymer. When fatty foods come in contact with these polymers, this value is low (k. P < 1); for water, it is very high (k. P > 1. 00. 0) (Piringer 2. However, the coefficients can vary with concentration and time, leading to non- Fickian diffusion, resulting from the solvent penetration- induced swelling phenomenon (Piringer 2. Changes in temperature may influence the partition coefficient, as the solubility of the migrant changes both in the polymer and food phases at equilibrium. The temperature dependence of partition coefficient is also described with the Arrhenius equation (Bastarrachea and others 2. The process of diffusion is also influenced by temperature. The fundamental equation correlating diffusion coefficient and temperature is the Arrhenius type equation (Bastarrachea and others 2. D0 is the pre- exponential factor, E is the activation energy for diffusive molecules, R is the gas constant, and T is the absolute temperature of the system. Several approaches have been carried out to develop a new model for predicting diffusion of compounds, where Dp = f (molecular mass of migrant, absolute temperature). This correlation was developed by Brandsch and others (2. AP=AP. Diffusion in glassy polymers is much slower than in rubbery polymers. The likelihood of monomer and oligomer migration increases when a plastic is exposed to high temperatures during thermal processing or when food is stored for extended periods. Transfer of chemical compounds from plastics into food has raised concerns about the potentially adverse effects of food products on human health. Much of the initial work in this area was conducted in the 1. A susceptor is a lightly metalized polyethylene terephthalate (PET) that absorbs electromagnetic waves such as microwave (MW) radiation, converting this energy to heat, which is then transferred from the susceptor to the food product by conduction, creating localized areas of high temperature on the product surface. These new MW- specific packaging materials facilitated the development of foods such as microwaveable popcorn and required testing of packaging materials under conditions that were completely new to the food industry. To analyze the overall migration (OM) from the food- contact plastic layer, 4 food simulants are most commonly used to simplify testing for regulatory compliance purposes since the simulants are less chemically complex (Grob 2. The simulants recommended for migration testing are: water (simulant A) to represent aqueous foods (p. H > 4. 5); 3% aqueous acetic acid (simulant B) to represent acidic aqueous foods (p. H < 4. 5); 1. 0% aqueous ethanol (simulant C) to simulate alcoholic food products, and olive oil (simulant D) for fatty foods. Recent regulations on food simulants provided by EU 1. Ethanol 1. 0% (v/v) for aqueous food (simulant A); acetic acid 3% (w/v) for acidic food (simulant B); 2. C); for fatty food, 5. D1) and vegetable oil (simulant D2), and lastly, Tenax (PPPO) for dry food (simulant E). However, the U. S. Food and Drug Administration recommends 1. I, II, IVB, VIB, and VIIB in Table 1); 1. VIA, VIC), and food oil, HB3. Miglyol 8. 12 for fatty foods (type III, IVA, V, VIIA, IX). HB3. 07 is a mixture of synthetic triglycerides, and Miglyol 8. HB3. 07 is the product of NATEC, Hamburg, Germany. Miglyol 8. 12 is a fractionated coconut oil that is composed of saturated C8 (5. C1. 0 (3. 0–4. 5%) triglycerides with boiling point range of 2. This product is made by Dynamit Nobel Chemicals, HULS America Inc., Piscataway, NJ. Table 1 shows the classification of types of food and food simulants recommended for FCM (Barnes and others 2. Table 1. Classification of food types and food simulants for food- contact materials recommended by FDA (reproduced from chemical migration and food- contact materials by Barnes and others 2. INonacid, aqueous products; may contain salt, sugar, or both (p. H > 5)Aqueous. IIAcid, aqueous products; may contain salt, sugar, or both, and including oil- in- water emulsions of low- or high- fat content. Acidic. 10% ethanol. IIIAqueous, acid or nonacid products containing free oil or fat; may contain salt, and including water- in- oil emulsions of low- or high- fat content. Fatty. Food oil, HB3. Miglyol 8. 12. IVDairy products and modifications A. Water- in- oil emulsions, high or low fat. Fatty. Food oil, HB3. Miglyol 8. 12 B. Oil- in- water emulsions, high or low fat. Aqueous. 10% ethanol. VLow- moisture fats and oils. Fatty. Food oil, HB3. Miglyol 8. 12. VIBeverages A. Containing up to 8% alcohol. Low alcohol. 10% ethanol B. Nonalcoholic. Aqueous. C. Containing more than 8% alcohol. High alcohol. 50% ethanol. VIIBakery products (other than those under types VIII or IX) A. Moist bakery products with surface containing free fat or oil. Fatty. Food oil, HB3. Miglyol 8. 12 B. Moist bakery products with surface containing no free fat or oil. Aqueous. 10% ethanol. VIIIDry solids with the surface containing no free fat or oil. Dry. Tenax. IXDry solids with the surface containing free fat or oil. Fatty. Food oil, HB3. Miglyol 8. 12. Testing the migration of chemical compounds from food packaging into food simulants involves 2 steps (Castle 1. Comprehensive Organic Synthesis - (Second Edition)Comprehensive Organic Synthesis(Second Edition)Editors- in- Chief: Paul Knochel and Gary A. Molander. ISBN: 9. Copyright . 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