144 Reasons Why Sugar Is Ruining Your Health

Contributed by Nancy Appleton, Ph.D.

Author of the book "Lick The Sugar Habit"

In addition to throwing off the body's homeostasis, excess sugar may result in a number of other significant consequences. The following is a listing of some of the metabolic consequences from a variety of medical journals and other scientific publications.

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Can suppress the immune system.

Upset the mineral relationships in the body.

Cause hyperactivity, anxiety, difficulty concentrating, and crankiness in children.

It can produce a significant rise in triglycerides.

Contributes to the reduction in defense against bacterial infection (infectious diseases).

It causes a loss of tissue elasticity and function, the more you eat the more elasticity and function you loose.

It reduces high-density lipoproteins.

Leads to chromium deficiency.

Leads to cancer of the ovaries.

Can increase fasting levels of glucose.

It causes copper deficiency.

Interferes with absorption of calcium and magnesium.

May make eyes more vulnerable to age-related macular degeneration.

Raises the level of a neurotransmitters: dopamine, serotonin, and norepinephrine.

Can cause hypoglycemia.

Can produce an acidic digestive tract.

Can cause a rapid rise of adrenaline levels in children.

Sugar malabsorption is frequent in patients with functional bowel disease.

Can cause premature aging.

Can lead to alcoholism.

Can cause tooth decay.

It contributes to obesity.

High intake of sugar increases the risk of Crohn's disease, and ulcerative colitis.

It can cause changes frequently found in person with gastric or duodenal ulcers.

Can cause arthritis.

Can cause asthma.

It greatly assists the uncontrolled growth of Candida Albicans (yeast infections).

Can cause gallstones.

Can cause heart disease.

Can cause appendicitis.

Can cause hemorrhoids.

Can cause varicose veins.

Can elevate glucose and insulin responses in oral contraceptive users.

Can lead to periodontal disease.

Can contribute to osteoporosis.

It contributes to saliva acidity.

Can cause a decrease in insulin sensitivity.

Can lower the amount of Vitamin E (alpha-Tocopherol) in the blood.

Can decrease growth hormone.

Can increase cholesterol.

Can increase the systolic blood pressure.

High sugar intake increases advanced glycation end products. (AGEs)(Sugar bound non-enzymatically to protein)

It can interfere with the absorption of protein.

It causes food allergies.

Can contribute to diabetes.

Can cause toxemia during pregnancy.

Can contribute to eczema in children.

Can cause cardiovascular disease.

Can impair the structure of DNA.

Can change the structure of protein.

Can make our skin age by changing the structure of collagen.

Can cause cataracts.

Can cause emphysema.

Can cause atherosclerosis.

Can promote an elevation of low-density lipoproteins. (LDL)

High sugar intake can impair the physiological homeostasis of many systems in the body.

It lowers the enzymes ability to function.

Sugar intake is higher in people with Parkinson’s disease.

Can increase the size of the liver by making the liver cells divide.

Can increase the amount of liver fat.

Can increase kidney size and produce pathological changes in the kidney.

Can damage the pancreas.

Can increase the body's fluid retention.

It is enemy #1 of the bowel movement.

Can cause myopia. (nearsightedness)

Can compromise the lining of the capillaries.

Can make the tendons more brittle.

Can cause headaches, including migraine.

It plays a role in pancreatic cancer in women.

Can adversely affect school children's grades and cause learning disorders.

Can cause depression.

It increases the risk of gastric cancer.

It can cause dyspepsia. (indigestion)

Can increase your risk of getting gout.

Can increase the levels of glucose in an oral glucose tolerance test over the ingestion of complex carbohydrates.

Can increase the insulin responses in humans consuming high-sugar diets compared to low-sugar diets.

A diet high in refined sugar reduces learning capacity.

It can cause less effective functioning of two blood proteins, albumin, and lipoproteins, which may reduce the body’s ability to handle fat and cholesterol.

It can contribute to Alzheimer’s disease.

Can cause platelet adhesiveness.

Can cause hormonal imbalance; some hormones become under active and others become overactive.

Can lead to the formation of kidney stones.

Diets high in sugar can cause free radicals and oxidative stress.

High sugar diet can lead to biliary tract cancer.

High sugar consumption of pregnant adolescents is associated with a twofold-increased risk for delivering a small-for-gestational-age (SGA) infant.

High sugar consumption can lead to substantial decrease in gestation duration among adolescents.

It slows food's travel time through the gastrointestinal tract.

It increases the concentration of bile acids in stools and bacterial enzymes in the colon. This can modify bile to produce cancer-causing compounds and colon cancer.

It increases estradiol (the most potent form of naturally occurring estrogen) in men.

It combines with and destroys phosphatase, an enzyme, which makes the process of digestion more difficult.

It can be a risk factor of gallbladder cancer.

It is an addictive substance.

Can be intoxicating, similar to alcohol.

Can exacerbate PMS.

Sugar given to premature babies can affect the amount of carbon dioxide they produce.

Decrease in sugar intake can increase emotional stability.

The rapid absorption of sugar promotes excessive food intake in obese subjects.

It can worsen the symptoms of children with attention deficit hyperactivity disorder. (ADHD)

It adversely affects urinary electrolyte composition.

Can slow down the ability of the adrenal glands to function.

I.Vs (intravenous feedings) of sugar water can cut off oxygen to the brain.

High sucrose intake could be an important risk factor in lung cancer.

It increases the risk of polio.

High sugar intake can cause epileptic seizures.

It causes high blood pressure in obese people.

In Intensive Care Units, limiting sugar saves lives.

It may induce cell death.

Can increase the amount of food that you eat.

In juvenile rehabilitation camps, when children were put on a low sugar diet, there was a 44% drop in antisocial behavior.

It can lead to prostrate cancer.

It dehydrates newborns.

Can cause low birth weight babies.

Greater consumption of refined sugar is associated with a worse outcome of schizophrenia.

It can raise homocysteine levels in the blood stream.

Sweet food items increase the risk of breast cancer.

It is a risk factor in cancer of the small intestine.

It may cause laryngeal cancer.

It induces salt and water retention.

It may contribute to mild memory loss.

The more sodas a 10 year old child consumes, the less milk.

It can increase the total amount of food consumed.

Exposing a newborn to sugar results in a heightened preference for sucrose relative to water at 6 months and 2 years of age.

It causes constipation.

It causes varicose veins.

Can cause brain decay in prediabetic and diabetic women.

Can increase the risk of stomach cancer.

Can cause metabolic syndrome.

Sugar ingestion by pregnant women increases neural tube defects in embryos.

Can be a factor in asthma.

The higher the sugar consumption the more chances of getting irritable bowel syndrome.

It can affect the brain’s ability to deal with rewards and consequences.

Can cause cancer of the rectum.

Can cause endometrial cancer.

Can cause renal (kidney) cell carcinoma.

Can cause liver tumors.

Can increase inflammatory markers in the blood stream of overweight people.

Can lower Vitamin E levels in the blood stream.

Can increase your appetite for all food.

It plays a role in the etiology and the continuation of acne.

Too much sugar can kill your sex life.

It saps school performance in children.

It can cause fatigue, moodiness, nervousness and depression.

It is common choice of obese individuals.

A linear decrease in the intake of many essential nutrients is associated with increasing total sugar intake.

References:

Note: The word Sugar or Sugars has been changed here to [S] so as to satisfy the Search Engines.

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2. Couzy, F., et al."Nutritional Implications of the Interaction Minerals," Progressive Food and Nutrition Science. 17;1933:65-87.

3. Goldman, J., et al. "Behavioral Effects of Sucrose on Preschool Children." J Abnormal Child Psychol. 1986;14(4):565-577.

4. Scanto, S. and Yudkin, J. "The Effect of Dietary Sucrose on Blood Lipids, Serum Insulin, Platelet Adhesiveness and Body Weight in Human Volunteers." J Postgrad Med. 1969;45:602-607.

5. Ringsdorf, W., Cheraskin, E. and Ramsay R. "Sucrose, Neutrophilic Phagocytosis and Resistance to Disease," Dental Surv. 1976;52(12):46-48.

6. Cerami, A., et al. "Glucose and Aging." Scientific American. May 1987:90. Lee, A. T. and Cerami, A. "The Role of Glycation in Aging." Ann N Y Acad Sci. 663:63-67.

7. Albrink, M. and Ullrich I. H. "Interaction of Dietary Sucrose and Fiber on Serum Lipids in Healthy Young Men Fed High Carbohydrate Diets." Am J Clin Nutr. 1986;43:419-428. Pamplona, R., et al. “Mechanisms of Glycation in Atherogenesis.” Med Hypotheses. Mar 1993;40(3):174-81.

8. Kozlovsky, A., et al. "Effects of Diets High in Simple [S] on Urinary Chromium Losses." Metabolism. June 1986;35:515-518.

9. Takahashi, E., Tohoku University School of Medicine, Wholistic Health Digest. October 1982:41.

10. Kelsay, J., et al. "Diets High in Glucose or Sucrose and Young Women." Am J Clin Nutr. 1974;27:926-936. Thomas, B. J., et al. “Relation of Habitual Diet to Fasting Plasma Insulin Concentration and the Insulin Response to Oral Glucose,” Hum Nutr Clin Nutr. 1983; 36C(1):49_51.

11. Fields, M.., et al. "Effect of Copper Deficiency on Metabolism and Mortality in Rats Fed Sucrose or Starch Diets," Am J Clin Nutr. 1983;113:1335-1345.

12. Lemann, J. "Evidence that Glucose Ingestion Inhibits Net Renal Tubular Reabsorption of Calcium and Magnesium." Am J Clin Nutr. 1976 ;70:236-245.

13. Chiu, C. Am J Clin Nutr. July 2007;86:180-188.

14. "[S], White Flour Withdrawal Produces Chemical Response." The Addiction Letter. Jul 1992:4.

15. Dufty, William. [S] Blues. (New York:Warner Books, 1975)

16. Ibid.

17. Jones, T. W., et al. “Enhanced Adrenomedullary Response and Increased Susceptibility to Neuroglygopenia: Mechanisms Underlying the Adverse Effect of [S] Ingestion in Children.” J Pediatrics. Feb 1995;126:171-7.

18. Ibid.

19. Lee, A. T. and Cerami A. "The Role of Glycation in Aging." Annals of the New York Academy of Science. 1992;663:63-70.

20. Abrahamson, E. and Peget, A. Body, Mind and [S]. (New York: Avon, 1977)

21. Glinsmann, W., et al. “Evaluation of Health Aspects of [S] Contained in Carbohydrate Sweeteners.” F. D. A. Report of [S] Task Force. 1986:39. Makinen K.K.,et al. “A Descriptive Report of the Effects of a 16_month Xylitol Chewing_Gum Programme Subsequent to a 40_Month Sucrose Gum Programme.” Caries Research. 1998; 32(2)107-12. Riva Touger-Decker and Cor van Loveren, “[S] and Dental Caries.” Am.J. Clin.Nutr. Oct 2003; 78:881-892.

22. Keen, H., et al. "Nutrient Intake, Adiposity, and Diabetes." Brit Med J. 1989; 1: 655-658.

23. Tragnone, A. et al. “Dietary Habits as Risk Factors for Inflammatory Bowel Disease.” Eur J Gastroenterol Hepatol. Jan 1995;7(1):47-51.

24. Yudkin, J. Sweet and Dangerous. (New York;Bantam Books:1974), 129.

25. Darlington, L., Ramsey, et al. "Placebo-Controlled, Blind Study of Dietary Manipulation Therapy in Rheumatoid Arthritis," Lancet. Feb 1986;8475(1):236-238.

26. Powers, L. "Sensitivity: You React to What You Eat." Los Angeles Times. Feb. 12, 1985. Cheng, J., et al. “Preliminary Clinical Study on the Correlation Between Allergic Rhinitis and Food Factors.” Lin Chuang Er Bi Yan Hou Ke Za Zhi Aug 2002;16(8):393-396.

27. Crook, W. J. The Yeast Connection. (TN:Professional Books, 1984)

28. Heaton, K. "The Sweet Road to Gallstones." Brit Med J. Apr 14, 1984; 288:1103-1104. Misciagna, G., et al. Am J Clin Nutr. 1999;69:120-126.

29. Yudkin, J. "[S] Consumption and Myocardial Infarction." Lancet. Feb 6, 1971;1(7693):296-297. Chess DJ, et al. “Deleterious Effects of [S] and Protective Effects of Starch on Cardiac Remodeling, Contractile Dysfunction, and Mortality in Response to Pressure Overload.” Am J Physiol Heart Circ Physiol. Sept. 2007;293(3):H1853-H1860.

30. Cleave, T. The Saccharine Disease. (New Canaan, CT: Keats Publishing, 1974)

31. op. cit.

32. Cleave, T. and Campbell, G. Diabetes, Coronary Thrombosis and the Saccharine Disease. (Bristol, England, John Wright and Sons, 1960)

33. Behall, K. "Influence of Estrogen Content of Oral Contraceptives and Consumption of Sucrose on Blood Parameters." Disease Abstracts International. 1982;431-437.

34. Glinsmann, W., et al. “Evaluation of Health Aspects of [S] Contained in Carbohydrate Sweeteners.” F. D. A. Report of [S] Task Force. 1986;39:36_38.

35. Tjäderhane, L. and Larmas, M. “A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats.” Am J Clin Nutr. 1998:128:1807-1810.

36. Wilson R.F. and Ashley F.P. “The Effects of Experimental Variations in Dietary [S] Intake and Oral hygiene on the Biochemical Composition and pH of Free Smooth-surface and Approximal Plaque.” J Dent Res. June 1988;67(6):949-953.

37. Beck-Nielsen H., et al. “Effects of Diet on the Cellular Insulin Binding and the Insulin Sensitivity in Young Healthy Subjects." Diabetes. 1978;15:289-296.

38. Mohanty P. et al. “Glucose Challenge Stimulates Reactive Oxygen Species (ROS) Generation by Leucocytes.” J Clin Endocrin Metabol. Aug 2000; 85(8):2970-2973.

39. Gardner, L. and Reiser, S. "Effects of Dietary Carbohydrate on Fasting Levels of Human Growth Hormone and Cortisol." Proc Soc Exp Biol Med. 1982;169:36-40.

40. Ma Y. et al. “Association Between Carbohydrate Intake and Serum Lipids.” J Am Coll Nutr. Apr 2006;25(2):155-163.

41. Preuss, H. G. “[S]-Induced Blood Pressure Elevations Over the Lifespan of Three Substrains of Wistar Rats.” J Am Coll of Nutr. 1998;17(1) 36-37.

42. Furth, A. and Harding, J. "Why [S] Is Bad For You." New Scientist. Sep 23, 1989;44.

43. Lee AT, Cerami A. “Role of Glycation in Aging.” Ann N Y Acad Sci. Nov 21, 1992; 663:63-70.

44. Appleton, N. Lick the [S] Habit. (New York: Avery Penguin Putnam:1988)

45. Henriksen H. B. and, Kolset S.O. Tidsskr Nor Laegeforen. Sep 6, 2007;127(17):2259-62.

46. Cleave, T.: The Saccharine Disease. (New Canaan Ct: Keats Publishing, Inc., 1974).131.

47. Ibid. 132.

48. Vaccaro O., et al. “Relationship of Postload Plasma Glucose to Mortality with 19 Year Follow-up.” Diabetes Care. Oct 15, 1992;10:328-334. Tominaga, M., et al, “Impaired Glucose Tolerance Is a Risk Factor for Cardiovascular Disease, but Not Fasting Glucose.” Diabetes Care. 1999:2(6):920-924.

49. Lee, A. T. and Cerami, A. "Modifications of Proteins and Nucleic Acids by Reducing [S]: Possible Role in Aging." Handbook of the Biology of Aging. (New York: Academic Press, 1990)

50. Monnier, V. M. "Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process." J Gerontol. 1990:45(4 ):105-110.

51. Dyer, D. G., et al. "Accumulation of Maillard Reaction Products in Skin Collagen in Diabetes and Aging." J Clin Invest. 1993:93(6):421-422.

52. Veromann, S. et al. ”Dietary [S] and Salt Represent Real Risk Factors for Cataract Development.” Ophthalmologica. Jul-Aug 2003 ;217(4):302-307.

53. Monnier, V. M. "Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process." J Gerontol. 1990:45(4):105-110.

54. Schmidt A.M. et al. “Activation of Receptor for Advanced Glycation End Products: a Mechanism for Chronic Vascular Dysfunction in Diabetic Vasculopathy and Atherosclerosis.” Circ Res. Mar 1999 19;84(5):489-97.

55. Lewis, G. F. and Steiner, G. “Acute Effects of Insulin in the Control of VLDL Production in Humans. Implications for The Insulin-resistant State.” Diabetes Care. Apr 1996;19(4):390-3 R. Pamplona, M. .J., et al. "Mechanisms of Glycation in Atherogenesis." Med Hypotheses. 1990;40:174-181.

56. Ceriello, A. “Oxidative Stress and Glycemic Regulation.” Metabolism. Feb 2000;49(2 Suppl 1):27-29.

57. Appleton, N. Lick the [S] Habit. (New York: Avery Penguin Putnam, 1988)

58. Hellenbrand, W. ”Diet and Parkinson's Disease. A Possible Role for the Past Intake of Specific Nutrients. Results from a Self-administered Food-frequency Questionnaire in a Case-control Study.” Neurology. Sep 1996;47(3):644-650 Cerami, A., et al. "Glucose and Aging." Scientific American. May 1987: 90.

59. Goulart, F. S. "Are You [S] Smart?" American Fitness. Mar-Apr 1991: 34-38.

60. Scribner, K.B. et al. “Hepatic Steatosis and Increased Adiposity in Mice Consuming Rapidly vs. Slowly Absorbed Carbohydrate.” Obesity. 2007;15:2190-2199.

61. Yudkin, J., Kang, S. and Bruckdorfer, K. "Effects of High Dietary Sugar." Brit J Med. Nov 22, 1980;1396.

62. Goulart, F. S. "Are You [S] Smart?" American Fitness. March-April 1991: 34-38.

63. Ibid.

64. Ibid.

65. Ibid.

66. Ibid.

67. Nash, J. "Health Contenders." Essence. Jan 1992-23: 79-81.

68. Grand, E. "Food Allergies and Migraine." Lancet. 1979:1:955-959.

69. Michaud, D. ”Dietary [S], Glycemic Load, and Pancreatic Cancer Risk in a Prospective Study.” J Natl Cancer Inst. Sep 4, 2002;94 (17):1293-300.

70. Schauss, A. Diet, Crime and Delinquency. (Berkley Ca; Parker House, 1981)

71. Peet, M. "International Variations in the Outcome of Schizophrenia and the Prevalence of Depression in Relation to National Dietary Practices: An Ecological Analysis." Brit J Psych. 2004;184:404-408.

72. Cornee, J., et al. "A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France, " Eur J Epidemiol. 1995;11:55-65.

73. Yudkin, J. Sweet and Dangerous. (New York: Bantam Books,1974) 129.

74. Ibid, 44.

75. Reiser, S., et al. “Effects of [S] on Indices on Glucose Tolerance in Humans." Am J Clin Nutr. 1986:43;151-159.

76. Reiser, S., et al. “Effects of [S] on Indices on Glucose Tolerance in Humans." Am J Clin Nutr. 1986;43:151-159.

77. Molteni, R, et al. “A High-fat, Refined [S] Diet Reduces Hippocampal Brain-derived Neurotrophic Factor, Neuronal Plasticity, and Learning.” NeuroScience. 2002;112(4):803-814.

78. Monnier, V., “Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process.” J Gerontol. 1990;45:105-111.

79. Frey, J. “Is There [S] in the Alzheimer’s Disease?” Annales De Biologie Clinique. 2001; 59 (3):253-257.

80. Yudkin, J. "Metabolic Changes Induced by [S] in Relation to Coronary Heart Disease and Diabetes." Nutrition and Health. 1987;5(1-2):5-8.

81. Ibid.

82. Blacklock, N. J., "Sucrose and Idiopathic Renal Stone." Nutrition and Health. 1987;5(1-2):9-12. Curhan, G., et al. “Beverage Use and Risk for Kidney Stones in Women.” Ann Inter Med. 1998:28:534-340.

83. Ceriello, A. “Oxidative Stress and Glycemic Regulation.” Metabolism. Feb 2000;49(2 Suppl 1):27-29.

84. Moerman, C. J., et al. “Dietary [S] Intake in the Etiology of Biliary Tract Cancer.” Internat J Epidemiol. Apr 1993;2(2):207-214.

85. Lenders, C. M. “Gestational Age and Infant Size at Birth Are Associated with Dietary Intake among Pregnant Adolescents.” Am J Nutr. Jun 1997;1113-1117.

86. Ibid.

87. Bostick, R. M., et al. "[S], Meat.and Fat Intake and Non-dietary Risk Factors for Colon Cancer Incidence in Iowa Women." Cancer Causes & Control. 1994:5:38-53.

88. Ibid. Kruis, W., et al. "Effects of Diets Low and High in Refined [S] on Gut Transit, Bile Acid Metabolism and Bacterial Fermentation.” Gut. 1991;32:367-370. Ludwig, D. S., et al. “High Glycemic Index Foods, Overeating, And Obesity.” Pediatrics. Mar 1999;103(3):26-32.

89. Yudkin, J and Eisa, O. “Dietary Sucrose and Oestradiol Concentration in Young Men.” Ann Nutr Metabol. 1988:32(2):53-55.

90. Lee, A. T. and Cerami A. "The Role of Glycation in Aging." Ann N Y Acad Sci. 1992; 663:63-70.

91. Moerman, C. et al."Dietary [S] Intake in the Etiology of Gallbladder Tract Cancer." Internat J of Epi. Apr 1993; 22(2):207-214.

92. Avena N.M. “Evidence for [S] Addiction: Behavioral and Nuerochemical Effects of Intermittent, "Excessive [S] Intake." Neurosci Biobehav Rev. 2008;32(1):20-39. Colantuoni, C., et al. “Evidence That Intermittent, Excessive [S] Intake Causes Endogenous Opioid Dependence.” Obes Res. Jun 2002 ;10(6):478-488.

93. Ibid.

94. The Edell Health Letter. Sept 1991;7:1.

95. Sunehag, A. L., et al. “Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition.” Diabetes. 1999 ;48 7991-8000.

96. Christensen L. et al. “Impact of A Dietary Change on Emotional Distress.” J Abnor Psychol. 1985;94(4):565-79.

97. Ludwig, D. S., et al. “High Glycemic Index Foods, Overeating and Obesity.” Pediatrics. Mar1999;103(3):26-32.

98. Girardi, N.L.” Blunted Catecholamine Responses after Glucose Ingestion in Children with Attention Deficit Disorder.” Pediatrics Res. 1995;38:539-542. Berdonces, J. L. “Attention Deficit and Infantile Hyperactivity.” Rev Enferm. Jan 2001;4(1)11-4.

99. Blacklock, N. J. “Sucrose and Idiopathic Renal Stone.” Nutrition and Health. 1987;5(1 & 2):9-17.

100. Lechin, F., et al. “Effects of an Oral Glucose Load on Plasma Neurotransmitters in Humans.” Neurophychobiology. 1992;26(1-2):4-11.

101. Arieff, A. I. “IVs of [S] Water Can Cut Off Oxygen to the Brain.” Veterans Administration Medical Center in San Francisco. San Jose Mercury; June 12/86.

102. De Stefani, E. “Dietary [S] and Lung Cancer: a Case Control Study in Uruguay.” Nutr and Cancer. 1998;31(2):132_7.

103. Sandler, B.P. Diet Prevents Polio. (Milwakuee, WI,: The Lee Foundation for Nutritional Research, 1951)

104. Murphy, P. “The Role of [S] in Epileptic Seizures.” Townsend Letter for Doctors and Patients. May, 2001.

105. Stern, N. & Tuck, M. “Pathogenesis of Hypertension in Diabetes Mellitus.” Diabetes Mellitus, a Fundamental and Clinical Test. 2nd Edition, (Phil. A: Lippincott Williams & Wilkins, 2000)943-957.

106. Christansen, D. “Critical Care: [S] Limit Saves Lives.” Science News. June 30, 2001;159:404.

107. Donnini, D. et al. “Glucose May Induce Cell Death through a Free Radical-mediated Mechanism.” Biochem Biohhys Res Commun. Feb 15, 1996:219(2):412-417.

108. Levine, A.S, et al. “[S] and Fats: The Neurobiology of Preference “ Am J Nutr. 2003 133:831S-834S.

109. Schoenthaler, S. “The Los Angeles Probation Department Diet-Behavior Program: Am Empirical Analysis of Six Institutional Settings.” Int J Biosocial Res. 5(2):88-89.

110. Deneo-Pellegrini H,. et al.Foods, “Nutrients and Prostate cancer: a Case-control study in Uruguay"Br J Cancer. 1999 May;80(3-4):591-7.

111. “Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition.” Diabetes. 1999 Apr;48(4):791-800.

112. Lenders, C. M. “Gestational Age and Infant Size at Birth Are Associated with Dietary Intake Among Pregnant Adolescents.” Am Jf Nutr. 1998;128:807-1810.

113. Peet, M. “International Variations in the Outcome of Schizophrenia and the Prevalence of Depression in Relation to National Dietary Practices: An Ecological Analysis.” Brit J Psychiatry. 2004;184:404-408.

114. Fonseca, V. et al. “Effects of a High-fat-sucrose Diet on Enzymes in Homosysteine Metabolism in the Rat.” Metabolism. 200; 49:736-41.

115. Potischman, N, et.al. “Increased Risk of Early-stage Breast Cancer Related to Consumption of Sweet Foods among Women Less than Age 45 in the United States." Cancer Causes Control. 2002 Dec;13(10):937-46.

116. Negri. E. et al. “Risk Factors for Adenocarcinoma of the Small Intestine.” Intern J Cancer. 1999:82:I2:171-174.

117. Bosetti, C. et al. “Food Groups and Laryngeal Cancer Risk: A Case-control Study from Italy and Switzerland.” Inter J Cancer. 2002:100(3): 355-358.

118. Shannon, M. “An Empathetic Look at Overweight.” CCL Family Found. Nov-Dec.1993. 20(3):3-5.

119. "Health After 50." Johns Hopkins Med Letter. May 1994.

120. Rajeshwari, R. et al.”Secular Trends in Children’s Sweetened-beverage Consumption (1973 to 1994): The Bogalusa Heart Study.” J AM Diet Assoc. Feb 205;105(2):208-214.

121. Levine, A.S. et al. "[S] and Fats: The Neurobiology of Preference." Am J Nutr, 2003;133:831S-834S.

122. Booth, D.A.M. et al. “Sweetness and Food Selection: Measurement of Sweeteners’ Effects on Acceptance.” Sweetness. Dobbing, J., Ed., (London:Springer-Verlag, 1987)

123. Cleve, T.L On the Causation of Varicose Veins. (Bristol, England, John Wright, 1960)

124. op. cit.

125. Ket, Y. et al. “Diabetes, Impaired Fasting Glucose and Development of Cognitive Impairment in Older Women.” Neurology. 2004;63:658–663.

126. Chatenoud, Liliane et al. “Refined-cereal Intake and Risk of Selected Cancers in Italy.” Am. J. Clin Nutr. Dec 1999;70:1107-1110.

127. Yoo, S. et al. “Comparison of Dietary Intakes Associated with Metabolic Syndrome Risk Factors in Young Adults: the Bogalusa Heart Study” Am J Clin Nutr. 2004 Oct;80(4):841-848.

128. Shaw, Gary M. et al. “Neural Tube Defects Associated with Maternal Periconceptional Dietary Intake of Simple [S] and Glycemic Index.” Am. J. Clin Nutr. Nov 2003;78:972-978.

129. Krilanovich, Nicholas J. “Fructose Misuse, the Obesity Epidemic, the Special Problems of the Child, and a Call to Action “ Am. J. Clin Nutr. Nov 2004;80:1446-1447.

130. Jarnerot, G., “Consumption of Refined [S] by Patients with Crohn's Disease, Ulcerative colitis, or Irritable Bowel Syndrome.” Scand J Gastroenterol. 1983 Nov;18(8):999-1002.

131. Allen, S. "[S] and Fats: The Neurobiology of Preference." Am J Nutr. 2003;133:831S-834S.

132. De Stefani E, et al. “Sucrose as a Risk Factor for Cancer of the Colon and Rectum: a Case-control Study in Uruguay.” Int J Cancer. 1998 Jan 5;75(1):40-4.

133. Levi F, et al. “Dietary Factors and the Risk of Endometrial Cancer.” Cancer. 1993 Jun 1;71(11):3575-3581.

134. Mellemgaard A. et al. “Dietary Risk Factors for Renal Cell Carcinoma in Denmark.” Eur J Cancer. Apr 1996;32A(4):673-82.

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