Sugar | Rejuvenation Institute of Natural Health

No Sweeteners For You and That Includes Agave!

January 18, 2011February 19, 2012
by RejuvInstitute

Nancy Appleton Ph.D. & G.N. Jacobs
www.nancyappleton.com
December 14, 2009

We get asked about every new sweetener put out by the purveyors of unhealthy sweetness, and agave nectar or syrup is the most recent. Put a gun to our heads and we’ll tell you not to eat it. Actually, we’ll do that without the pistol and dramatics, we’re quite consistent that way.

Our basic position is always in favor of whole foods, because when a food processor converts a naturally sugary food like an apple or generous hunk of agave cactus into a syrup or nectar everything good about the whole food is lost in the production vat.

Whole foods have fiber, and slow down the sugar hit to the body that comes from glucose and fructose. So when a food distributor converts this semi-solid goodness into liquid sweetness, you are loading the revolver for a game of Russian roulette.

In the specific case of agave, the debate comes down to whether glucose or fructose is more harmful to the body. Natural agave, the plant from which tequila is derived, is approximately half and half glucose to fructose. The nectar or syrup appears to be 90% fructose according to published statistics from agave distributors.₁ “It’s almost all fructose, highly processed sugar with great marketing,” said Dr. Ingrid Kohlstadt, a fellow of the American College of
Nutrition and an associate faculty member at Johns Hopkins School of Public Health. “Fructose has a low glycemic index so it doesn’t raise blood glucose.” But it raises blood fructose, which is worse.₂

Fructose has been linked to raised triglycerides₃, more belly fat and contributes to fatty liver disease,
diabetes, heart disease and hypertension₄, which can all be collected together as Metabolic Syndrome.
Fructose doesn’t raise glucose levels in the bloodstream, but there seems to still be an insulin response which does not make it better for diabetics or anyone.₅

Agave seems to have other drawbacks. The first one that sets our teeth on edge is the thought that agave nectar might not actually be agave nectar. According to reporting by the Chicago Tribune, products labeled as being from the blue agave plant may in fact be mostly corn syrup or high-fructose corn syrup. Tequila manufacturers get first call on the expensive blue agave cactus that grows in Mexico. There are strict requirements for tequila to come from the blue agave in the same way the German Beer Purity Law says beer is wheat or barley, hops, water and fermenting yeast. So the nectar producers have a demand for agave that can’t be met by supply and decide to cut what agave they have with similar corn-based fructose.

“Agave is really chemically refined hydrolyzed high-fructose syrup and not from the blue agave plant, organic or raw, as claimed,” says Russ Bianchi, a food and beverage formulator. The Food and Drug Administration says there is no evidence of safety concerns. But in the past, agave products may have been “economically adulterated or misbranded by adding corn syrup or high-fructose corn syrup [HFCS],” said FDA spokesman Michael Herndon.₆

The Chicago Tribune also reports some less well-documented effects of agave nectar consumption that may be a concern. Apparently, some agave products and other sweeteners may have botulism spores and thus shouldn’t be given to small children.

There are assertions that agave may cause miscarriages and/or other harm to pregnant or lactating mothers and agave, like many other sugary products, has also been linked to increased acne.₇

Dr. Ingrid Kohlstadt of the American College of Nutrition and the Johns Hopkins School of Public Health tells us, “Fructose interferes with healthy metabolism when taken at higher doses. Many people have fructose intolerance like lactose intolerance. They get acne or worse diabetes symptoms even though blood glucose is OK.”

Our body can handle two teaspoons a day for any added sweetener to avoid the many related health effects. We live in the same world you do and we understand about occasionally unavoidable sugars and falling off the wagon, but any sweetener removed from its natural state is a refined sweetener that should be avoided as much as possible. Agave
is no different. Now you know.

Editor Note: Young Living’s Agave Nectar is listed on their website as “Organic nectar from Agave Tequilana.” It states, “Organic Blue Agave is much sweeter than sugar, but with a glycemic index of only 11 (sugar has a glycemic index of 68-85). In recipes, use 1/2 to 3/4 cup in place of 1 cup sugar.

References:

¹ Sweet Cactus Farms, www.sweetcactusfarms.com/products.htm
² Agave Provokes a Bitter Debate as a Sweetener, Chicago Tribune March 23, 2008 http://archives.chicagotribune.com/2008/mar/23/food/chi-0323deardorffmar23 ,br />
³ Bantle, J.P. “Effects of Dietary Fructose on Plasma Lipids in Healthy Subjects.” Bantle, J.P. “Effects of Dietary Fructose on Plasma Lipids in Healthy Subjects.”
⁴ Hallfrisch, J., et al. “The Effects of Fructose on Blood Lipid Levels.” Am J Clin Nutr.1983; 37(3): 740–748.
⁵ Basciano, H. et al. “Fructose, Insulin Resistance, and Metabolic Dyslipidemia.”
⁶ Blue Agave Form. “Agave Provokes a Bitter Debate.” www.ianchadwick.com/forum/index.php?/topic/4205-agave-provokes-a-bitter-debate/
⁷ Chicago Tribune. www.chicagotribune.com/features/chi-0323deardorffmar23,1,7478086. story

Sugar

141 Reasons Sugar Ruins Your Health

January 18, 2011February 19, 2012
by RejuvInstitute

(Just Kidding, it’s 143)

By Nancy Appleton PhD (http://www.nancyappleton.com/) & G.N. Jacobs

Excerpted from Suicide by Sugar

Used with permission

Sugar can suppress your immune system.
Sugar upsets the mineral relationships in the body.
Sugar can cause juvenile delinquency in children.
Sugar eaten during pregnancy and lactation can influence muscle force production in offspring, which can affect an individual’s ability to exercise.
Sugar in soda, when consumed by children, results in the children drinking less milk.
Sugar can elevate glucose and insulin responses and return them to fasting levels slower in oral contraceptive users.
Sugar can increase reactive oxygen species (ROS), which can damage cells and tissues.
Sugar can cause hyperactivity, anxiety, inability to concentrate and crankiness in children.
Sugar can produce a significant rise in triglycerides.
Sugar reduces the body’s ability to defend against bacterial infection.
Sugar causes a decline in tissue elasticity and function – the more sugar you eat, the more elasticity and function you lose.
Sugar reduces high-density lipoproteins (HDL).
Sugar can lead to chromium deficiency.
Sugar can lead to ovarian cancer.
Sugar can increase fasting levels of glucose.
Sugar causes copper deficiency.
Sugar interferes with the body’s absorption of calcium and magnesium.
Sugar may make eyes more vulnerable to age-related macular degeneration.
Sugar raises the level of neurotransmitters: dopamine, serotonin, and norepinephrine.
Sugar can cause hypoglycemia.
Sugar can lead to an acidic digestive tract.
Sugar can cause a rapid rise of adrenaline levels in children.
Sugar is frequently malabsorbed in patients with functional bowel disease.
Sugar can cause premature aging.
Sugar can lead to alcoholism.
Sugar can cause tooth decay.
Sugar can lead to obesity.
Sugar increases the risk of Crohn’s disease and ulcerative colitis.
Sugar can cause gastric or duodenal ulcers.
Sugar can cause arthritis.
Sugar can cause learning disorders in school children.
Sugar assists the uncontrolled growth of Candida Albicans (yeast infections).
Sugar can cause gallstones.
Sugar can cause heart disease.
Sugar can cause appendicitis.
Sugar can cause hemorrhoids.
Sugar can cause varicose veins.
Sugar can lead to periodontal disease.
Sugar can contribute to osteoporosis.
Sugar contributes to saliva acidity.
Sugar can cause a decrease in insulin sensitivity.
Sugar can lower the amount of Vitamin E in the blood.
Sugar can decrease the amount of growth hormones in the body.
Sugar can increase cholesterol.
Sugar increases advanced glycation end products (AGEs), which form when sugar binds non-enzymatically to protein.
Sugar can interfere with the absorption of protein.
Sugar causes food allergies.
Sugar can contribute to diabetes.
Sugar can cause toxemia during pregnancy.
Sugar can lead to eczema in children.
Sugar can cause cardiovascular disease.
Sugar can impair the structure of DNA.
Sugar can change the structure of protein.
Sugar can make the skin wrinkle by changing the structure of collagen.
Sugar can cause cataracts.
Sugar can cause emphysema.
Sugar can cause atherosclerosis.
Sugar can promote an elevation of low-density lipoproteins (LDL).
Sugar can impair the physiological homeostasis of many systems in the body.
Sugar lowers enzymes ability to function.
Sugar intake is associated with the development of Parkinson’s disease.
Sugar can increase the size of the liver by making the liver cells divide.
Sugar can increase the amount of liver fat.
Sugar can increase kidney size and produce pathological changes in the kidney.
Sugar can damage the pancreas.
Sugar can increase the body’s fluid retention.
Sugar is the number one enemy of the bowel movement.
Sugar can cause myopia (nearsightedness).
Sugar can compromise the lining of the capillaries.
Sugar can make tendons more brittle.
Sugar can cause headaches, including migraines.
Sugar plays a role in pancreatic cancer in women.
Sugar can adversely affect children’s grades in school.
Sugar can cause depression.
Sugar increases the risk of gastric cancer.
Sugar can cause dyspepsia (indigestion).
Sugar can increase the risk of developing gout.
Sugar can increase the levels of glucose in the blood much higher than complex carbohydrates in a glucose tolerance test can.
Sugar reduces learning capacity.
Sugar can cause two blood proteins – albumin and lipoproteins – to function less effectively, which may reduce the body’s ability to handle fat and cholesterol.
Sugar can contribute to Alzheimer’s disease.
Sugar can cause platelet adhesiveness, which causes blood clots.
Sugar can cause hormonal imbalance – some hormones become underactive and others become overactive.
Sugar can lead to the formation of kidney stones.
Sugar can cause free radicals and oxidative stress.
Sugar can lead to biliary tract cancer.
Sugar increases the risk of pregnant adolescents delivering a small-for-gestational-age (SGA) infant.
Sugar can lead to a substantial decrease the in the length of pregnancy among adolescents.
Sugar slows food’s travel time through the gastrointestinal tract.
Sugar increases the concentration of bile acids in stool and bacterial enzymes in the colon, which can modify bile to produce cancer-causing compounds and colon cancer.
Sugar increases estradiol (the most potent form of naturally occurring estrogen) in men.
Sugar combines with and destroys phosphatase, a digestive enzyme, which makes digestion more difficult.
Sugar can be a risk factor for gallbladder cancer.
Sugar is an addictive substance.
Sugar can be intoxicating, similar to alcohol.
Sugar can aggravate premenstrual syndrome (PMS).
Sugar can decrease emotional stability.
Sugar promotes excessive food intake in obese people.
Sugar can worsen the symptoms of children with attention deficit disorder (ADD).
Sugar can slow the ability of the adrenal glands to function.
Sugar can cut off oxygen to the brain when given to people intravenously.
Sugar is a risk factor for lung cancer.
Sugar increases the risk of polio.
Sugar can cause epileptic seizures.
Sugar can increase systolic blood pressure (pressure when the heart is contracting).
Sugar can induce cell death.
Sugar can increase the amount of food that you eat.
Sugar can cause antisocial behavior in juvenile delinquents.
Sugar can lead to prostate cancer.
Sugar dehydrates newborns.
Sugar can cause women to give birth to babies with low birth weight.
Sugar is associated with a worse outcome of schizophrenia.
Sugar can raise homocysteine levels in the bloodstream.
Sugar increases the risk of breast cancer.
Sugar is a risk factor in small intestine cancer.
Sugar can cause laryngeal cancer.
Sugar induces salt and water retention.
Sugar can contribute to mild memory loss.
Sugar water, when given to children shortly after birth, results in those children preferring sugar water to regular water throughout childhood.
Sugar causes constipation.
Sugar can cause brain decay in pre-diabetic and diabetic women.
Sugar can increase the risk of stomach cancer.
Sugar can cause metabolic syndrome.
Sugar increases neural tube defects in embryos when it is consumed by pregnant women.
Sugar can cause asthma.
Sugar increases the chances of getting irritable bowl syndrome.
Sugar can affect central reward systems.
Sugar can cause cancer of the rectum.
Sugar can cause endometrial cancer.
Sugar can cause renal (kidney) cell cancer.
Sugar can cause liver tumors.
Sugar can increase inflammatory markers in the bloodstreams of overweight people.
Sugar plays a role in the cause and the continuation of acne.
Sugar can ruin the sex life of both men and women by turning off the gene that controls the sex hormones.
Sugar can cause fatigue, moodiness, nervousness, and depression.
Sugar can make many essential nutrients less available to cells.
Sugar can increase uric acid in blood.
Sugar can lead to higher C-peptide concentrations.
Sugar causes inflammation.
Sugar can cause diverticulitis, a small bulging sac pushing outward from the colon wall that is inflamed.
Sugar can decrease testosterone production.
Sugar impairs spatial memory.
Sugar can cause cataracts.

Citations:

1. Sanchez, A, et al. “Role of Sugars in Human Neutrophilic Phagocytosis.” Am J Clin Nutr. Nov 1973; 261: 1180-1184.

2. Bernstein, L et al. “Depression of Lymphocyte Transformation Following Oral Glucose Ingestion.” Am J Clin Nutr. 1997; 30: 613.

3. Schauss, A. Diet, Crime and Delinquency. (Berkley, CA: Parker House, 1981).

4. Bayol, S.A “Evidence that a Maternal ‘Junk Food’ Diet during Pregnancy and Lactation Can Reduce Muscle Force in Offspring.” Eur J Nutr. Dec 19, 2008.

5. Rajeshwari, R, et al. “Secular Trends in Children’s Sweetened-beverage Consumption (1973 to 1994): The Bogalusa Heart Study.” J Am Diet Assoc. Feb 2005; 105(2): 208-214.

6. Behall, K. “Influence of Estrogen Content of Oral Contraceptives and Consumption of Sucrose on Blood Parameters.” Disease Abstracts International.1982; 431-437. POPLINE Document Number: 013114.

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

Couzy, F., et al. “Nutritional Implications of the Interaction Minerals.”Progressive Food & Nutrition Science. 1933; 17: 65-87.

8. Goldman, L et al. “Behavioral Effects of Sucrose on Preschool Children.” J Abnorm Child Psy. 1986; 14(4): 565-577.

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

10. Ringsdorf, w., Cheraskin, E., and Ramsay. R “Sucrose, Neutrophilic Phagocytosis and Resistance to Disease.” Dental Survey. 1976; 52(12): 46-48.

11. Cerami, A, et al. “Glucose and Aging.” Scientific American. May 1987: 90.

Lee, A T. and Cerami, A “The Role of Glycation in Aging.” Annals N Y Acad Sci. 663: 63-67.

12. Albrink, M. and Ullrich, LH. “Interaction of Dietary Sucrose and Fiber on Serum Lipids in Healthy Young Men Fed High Carbohydrate Diets.” Clin Nutr.1986;43: 419-428.

Pamplona, R, et al. “Mechanisms of Glycation in Atherogenesis.” Medical Hypotheses. Mar 1993; 40(3): 174-81.

13. Kozlovsky, A, et al. “Effects of Diets High in Simple Sugars on Urinary Chromium Losses.” Metabolism. Jun 1986; 35: 515-518.

14. Takahashi, E. Tohoku, University School of Medicine. Wholistic Health Digest. Oct 1982: 41.

15. Kelsay, L et al. “Diets High in Glucose or Sucrose and Young Women.” Am J Clin Nutr. 1974; 27: 926-936.

Thomas, B. L 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.

16. 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.

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

18. Chiu, C. “Association between Dietary Glycemic Index and Age-related Macular Degeneration in Nondiabetic Participants in the Age-Related Eye Disease Study.” Am J Clin Nutr. Jul 2007; 86: 180-188.

19. “Sugar, White Flour Withdrawal Produces Chemical Response.” The Addiction Letter. Jul1992: 4.

20. Dufty, William. Sugar Blues. (New York: Warner Books, 1975).

21. Ibid.

22. Jones, T.W., et al. “Enhanced Adrenomedullary Response and Increased Susceptibility to Neuroglygopenia: Mechanisms Underlying the Adverse Effect of Sugar Ingestion in Children.” J Ped. Feb 1995; 126: 171-177.

23. Ibid.

24. Lee, A. T. and Cerami, A. “The Role of Glycation in Aging.” Annals NY Acad Sci. 1992; 663: 63-70.

25. Abrahamson, E. and Peget, A. Body, Mind and Sugar. (New York: Avon, 1977).

26. Glinsmann, w., et al. “Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners.” FDA Report of Sugars 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 Res. 1998; 32(2): 107-12.

Riva Touger-Decker and Cor van Loveren, “Sugars and Dental Caries.” Am J Clin Nutr. Oct 2003; 78: 881-892.

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

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

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

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

31. Schauss, A. Diet, Crime and Delinquency. (Berkley, CA: Parker House, 1981).

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

33. Heaton, K. “The Sweet Road to Gallstones.” Brit Med J. Apr 14, 1984; 288: 1103-1104.

Misciagna, G., et al. “Insulin and Gallstones.” Am J Clin Nutr. 1999; 69: 120-126.

34. Yudkin, J. “Sugar Consumption and Myocardial Infarction.” Lancet. Feb 6, 1971; 1(7693): 296-297.

Chess, D.J., et al. “Deleterious Effects of Sugar and Protective Effects of Starch on Cardiac Remodeling, Contractile Dysfunction, and Mortality in Response to Pressure Overload.” Am J Physiol Heart Circ Physiol. Sep 2007; 293(3): H1853-H1860.

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

36. Ibid.

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

38. Glinsmann, W., et al. “Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners.” F.D.A. Report of Sugars Task Force. 1986; 39: 36-38.

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

40. Wilson, RE and Ashley, EP. “The Effects of Experimental Variations in Dietary Sugar Intake and Oral Hygiene on the Biochemical Composition and pH of Free Smooth-surface and Approximal Plaque.” J Dent Res. Jun 1988; 67(6): 949-953.

41. 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.

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

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

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

45. Furth, A and Harding, J. “Why Sugar Is Bad For You.” New Scientist. Sep 23, 1989; 44.

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

47. Appleton, N. Lick the Sugar Habit. (New York: Avery Penguin Putnam, 1988).

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

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

50. Ibid., at 132.

51. Vaccaro, 0., 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.

52. Lee, A T. and Cerami, A “Modifications of Proteins and Nucleic Acids by Reducing Sugars: Possible Role in Aging.” Handbook of the Biology of Aging. (New York: Academic Press, 1990).

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

54. 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.

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

56. Monnier, V. M. “Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process.” J Ger. 1990; 45(4): 105-110.

57. Schmidt, AM., 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; 1984(5): 489-97.

58. 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): 390-393.

R. Pamplona, M.J., et al. “Mechanisms of Glycation in Atherogenesis.” Medical Hypotheses. 1990; 40: 174-181.

59. Ceriello, A “Oxidative Stress and Glycemic Regulation.” Metabolism. Feb 2000; 49(2 Suppl1): 27-29.

60. Appleton, Nancy. Lick the Sugar Habit. (New York: Avery Penguin Putnam, 1988).

61. Hellenbrand, W., et al. “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: 644-650.

Cerami, A, et al. “Glucose and Aging.” Sci Am. May 1987: 90.

62. Goulart, F. S. “Are You Sugar Smart?” American Fitness. Mar-Apr 1991: 34-38.

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

64. Yudkin, L Kang, S., and Bruckdorfer, K. “Effects of High Dietary Sugar.” Brit Med J. Nov 22, 1980; 1396.

65. Goulart, F. S. “Are You Sugar Smart?” American Fitness. Mar-Apr 1991: 34-38

66. Ibid.

67. Ibid.

68. Ibid.

69. Ibid.

70. Nash, J. “Health Contenders.” Essence. Jan 1992; 23: 79-81.

71. Grand, E. “Food Allergies and Migraine.” Lancet. 1979; 1: 955-959.

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

73. Schauss, A. Diet, Crime and Delinquency. (Berkley, CA: Parker House, 1981).

74. 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 Psy. 2004; 184: 404-408.

75. Cornee, L et al. “A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France.” Eur J Epid. 1995; 11: 55-65.

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

77. Ibid., at 44.

78. Reiser, S., et al. “Effects of Sugars on Indices on Glucose Tolerance in Humans.” Am J Clin Nutr. 1986: 43; 151-159.

79. Ibid.

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

80. Monnier, v., “Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process.” J Ger. 1990; 45: 105-111.

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

82. Yudkin, J. “Metabolic Changes Induced by Sugar in Relation to Coronary Heart Disease and Diabetes.” Nutr Health. 1987; 5(1-2): 5-8.

83. Ibid.

84. Blacklock, N.J., “Sucrose and Idiopathic Renal Stone.” Nutr 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.

85. Ceriello, A “Oxidative Stress and Glycemic Regulation.” Metabolism. Feb 2000; 49(2 Suppl1): 27-29.

86. Moerman, C. L et al. “Dietary Sugar Intake in the Etiology of Biliary Tract Cancer.” Inter J Epid. Apr 1993; 2(2): 207-214.

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

88. Ibid.

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

90. Bostick, RM., et al. “Sugar, Meat, and Fat Intake and Non-dietary Risk Factors for Colon Cancer Incidence in Iowa Women.” Cancer Causes & Control. 1994; 5: 38-53.

Kruis, w., et al. “Effects of Diets Low and High in Refined Sugars 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.

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

92. Lee, AT. and Cerami, A “The Role of Glycation in Aging.” Annals N Y Acad Sci. 1992; 663: 63-70.

93. Moerman, c., et al.”Dietary Sugar Intake in the Etiology of Gallbladder Tract Cancer.” Inter J Epid. Apr 1993; 22(2): 207-214.

94. Avena, N.M. “Evidence for Sugar Addiction: Behavioral and Nuerochemical Effects of Intermittent, Excessive Sugar Intake.” Neurosci Biobehav Rev. 2008; 32(1): 20-39.

Colantuoni, c., et al. “Evidence That Intermittent, Excessive Sugar Intake Cause Endogenous Opioid Dependence.” Obesity. Jun 2002; 10(6): 478-488.

95. Ibid.

96. The Edell Health Letter. Sep 1991; 7: 1.

97. Christensen, L., et al. “Impact of A Dietary Change on Emotional Distress.” J Abnorm Psy. 1985; 94(4): 565-79.

98. Ludwig, D.S., et al. “High Glycemic Index Foods, Overeating and Obesity.”Pediatrics. Mar 1999; 103(3): 26-32.

99. Girardi, N.L.” Blunted Catecholamine Responses after Glucose Ingestion in Children with Attention Deficit Disorder.” Pediatr Res. 1995; 38: 539-542.

Berdonces, J.L. “Attention Deficit and Infantile Hyperactivity.” Rev Enferm. Jan 2001; 4(1): 11-4.

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

101. Arieff, AI. “IVs of Sugar Water Can Cut Off Oxygen to the Brain.” Veterans Administration Medical Center in San Francisco. San Jose Mercury. Jun 12/86.

102. De Stefani, E. “Dietary Sugar and Lung Cancer: a Case Control Study in Uruguay.” Nutr Cancer. 1998; 31(2): 132-7.

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

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

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

Citation Preuss, H.G., et al. “Sugar-Induced Blood Pressure Elevations Over the Lifespan of Three Substrains of Wistar Rats.” J Am Coli Nutr. 1998; 17(1): 36-37.

106. Christansen, D. “Critical Care: Sugar Limit Saves Lives.” Science News. Jun 30, 2001; 159: 404.

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

107. Levine, AS., et al. “Sugars and Fats: The Neurobiology of Preference” J Nutr. 2003; 133: 831S-834S.

108. 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.

109. Deneo-Pellegrini H., et al. “Foods, Nutrients and Prostate Cancer: a Casecontrol Study in Uruguay.” Br J Cancer. May 1999; 80(3-4): 591-7.

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

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

112. 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 Psy. 2004; 184: 404-408.

113. Fonseca, v., et al. “Effects of a High-fat-sucrose Diet on Enzymes in Homosysteine Metabolism in the Rat.” Metabolism. 2000; 49: 736-41.

114. 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. Dec 2002; 13(10): 937-46.

115. Negri, E., et al. “Risk Factors for Adenocarcinoma of the Small Intestine.” Int J Cancer. Jul1999; 2(2): 171-4.

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

117. Shannon, M. “An Empathetic Look at Overweight.” CCL Family Found. NovDec 1993; 20(3): 3-5. POPLINE Document Number: 091975.

118. Harry, G. and Preuss, MD, Georgetown University Medical School. http://www.usa.weekend.com/food/carper_archive/961201carper_eatsmart.html.

119. Beauchamp, G.K., and Moran, M. “Acceptance of Sweet and Salty Tastes in 2-year-old Children.” Appetite. Dec 1984; 5(4): 291-305.

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

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

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

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

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

125. Powers, L. “Sensitivity: You React to What You Eat.” Los Angeles Times. Feb 12, 1985.

Cheng, L 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.

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

127. Allen, S. “Sugars and Fats: The Neurobiology of Preference.” J Nutr. 2003; 133: 831S-834S.

128. 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. Jan 5, 1998; 75(1): 40-4.

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

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

131. Rogers, AE., et al. “Nutritional and Dietary Influences on Liver Tumorigenesis in Mice and Rats.” Arch Toxicol Suppl. 1987; 10: 231-43. Review.

132. Sorensen, L.B., et al. “Effect of Sucrose on Inflammatory Markers in Overweight Humans” Am J Clin Nutr. Aug 2005; 82(2).

133. Smith, R.N., et al. “The Effect of a High-protein, Low Glycemic-load Diet Versus a Conventional, High Glycemic-load Diet on Biochemical Parameters Associated with Acne Vulgaris: A Randomized, Investigator-masked, Controlled TriaL” JAm Acad Dermatol. 2007; 57: 247-256.

134. Selva, D.M., et al. “Monosaccharide-induced Lipogenesis Regulates the Human Hepatic Sex Hormone-binding Globulin Gene.” J Clin Invest. 2007. doi:10.1172/JCI32249.

135. Krietsch, K., et al. “Prevalence, Presenting Symptoms, and Psychological Characteristics of Individuals Experiencing a Diet-related Mood-disturbance.”Behavior Therapy. 1988; 19(4): 593-604.

136. Berglund, M., et al. “Comparison of Monounsaturated Fat with Carbohydrates as a Replacement for Saturated Fat in Subjects with a High Metabolic Risk Profile: Studies in the Fasting and Postprandial States.” Am J Clin Nutr. Dec 1, 2007; 86(6): 1611-1620.

137. Gao, X., et al. “Intake of Added Sugar and Sugar-Sweetened Drink and Serum Uric Acid Concentration in US Men and Women.” Hypertension. Aug 1, 2007; 50(2): 306-312.

138. Wu, T., et al. Fructose, Glycemic Load, and Quantity and Quality of Carbohydrate in Relation to Plasma C-peptide Concentrations in US Women.” Am J Clin Nutr. Oct 2004; (4):1043-1049.

139. Matthias, B. and Schulze, M.B. “Dietary Pattern, Inflammation, and Incidence of Type 2 Diabetes in Women.” Am J Clin Nutr. Sep 2005; 82: 675-684.

140. Yudkin, J. Sweet and Dangerous. (New York: Bantam Books: 1974) 169.

141. http://www.endo-society.org/media/press/upload/CARONIA_FINAL.pdfdated June 13, 2009

142. Ross, AP, et. al. “A High Fructose Diet Impairs Spatial Memory in Male Rats” Neurobiol Learn Mem. 2009 Jun 12. [Epub ahead of print]

143. Gul, A. et al. “Role of fructose concentration on cataractogenesis in senile diabetic and non-diabetic patients.” Graefes Arch Clin Exp Ophthalmol. 2009 Jun;247(6):809-14. Epub 2009 Feb 6.

Back to Sugar

Category: Sugar

Sugar Under Fire For Causing Fat and Disease

Sugar: The Bitter Truth – Video

No Sweeteners For You and That Includes Agave!

References:

141 Reasons Sugar Ruins Your Health