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REFERENCES
Date:
June 25, 2005 08:13 PM
Author: 
Darrell Miller
(dm@vitanetonline.com)
Subject: REFERENCES
REFERENCES
1 a. The Surgeon General’s “Nutrition and Health Report.” b. The Centers for Disease Control and Prevention’s “National Health and Examination Survey (NHANES III)” c. The National Academy of Science’s. Diet and Health Report: Health Promotion and Disease Objectives (DHHS Publication No. (PHS) 91-50213, Washington, DC: US Government Printing Office, 1990). e. Dietary Guidelines for Americans. 2 Rolls BJ. Carbohydrates, fats, and satiety. Am J Clin Nutr 1995; 61(4 Suppl):960S-967S. 3 McDowell MA, Briefel RR, Alaimo K, et al. Energy and macronutrient intakes of persons ages 2 months and over in the United States: Third National Health and Nutrition Examination Survey, Phase 1:1988-91. Advance data from vital and health statistics of the Centers for Disease Control and Prevention; No. 255. Hyattsville, Maryland: National Center for Health Statistics; 1994. 4 Center for Science in the Public Interest and McDonald’s Nutrition and You—A guide to Healthy Eating at McDonald’s: McDonald’s Corp,1991. 5 Bray GA. Appetite Control in Adults. In: Fernstrom JD, Miller GD eds. Appetite and Body Weight Regulation. Boca Raton: CRC Press, 1994:1-92. 6 Michnovicz JJ. How to Reduce Your Risk of Breast Cancer. New York: Warner Book Inc. 1994:54. 7 Carcinogens and Anticarcinogens in the Human Diet. National Research Council Report, National Academy of Sciences, 15 Feb. 1996. 8 Van Tallie TB. Obesity: adverse effects on health and longevity. Am J Clin Nutr 1979:32: 2723-33. 9 Somer E, M.A. R.D. Nutrition for Women. New York: Henry Hold and Company, 1993:273. 10 Swaneck GE, Fishman J. Covalent binding of the endogenous estrogen 16A-hydroxyestrone to estradiol in human breast concer cells: characterization and intranuclear localization. Proc Natl Acad Sci USA 1988:85;7831-5. 11 Colditz GA. Epidemiology of breast cancer. Findings from the nurses’ health study. Cancer1993;714:1480-9. 12 Hennen WJ. Breast Cancer Risk Reduction. The effects of supplementation with dietary indoles. Unpublished report 1992. 13 Deslypere BJ. Obesity and cancer. Metabolism 1995;44(93):24-7. 14 Somer E, M.A. R.D. Nutrition for Women. New York: Henry Hold and Company, 1993:281. 15 Whittemore AS, Kolonel LN, John M. Prostate cancer in relation to diet, physical activity, and body size in blacks, whites, and Asians in the United States and Canada. J Natl Cancer Inst 1995;87(9):629-31. 16 Key T. Risk factors for prostate cancer. Cancer Survivor 1995;23:63- 77. 17 Kondo Y, Homma Y, Aso Y, Kakizoe T. Promotional effects of twogeneration exposure to a high-fat diet on prostate carcinogenisis in ACI/Seg mice. Cancer Res 1994;54(23):6129-32. 18 Wang Y, Corr JG, Taler HT, Tao Y, Fair WR, Heston WD. Decreased growth of established human prostate LNCaP tumors in nude mice fed a low-fat diet. J Natl Cancer Inst. 1995;87(19):1456-62. 19 Nixon DW. Cancer prevention clinical trials. In-Vivo 1994;8(5):713-6. 20 Key T. Micronutrients and cancer aetiology: the epidmiological evidence. Proceed Nutr Soc 1994;53(3):605-14. 21 Gorbach SL, Goldin BR. The intestinal microflora and the colon cancer connection. Reviews of Infectious Diseases 1990;12(Suppl 2):S252-61. 22 Shrapnel WS, Calvert GD, Nestel PJ, Truswell AS. Diet and coronary heart disease. The National Heart Foundation of Australia. Med J Australia. 1995;156(Suppl):S9-S16. 23 Ellis JL, Campos-Outcalt D. Cardiovascular disease risk factors in native Americans: a literature review. Am. J. Preventive Med 1994;10(5):295-307. 24 DiBianco R. The changing syndrome of heart failure: an annotated review as we approach the 21st century. J. Hypertension 1994; 12(4 Suppl):S73- S87. 25 Van Itallie TB. Obesity: adverse effects on health and longevity. Am J Clin Nutr 1979;32(suppl):2723-33. 26 Kestin M, Moss R, Clifton PM, Nestel PJ. Comparative effects of three cereal brans on plasma lipids, blood pressure and glucose metabolism in mildly hyper-cholesterolemic men. Am J Clin Nutr 1990;52(4):661-6. 27 Story JA. Dietary fiber and lipid metabolism. In: Spiller GA, Kay RM. eds. Medical Aspects of Dietary Fiber. Penun Medical; New York, 1980, p.138. 28 Stein PP, Black HR. The role of diet in the genesis and treatment of hypertension. Med. Clin. North America. 1993;77(4):831-47. 29 Olin JW. Antihypertensive treatment in patients with peripheral vascular disease. Cleve. Clin. J. Medicine. 1994;61(5):337-44. 30 Tinker LF. Diabetes Mellitus—a priority health care issue for women. J. Am. Dietetic Association. 1994;94(9):976-85. 31 Gaspard UJ, Gottal JM, van den Brule FA. Postmenopausal changes of lipid and glucose metabolism: a review of their main aspects. Maturitas. 1995;21(3):71-8. 32 Coordt MC, Ruhe RC, McDonald RB. Aging and insulin secretion. Proc. Soc. Exp. Biology and Medicine. 1995;209(3):213-22. 33 Felber JP. From Obesity to Diabetes. Pathophysiological Considerations. Int. Journal of Obesity 1992;16:937-952. 34 Gillum RF. The association of body fat distribution with hypertension, hypertensive heart disease, coronary heart disease, diabetes, and cardiovascular risk factors in men and women age 18-79. J Chronic Diseases 1987;40:421-8. 35 Haffner SM, Stern MP, Hazuda HP, et al. Role of obesity and fat distribution in non-insulin-dependent diabetes mellits in Mexican Americans and non- Hispanic whites. Diabetes Care 1986;9:153-61. 36 Bonadonna RC, deFronzo RA. Glucose metabolism in obesity and type 2 diabetes. Diabetes and Metabolism. 1991;17(1 Pt. 2):12-35. 37 Shoemaker JK, Bonen A. Vascular actions of insulin in health and disease. Canadian J. of Applied Physiology. 1995;20(2):127-54. 38 Resnick LM. Ionic Basis of Hypertension, Insulin Resistaince, Vascular Disease, and Related Disorders. The Mechanism of ‘Syndrome X’. Am. J. Hypertension. 1993;6(suppl):123S-134S. 39 Trautwein EA. Dietetic influences on the formation and prevention of cholesterol gallstones. Z. Ernahrugswiss. 1994;33(1):2-15. 40 Cicuttini FM, Spector TD. Osteoarthritis in the aged. Epidemiological issues and optimal management. Drugs and Aging. 1995;6(5):409-20. 41 Melnyk MG, Wienstein E. Preventing obesity in black women by targeting adolescents: a literature review. J Am. Diet. Association. 1994;94(4):536-40. 42 Robinson BE, Gjerdingen Dk, Houge DR. Obesity: a move from traditional to more patient-oriented management. J. Am. Board of Family Practice. 1995;8(2):99-108. 43 Dulloo AG, Miller DS. Reversal of Obesity in the Genetically Obese fa/fa Zucker Rat with an Ehpedrine/Methylxanthines Thermogenic Mixture. J. Nutrition. 1987;117:383-9. 44 Dulloo AG, Miller DS. The thermogenic properties of ephedrin/methylxanthine mixtures: animal studies. Am J Clinical Nutr. 1986;43:388-394. 45 Richelsen B. Health risks of obesity. Significance of the regional distri-bution of adipose tissue. Ugeskr. Laeger. 1991;153(13):908-13. 46 Lissner L, Heitmann BL. Dietary fat and obesity: Evidence from epidemiology. European J. Clinical Nutrition. 1995;49(2):79-90. 47 Lissner L, Heitmann BL. The dietary fat: Carbohydrate ratio in relation to body weight, Current Opinion in Lipidology. 1995;6(1):8-13. 48 Ravussin E. Energy metabolism in obesity. Studies in the Pima Indians. Diabetes Care. 1993;16(1):232-8. 49 O’Dea K. Westernisation, insulin resistance and diabetes in Australian aborigines. Med J. Australia. 1991;155(4):258-64. 50 Bailey C. Fit or Fat . Houghton Mifflen, Boston, 1991. 51 McCarty MF. Optimizing Exercise for Fat Loss. Unpublished report. 52 Weinsier RL, Schutz Y, Bracco D. Reexamination of the relationship of resting metabolic rate and fat-free mass and the the metabolically active components of fat-free mass in humans. Am. J. Clinical Nutrition. 1992;55(4):790-4. 53 Evans WJ. Exercise, nutrition and aging. J. Nutrition. 1992;122(3 suppl):796-801. 54 Schlicker SA, Borra ST, Regan C. The weight and fitness status of United States children. Nutrition Reviews. 1994;52(1):11-7. 55 Raben A, Jensen ND, Marckmann P, Sandstrom B and Astrup A. Spontaeous weight loss during 11 weeks’ ad libitum intake of a low fat/high fiber diet in young, normal weight subjects. Stockholm Press. 1995;916-23. 56 Blundell JE, Cotton JR, Delargy H, Green S, Greenough A, King NA, Lawton, CL. The fat paradox: fat-induced satiety signals versus high fat overconsumption. Short Communication 1995:832-835. 57 Reinhold RB. Late results of gastric bypass surgery for morbid obesity. J Am Coll Nutr 1994;13(4):307-8. 58 McCredie M, Coates M Grulich A. Cancer incidence in migrants to New South Wales (Australia) from the Middle East, 1972-1991. Cancer Causes Control 1994:5(5):414-21. 59 Schiff ER, Dietschy JM. Steatorrhea Associated with Disordered Bile Acid Metabolism. Am. J. Digestive Diseases. 1969;14(6) 60 Nauss JL , Thompson JL and Nagyvary J. The binding of micellar lipids to Chitosan. Lipids. 1983;18(10):714-19. 61 Braconnot H, Sue la natrue ces champignons. Ann Chim Phys 1811;79:265. 62 Odier A. Memoire sur la composition chemique des parties cornees des insectes. Mem Soc Hist Nat Paris 1823;1:29. 63 Johnson EL, Peniston QP. Utilization of shellfish waste for chitin and Chitosan production. Chp 19 In: Chemistry and Biochemistry of Marine Food Products. Martin RE, Flick GJ, Hebard CE and Ward DR (eds.) 1982. p.415-. AVI Publishing Co., Westport, CT. 64 Shahram H. Seafood waste: the potential for industrial use. Kem Kemi 1992;19(3),256-8. 65 Rouget C. Des substances amylacees dans le tissue des animux, specialement les Articules (Chitine). Compt Rend 1859;48:792. Commission on Natural Health Products. 1995 67 Peniston QP and Johnson EL. Method for Treating an Aqueous Medium with Chitosan and Derivatives of Chitin to Remove an Impurity. US Patent 3,533,940. Oct. 30:1970. 68 Poly-D-Glucosamine (Chitosan); Exemption from the Requirement of a Tolerance. Federal Register. 1995;60(75):19523-4. Rules and Regulations. Environmental Protection Agency 40 CFR Part 180. April, 19, 1995. 69 Arul J. “Use of Chitosan films to retard post-harvest spoilage of fruits and vegetables,” Chitin Workshop. ICNHP, North Carolina State University, Raleigh, NC. 70 Karlsen J, Skaugrud O. “Excipient properties of Chitosan,” Manufacturing Chemist. 1991;62:18-9. 71 Winterowd JG, Sandford PA. Chitin and Chitosan. In: Food Polysaccharides and their Applications. Ed: Stephen AM. Marcel Dekker 1995. 72 Chitin Workshop. ICNHP, North Carolina State University, Raleigh, NC. 73 Advances in Chitin and Chitosan. Eds: CJ Brine, PA Sandford, JP Zikakis. Elsevier Applied Science. London. 1992. 74 Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 75 Zikakis, JP. Chitin, Chitosan and Related Enzymes. Academic Press, Inc. 1984. 76 Abelin J and Lassus A. Fat binder as a weight reducer in patients with moderate obesity. ARS Medicina, Helsinki, Aug- October, 1994. 77 Kanauchi O, Deuchi K, Imasato Y, Shizukuishi M, Kobayashi E. Increasing effect of a Chitosan and ascorbic acid mixture on fecal dietary fat excretion. Biosci Biotech Biochem 1994;58(9):1617-20. 78 Maezaki Y, Tsuji K, Nakagawa Y, et al. Hypocholesterolemic effect of Chitosan in adult males. Biosci Biotchnol Biochem1993;57(9):1439-44. 79 Kobayashi T, Otsuka S, Yugari Y. Effect of Chitosan on serum and liver cholesterol levels in cholesterol-fed rats. Nutritional Rep. Int., 1979;19(3):327-34. 80 Sugano M, Fujikawa T, Hiratsuji Y, Hasegawa Y. Hypocholesterolemic effects of Chitosan in cholesterol-fed rats. Nutr Rep. Int. 1978;18(5):531-7. 81 Vahouny G, Satchanandam S, Cassidy M, Lightfoot F, Furda I. Comparative effects of Chitosan and cholestryramine on lymphatic absorption of lipids in the rat. Am J Clin Nutr, 1983;38(2):278-84 82 Suzuki S, Suzuki M, Katayama H. Chitin and Chitosan oligomers as hypolipemics and formulations containing them. Jpn. Kokai Tokkyo Koho JP 63 41,422 [88,422] 22 Feb1988. 83 Ikeda I, Tomari Y, Sugano M. Interrelated effects of dietary fiber on lymphatic cholesterol and triglyceride absorption in rats. J Nutr 1989;119(10):1383- 7. 84 LeHoux JG and Grondin F. Some effects of Chitosan on liver function in the rat. Endocrinology. 1993;132(3):1078-84. 85 Fradet G, Brister S, Mulder D, Lough J, Averbach BL. “Evaluation of Chitosan as a New Hemostatic Agent: In Vitro and In Vivo Experiments In Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 86 Malette W, Quigley H, Gaines R, Johnson N, Rainer WG. Chitosan A New Hemostatic. Annals of Thorasic Surgery. 1983;36:55. 87 Malette W, Quigley H, Adickes ED. Chitosan effect in Vascular Surgery, Tissue Culture and Tissue Regeneration. In R Muzzarelli, C Jeuniaux, GW Gooday, Eds: Chitin in Nature and Technology. Plenum Press, New York. 1986. 88 Okamoto Y, Tomita T, Minami S, et al. Effects of Chitosan on experimental abscess with Staphylococcus aureus in dogs. J. Vet. Med., 1995;57(4):765-7. 89 Klokkevold PR, Lew DS, Ellis DG, Bertolami CN. Effect of Chitosan on lingual hemostasis in rabbits. Journal of Oral-Maxillofac-Surg, 1991;Aug. 49(8):858-63. 89 Surgery, Tissue Culture and Tissue Regeneration. In Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 90 Hiroshi S, Makoto K, Shoji A, Yoshikazu S. Antibacterial fiber blended with Chitosan. Sixth International Conference on Chitin and Chitosan. Sea Fisheries Institute, Gdynia, Poland. August 1994;16-19. 91 Shimai Y, Tsukuda K, Seino H. Antiacne preparations containing chitin, Chitosan or their partial degradation products. Jpn. Kikai Tokkyo Koho JP 04,288,017 [92,288,017] 13 Oct 1992. 92 Suzuki K, Okawa Y, Suzuki S, Suzuki M. Candidacidal effect of peritoneal exudate cells in mice administered with chitin or Chitosan: the role of serine protease in the mechanism of oxygen-independent candidacidal effect. Microbiol Immunol. 1987;31(4):375-9. 93 Sawada G, Akaha Y, Naito H, Fujita M. Synergistic food preservatives containing organic acids, Chitosan and citrus seed extracts. Jpn, Kokai Kokkyo Koho JP 04 27,373 [92 27,373] 30 Jan 1992. 94 Min H-K, Hatai K, Bai S. Some inhibitory effects of Chitosan on fishpathogenic oomycete, Saprolegnia parasitic. Gyobyo Kenkyu, 1994;29(2):73-4. 95 Nelson JL, Alexander JW, Gianotti L, Chalk CL, Pyles T. The influence of dietary fiber on microbial growth in vitro and bacterial translocation after burn injury in mice. Nutr 1994;10(1):32-6. 96 Ochiai Y, Kanazawa Y. Chitosan as virucide. Jpn Kokai Tokkyo Koho 79 41,326. 97 Hillyard IW, Doczi J, Kiernan. Antacid and antiulcer properties of the polysaccharide Chitosan in the rat. Proc Soc Expl Biol Med 1964; 115:1108-1112. 98 Shibasaki K, Sano H, MatsukuboT, Takaesu Y. pH response of human dental plaque to chewing gum supplemented with low molecular Chitosan. Bull- Tokyo-Dent-Coll, 1994:35(2): 61-6. 99 Kato H, Okuda H. Chitosan as antihypertensive. Jpn. Kikoi Tokyo Koho JP 06 56,674 [94 56,674] 100 Kato H, Taguchi T. Mechanism of the rise in blood pressure by sodium chloride and decrease effect of Chitosan on blood pressure. Baiosaiensu to Indasutori 1993;51(12):987-8. 101 Muzzarelli R, Biagini G, Pugnaoni A, Filippini O, Baldassarre V, Castaldini C, and Rizzoli C. Reconstruction of Periodontal Tissue with Chitosan. Biomaterials. 1989;10:598-603. 102 Sapelli P, Baldassarre V, Muzzarelli R, Emanuelli M. Chitosan in Dentistry. In Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 103 Borah G, Scott G, Wortham K. Bone induction by Chitosan in endochrondral bones of the extremities. In Advances in Chitin and Chitosan. Eds: CJ Brine, PA Sandford, JP Zikakis. Elsevier Applied Science. London. 1992. 104 Ito F. Role of Chitosan as a supplementary food for osteoporosis. Gekkan Fudo Kemikaru, 1995;11(2):39-44. 105 Nakamura S, Yoshioka T, hamada S, Kimura I. Chitosan for enhancement of bioavailability of calcium. Jpn. Kokai Tokkyo Koho JP 07 194,316 [95 194,316] 01 Aug 1995. 106 Maekawa A, Wada M. Food Containing chitin or its derivatives for reduction of blood and urine uric acid. Jpn. Kokai Tokkyo Koho JP 03 280,852 [91 280,852], 11 Dec 1991. 107 Weisberg M, Gubner R. Compositions for oral administration comprising Chitosan and a pharmaceutically acceptable carrier. Antacid preparations for alleviating gastric hyperacidity. U.S. patent 3257275 108 Kanauchi O, Deuchi K, Imasato Y, Shizukuishi M, Kobayashi E. Mechanism for the inhibition of fat digestion by Chitosan and for the synergistic effect of ascorbate. Biosci Biotech Biochem1995;59(5):786-90. 109 McCausland CW. Fat Binding Properties of Chitosan as Compared to Other Dietary Fibers. Private communication. 24 Jan1995. 110 Deuchi K, Kanauchi O, Imasato Y, Kobayashi E. Biosci Biotech Biochem. 1994:58,1613-6. 111 Ebihara K, Schneeman BO. Interaction of bile acids, phospholipids, cholesterol and triglyceride with dietary fibers in the small intestine of rats. J Nutr 1989;119(8):1100-6. 112 Weil A, M.D. Natural Health Natural Medicine: Boston: Houghton Mifflin, 1990:182. 113 Chen Y-H, Riby Y, Srivastava P, Bartholomew J, Denison M, Bjeldanes L. Regualtion of CYP1A1 by indolo[3,2-b]carbazole in murine hepatoma cells. J Biol Chem 1995;270(38):22548-55. 114 Intestinal Absorption of metal ions and chelates. Ashmead HD, Graff DJ, Ashmead HH. Charles C Thomas, Springfield, IL 1985. 115 Nutrient Interactions. Bodwell CE, Erdman JW Jr. Marcel Dekker New York 1988. 116 Heleniak EP, Aston B. Prostaglandins, Brown Fat and Weight Loss. Medical Hypotheses 1989;28:13-33. 117 Connor WE, DeFrancesco CA, Connor SL. N-3 fatty acids from fish oil. Effects on plasma lipoproteins and hypertriglyceridemic patients. Ann NY Acad Sci 1993;683:16-34. 118 Conte AA. A non-prescription alternative in weight reduction therapy. The Bariatrician Summer 1993:17-19. 119 McCarty MF. Inhibition of citrate lyase may aid aerobic endurance. Unpublished manuscript. 120 Bray GA. Weight homeostasis. Annual Rev Med 1991;42:205-216. 121 Dulloo AG, Miller DS. The thermogenic properties of Ephedrin/Methylxanthine mixtures: Human studies. Intl J Obesity 986;10:467-481. 122 Arai K, Kinumaki T, Fujita, T. Bulletin Tokai Regional Fisheries Res Lab. 1968;No. 56. 123 Bough WA. Private communication. 124 Freidrich EJ, Gehan, EA, Rall DP, Schmidt LH, Skipper HE. Cancer Chemotherapy Reports 1966;50(4):219-244. 125 A Drovanti, AA Bignamini, AL Rovati. Therapeutic activity of oral glucosamine sulfate in osteoarthritis: A placebo-controlled double-blind investigation. Clinical Therapeutics 1980;3(4):260-272. 126 K Deuchi, O Kanauchi, M Shizukuishi, E Kobayashi. Continuous and massive intake of Chitosan affects mineral and fat-soluble vitamin status in rats fed on a high-fat diet. Biosci. Biotech. Biochemistry. 1995;59(7):1211-6. 127 . BesChitin W in Chitin Wound Healing (video), Unitika Corporation, April 1992.
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CHITOSAN: The Fiber that Binds Fat
Date:
June 25, 2005 07:55 PM
Author: Darrell Miller
(dm@vitanetonline.com)
Subject: CHITOSAN: The Fiber that Binds Fat
Overview
Chitosan is a natural product that inhibits fat absorption. It has the potential to revolutionize the process of losing weight and by so doing, reduce the incidence of some of the most devastating Western diseases we face today. Chitosan is indigestable and non-absorbable. Fats bound to chitosan become nonabsorbable thereby negating their caloric value. Chitosan-bound fat leaves the intestinal tract having never entered the bloodstream. Chitosan is remarkable in that it has the abilty to absorb an average of 4 to 5 times its weight in fat.60
The same features that allow chitosan to bind fats endow it with many other valuable properties that work to promote health and prevent disease. Chitosan is a remarkable substance whose time has come.
Chitosan: A Brief History
Chitin, the precursor to Chitosan, was first discovered in mushrooms by the French professor Henri Braconnot in 1811.61 In the 1820’s chitin was also isolated from insects.62 Chitin is an extremely long chain of N-acetyl-D-glucoseamine
FIGURE 2.
a) Chitosan full structure
b) Abbreviated Chitosan structure
c) Fanciful "crab oligomer" Chitosan structure showing functional claw
glucoseamine units. Chitin is the most abundant natural fiber next to cellulose and is similar to cellulose in many respects. The most abundant source of chitin is in the shells of shellfish such as crab and shrimp. The worldwide shellfish harvest is estimated to be able to supply 50,000 tons of chitin annually.63 The harvest in the United States alone could produce over 15,000 tons of chitin each year.64
Chitin has a wide range of uses but that is the subject of another book. Chitosan was discovered in 1859 by Professor C. Rouget.65 It is made by cooking chitin in alkali, much like the process for making natural soaps. After it
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• Waste Water Purification • Stabilizing Oil Spills • Stabilizing Fats in Food Preparation • Antibacterial Protection for Seeds • Flavor Stabilizer • Stabilizes Perishable Fruits/Vegetables • Ion Exchange Media • Bacterial Immobilizer • Cosmetic and Shampoo Additive • Tableting Excipient • Absorbant for Heavy Metal Removal
Table 5. Industrial Uses of Chitosan 66-75
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• Absorbs and Binds Fat • Promotes Weight Loss • Reduces LDL Cholesterol • Boosts HDL Cholesterol • Promotes Wound Healing • Antibacterial/Anticandida/Antiviral • Acts as Antacid • Inhibits the Formation of Plaque/Tooth Decay • Helps Control Blood Pressure • Helps Dental Restoration/Recovery • Helps to Speed Bone Repair • Improves Calcium Absorption • Reduces Levels of Uric Acid
Table 6. Health and Nutrition Uses of Chitosan 60,66,77-107
is cooked the links of the chitosan chain are made up of glucosamine units. Each glucosamine unit contains a free amino group. These groups can take on a positive charge which gives chitosan its amazing properties. The stucture of chitosan is represented schematically in Figure 2. Research on the uses of chitin and Chitosan flourished in the 1930s and early 1940s but the rise of synthetic fibers, like the rise of synthetic medicines, overshadowed the interest in natural products. Interest in natural products, including chitin and chitosan, gained a resurgence in the 1970s and has continued to expand ever since. Uses of Chit osan Some of Chitosan's major uses—both Industrial and Health and Nutritional—are listed in Tables 5 and 6.
Water Purification
Chitosan has been used for about three decades in water purification processes. 67 When chitosan is spread over oil Spills it holds the oil mass together making it easier to clean up the Spill. Water purification plants throughout the world use chitosan to remove oils, grease, heavy metals, and fine particulate matter that cause turbidity in waste water streams.
Fat Binding/ Weight Loss
Like some plant fibers, chitosan is not digestible; therefore it has no caloric value. No matter how much chitosan you ingest, its calorie count remains at
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Dietary Fiber % Fat Excreted Dietary Fiber %Fat Excreted Chitosan 50.8 + 21.6 Carrageen 9.6 + 1.9 Kapok 8.3 + 1.1 Sodium Alginate 8.1 + 2.2 Pectin 7.4 + 1.9 Locust Bean 6.0 + 1.8 Guar 6.0 + 1.7 Konjak 5.2 + 0.6 Cellulose 5.1 + 2.1 Karaya 4.9 + 1.5 Acacia 4.6 + 0.9 Furcellaran 4.4 + 0.9 Chitin 4.3 + 1.0 Agar 2.8 + 0.4
TABLE 7. Effects of Dietary Fibers on Fecal Lipid Excretion 109,110
fibers, chitosan’s unique properties give it the ability to significantly bind fat, acting like a “fat sponge” in the digestive tract. Table 7 shows a comparison of chitosan and other natural fibers and their ability to inhibit fat absorption. Under optimal conditions, Chitosan can bind an average of 4 to 5 times its weight with all the lipid aggregates tested.60 (NOTE: This assessment was made without the addition of ascorbic acid which potentiates this action even further.77 Studies in Helsinki have shown that individuals taking chitosan lost an average of 8 percent of their body weight in a 4-week period.76 Chitosan has increased oil-holding capacity over other fibers.108 Among the abundant natural fibers, chitosan is unique. This uniqueness is a result of chitosan’s amino groups which make it an acid absorbing (basic) fiber. Most natural fibers are neutral or acidic. Table 7 summarizes the in vivo effects in animals of various fibers on fecal lipid excretion. As can be seen from the results listed, ingestion of chitosan resulted in 5-10 times more fat excretion than any other fiber tested. D-Glucosamine, the building block of chitosan, is not able to increase fecal fat excretion. This is due to the fact that glucosamine is about 97 percent absorbed while chitosan is nonabsorbable. Fats bound to glucosamine would likely be readily absorbed along with the glucosamine. Chitosan, on the other hand, is not absorbed and therefore fats bound to chitosan can not be absorbed.
Cholesterol Control
Chitosan has the very unique ability to lower LDL cholesterol (the bad kind) while boosting HDL cholesterol (the good kind).78 Laboratory tests performed on rats showed that “chitosan depresses serum and liver cholesterol levels in cholesterol- fed rats without affecting performance, organ weight or the nature of the feces.”79 Japanese researchers have concluded that Chitosan “appears to be an effective hypocholesterolemic agent.”80 In other words, it can effectively lower blood serum cholesterol levels with no apparent side effects. A study reported in the American Journal of Clinical Nutrition found that Chitosan is as effective in mammals as cholestryramine (a cholesterol lowering drug) in controlling blood serum cholesterol without the deleterious side effects typical of cholestryramine. 81 Chitosan decreased blood cholesterol levels by 66.2 percent.82 It effectively lowered cholesterol absorption more than guar gum or cellulose.83 Laboratory test results indicated that a 7.5% chitosan formula maintained adequate cholesterol levels in rats, despite a dramatic increase in the intake of cholesterol. 84
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Bone Power - Natures Plus
Date:
June 11, 2005 04:41 PM
Author: Darrell Miller
(dm@vitanetonline.com)
Subject: Bone Power - Natures Plus
Bone Power by no author Energy Times, May 1, 1997
Patricia Q. stopped smoking 20 years ago. At 61, she is active, tries to exercise regularly, eats properly and takes a multivitamin. Most would consider Patricia's lifestyle a sufficient safeguard against the diseases of aging. But one debilitating possibility still concerns her: Osteoporosis-bone thinning. She worries that her bones may have begun weakening almost a decade ago. Although her good health habits can slow the demineralization of her bones, osteoporosis may still take its toll. And as her neck and back begin to obviously round, a possible sign of bone weakness, Patricia frets about her future.
The weakening of bones brought on by age makes them more prone to fracture. One of every two women older than age 50 suffers an osteoporosis-related fracture during her lifetime. Osteoporosis literally means "porous bones," bones that deteriorate and particularly increase the risk of damage to the hip, spine and wrist. In extreme cases, everyday activities assume danger: fractures can result from simply lifting a bag of groceries or from what would otherwise be a minor fall. Some women, fearful of fractures, eliminate many seemingly innocuous activities from their daily lives. Their fear is well founded. Complications from these fractures are a major killer of women.
As women grow older, the risk grows, too. Ten million individuals already have the disease, and 18 million have low bone mass, placing them at risk for osteoporosis.
But research shows that osteoporosis may be preventable and controllable. Regardless of age, eating right, getting enough calcium and performing weight-bearing exercises, can lower your risk for this disease.
Understanding Your Bones
Bones are not static structures but living tissue constantly reformed in a process called remodeling. Every day old bone is removed and replaced with new bone tissue. When more bone is broken down than is replaced (demineralization), bones weaken. When the structure loses sufficient density, you face eminent danger of a fracture.
Generally speaking, bones continue to increase their density and calcium content until you reach your 30s, at which point you probably have attained your peak bone mass. Afterward you may either maintain this mass or begin to lose calcium yearly, but you rarely can increase bone density. The loss of bone density can increase at menopause, when your body ceases producing estrogen, a hormone required to improve bone strength. In addition, some medications, used for a long period, compromise bone density.
Stop Calcium Loss
Eating a diet rich in nutrients that help your bones stay strong should be the first step in stopping or slowing the process of osteoporosis. Calcium, magnesium, vitamin D, phosphorus, soy-based foods and fluoride compose the major nutrients that strengthen bone.
At this moment, 98 percent of your body's calcium resides in your bones, the rest circulates in the blood, taking part in metabolic functions. Because the body cannot manufacture calcium, you must eat calcium in your daily diet to replace the amounts that are constantly lost. When the diet lacks sufficient calcium to replace the amount that is excreted, the body begins to break down bone for the calcium necessary for life-preserving metabolic processes.
Calcium in the diet can generally slow calcium loss from bones, but it usually doesn't seem to replace calcium already gone. The National Institutes of Health recommend 1000-1200 milligrams of dietary calcium per day for premenopausal women and 1200-1500 milligrams for menopausal and postmenopausal women
Good sources of calcium include milk and milk products, yogurt, ricotta, cheese, oysters, salmon, collard greens, spinach, ice cream, cottage cheese, kale, broccoli and oranges.
If you cannot tolerate dairy products, calcium supplements are an easy way to consume calcium. Take supplements with a meal to aid absorption of calcium from the stomach.
In Total Health for Women, Dr. Kendra Kale, clinical assistant professor of medicine at the University of Pennsylvania School of Medicine, urges women to read supplement labels. Scrutinize the fine print to see how many grams are considered "elemental"or "bioavailable"-the form of calcium your body will absorb. If you're taking a 750 milligram supplement, chances are only 300 milligrams are elemental. You should also check that the pill will dissolve within 30 minutes and meets the United States Pharmacopoeia (USP) standards. If tablets do not break down within 30 minutes, they may pass through you unabsorbed and you won't digest the calcium from them that you need.
Absorbing calcium from your digestive tract also requires the presence of vitamin D. Ten to 15 minutes of sun exposure daily usually satisfies vitamin D requirements since most people's bodies can use sunlight to manufacture this substance. So walking to work, or going outside for lunch should supply sufficient ultraviolet light to facilitate calcium absorption.
As we age, however, our body's ability to produce vitamin D gradually diminishes. Our diets can make up the difference: Good dietary sources of vitamin D include egg yolks, liver and fish or nutritional supplements. Many foods, like milk, are supplemented with vitamin D.
Magnesium is another mineral that helps to build bones. Found in leafy, green vegetables, nuts, soybeans, seeds and whole grains, your daily requirement of magnesium should be about half of your calcium intake.
Absorbing calcium for bone health also requires phosphorus, but be careful not to get too much of a good thing: excess phosphorus can actually increase your body's need for calcium. This can present a problem for people who drink bottle after bottle of cola soft drinks or who eat an abundance of processed foods which are often high in phosphorus.
New Soy Research
New research suggests that soy foods, like tofu or soy milk may be vital for preserving bones. A study of more than 60 postmenopausal women who consumed either diets rich in soy's isoflavones or milk protein found that eating soy restored calcium to some of the women's bones. Even though the researchers didn't think such a replacement due to soy was even possible!
The researchers at the University of Illinois believe that isoflavones behave in the body in some of the same ways that estrogen does. The study measured bone density at the lumbar spine, a part of the body at the small of the back that is liable to fractures due to osteoporosis.
Fluoride: Not Just For Teeth
Although most people associate the mineral fluoride with strong teeth, fluoride is just as important for bone strength. Surveys report that osteoporosis is reportedly less common in communities that drink fluoridated water. Fluoride combines with calcium in the bones to slow mineral loss after mid-life. Good sources of this mineral include fish, tea and most animal foods.
Cut Back on Alcohol and Coffee
According to the National Osteoporosis Foundation, consuming lots of caffeine is thought to increase the calcium excreted in your urine. In addition, high levels of protein and sodium in your diet are also believed to increase calcium excretion. And although more studies of protein and sodium are needed to precisely determine how these substances influence calcium loss you should limit the caffeine, protein and salt you take in.
On top of those findings, researchers say that the diuretic action of alcohol and caffeine speed skeletal calcium loss. They believe alcohol may interfere with intestinal absorption of calcium.
Pumping Up
Along with a bone-friendly diet, your exercise program should also be designed to preserve bone. Weight-bearing exercise-exercise that places stress on the bones-strengthens bone density and wards off osteoporosis. Weight-bearing exercises include weight lifting, walking, jogging and jumping rope.
Exercise possesses many benefits for preserving bone, according to Miriam Nelson, Ph.D., author of Strong Women Stay Young. Among them: exercise can help you retain the balance necessary to resist falls and strengthen the muscles that keep you erect. Studies performed on women of all ages found that by doing strength training exercises two times a week for a year, without use of estrogen or hormone replacement therapy (HRT), women, on average, added three pounds of muscle and lost three pounds of fat. They were also 75 percent stronger with improved balance and bone density.
Although strength training can be performed by anyone at any age, Nelson recommends that if you have an unstable medical condition or if you have recently undergone surgery, wait until you recover and speak with your doctor before beginning an exercise program. If you have not exercised in a long time, consult a health practitioner knowledgeable in sports medicine before beginning an exercise program.
Other Options
Drug therapies are now available to combat osteoporosis. One of the most popular is HRT, which supplies estrogen to women undergoing menopause. However, medical experts are still arguing over HRT 's possible role in increasing your risk of cancer, particularly breast cancer.
According to Jan Rattner-Heilman, co-author of Estrogen, the Facts Can Change Your Life, the conflicting studies that balance the benefits and risk of HRT are bound to confuse the average consumer. Estrogen is recommended to prevent bone loss and forestall heart disease and possibly Alzheimer's disease. Most women take estrogen to ease the discomforts of menopause such as hot flashes, and many experts do not believe that it unduly increases the risk of breast cancer for those at low risk.
Heilman warns, however, that estrogen probably should not be taken by women especially at risk for breast cancer risk or those who are already suffer the disease.
Patricia Q. is reluctant to try HRT. "I'm at risk for breast cancer-my mother had it-so I won't take estrogen. I'd rather do what I can without medications. My preference is to watch my diet and exercise as much as I can. That gives me my best chance to avoid osteoporosis."
Doctor Nelson agrees with this perspective She believes that exercise possesses enough benefits to make it the treatment of choice. "The difference between estrogen and strength training is that strength training has a huge Spillover effect; you aren't just decreasing one type of disease. You become stronger with more muscles and less fat, and you become more fit. This decreases your chances for many types of diseases, not just osteoporosis. It can decrease risks for heart disease, diabetes, sleep disturbances, hypertension and more."
If you believe you are at risk for osteoporosis, ask your doctor about the benefits of bone mineral density screening. DEXA scan (dual energy x-ray absorptiometry) measures the bone density in a 15-minute test. But the test is expensive: the cost of this test ranges from $75-200 or more and may not be covered by your health insurance. But financial help may be on the way. A Bone Mass Standardization Act has been introduced in Congress to ensure that the cost of bone mass measurement is covered under Medicare and that standards for coverage are clear and consistent for anyone with medical insurance.
Fighting Osteoporosis at Different Ages
Childbearing years (30-40): These years are particularly important for preserving bone through exercise and good nutrition. Eat plenty of low-fat dairy products, vegetables and soy. Perform weight-bearing exercise such as walking, jogging and weight lifting to attain the greatest amount of bone and muscle possible. Being active reduces risk of injury and makes you stronger. If you smoke, now's the time to stop.
Menopausal years (late 40s-50s): During this time, muscle, bone and estrogen decreases. Minimize loss through diet, walking and weight lifting. Your exercise intensity may have to be decreased but you should not stop being physically active.
Post Menopause (over 60): Focus on reducing your risk of falling. Minimize balance problems and increase muscle strength through exercise.
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ACTIVATED QUERCETIN: a truly hypoallergenic formula...
Date:
May 31, 2005 04:45 PM
Author: Darrell Miller
(dm@vitanetonline.com)
Subject: ACTIVATED QUERCETIN: a truly hypoallergenic formula...
Most of us like to stroll through the countryside. Or play with our pets. Or eat our favorite foods. Or just stop and smell the beautiful flowers. But when our bodily systems are at odds with the natural world, these simple pleasures can be difficult to enjoy. That’s why the nutrition experts at Source Naturals created ACTIVATED QUERCETIN: a truly hypoallergenic formula developed so we all can enjoy the pleasures of nature.
Quercetin: A Unique Bioflavonoid Quercetin is a unique bioflavonoid that has been extensively studied by researchers over the past 30 years. Bioflavonoids - first discovered by Nobel Prize Laureate Albert Szent-Györgyi in the 1930’s - occur as pigments in plants, where they usually are found in close association with vitamin C. Together, bioflavonoids and vitamin C provide antioxidant protection, helping plants withstand harsh variations in wind, rainfall, temperature, and sunlight. Bioflavonoids also can be important to our optimal health - but they cannot be manufactured by our bodies.
Quercetin is no stranger to the human diet: for example, onions may contain up to 6% quercetin (dry weight). As a food supplement, quercetin is hypoallergenic, containing no citrus, wheat, corn, or other common allergens.
Histamine and Leukotriene Inhibition: Helping Us Enjoy the Natural World
Quercetin has a strong affinity for mast cells, the body’s main storage unit for histamines. Like many other bioflavonoids, it has the ability to stabilize cell membranes, preventing histamines from Spilling out of mast cells into the bloodstream and surrounding tissues. Also, quercetin helps inhibit the action of two enzymes - phospholipase A2 and lipoxygenase - which act on arachidonic acid (a key fatty acid constituent of many cell membranes) to create leukotrienes. By inhibiting the release of histamines and leukotrienes into our bloodstreams, quercetin can leave us free to enjoy the natural world.
Activated for Absorption
Quercetin’s main disadvantage is that it is barely soluble in water, and therefore difficult for the body to absorb. Without biochemical help, its beneficial properties may be of very limited use to our bodies. There are lots of quercetin products on the market, but they won’t do much good if the quercetin is not activated for use by the body. Source Naturals combines its quercetin with bromelain, an enzyme derived from pineapple that is known to increase the body’s ability to absorb various substances. Bromelain also is known to have many of the same histamineand leukotriene-inhibiting properties as quercetin, so they enhance each others’ performance. Source Naturals ACTIVATED QUERCETIN contains vitamin C in a non-acidic form, magnesium ascorbate. Studies suggest that vitamin C has a synergistic relationship with quercetin, which improves quercetin’s use by the body. Since the acidic form of vitamin C (ascorbic acid) can create mild stomach irritation, and since quercetin is best taken on an empty stomach to maximize absorption, a pH-buffered form of vitamin C such as magnesium ascorbate is preferable.
Combined Excellence
Source Naturals ACTIVATED QUERCETIN is a state-of-the-art quercetin complex. With 333 mg of quercetin in each tablet, and key additional ingredients to maximize quercetin’s absorption and beneficial properties, ACTIVATED QUERCETIN is a potent formula. It gives you more help - so you can enjoy nature again. Source Naturals ACTIVATED QUERCETIN is available in 50, 100 and 200-tablet bottles.
References
• Busse, W.W., Kopp, D.E., and Middleton, E. (1984). “Flavonoid modulation of human neutrophil function.” Journal of Allergy and Clinical Immunology, 73: 801-809. • Middleton, E. (1981). “Quercetin: an inhibitor of antigen-induced human basophil histamine release.” Journal of Immunology, 127: 546-550. • Pearce, F., Befus, A.D., and Bienenstock, J. (1984). “Mucosal mast cells: III. Effect of Quercetin and other flavonoids on antigen-induced histamine secretion from rat intestinal mast cells.” Journal of Allergy and Clinical Immunology, 73: 819-823. • Tarayre, J.P. and Lauressergues, H., (1977). “Advantages of combination of proteolytic enzymes, flavonoids, and ascorbic acid in comparison with non-steroid anti-inflammatory drugs.” Arzneimforsch. 27: 1144-1149.
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VitaNet®
VitaNet ® Staff
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Celery seed extract is obtained from the fruits of celery. Powdered celery seeds are historically noted as a natural analgesic, and have been in use as a pain reliever throughout the ages. Modern science has found out that celery seeds are a good source of vitamins and minerals as well as phytochemicals that display pharmacological activity. In addition, it exhibits diuretic and hepatoprotective properties. 
