So distressing to find those pounds you laboriously managed to lose creeping back and bringing more of their unwanted friends along too. Here’s an explanation of why that happens and some hope from research on the gut microbiome.
It turns out that being obese alters the composition of micro-organisms residing in the gut microbiome, causing them to subvert any effort we make to keep lost weight off. In fact, just the opposite happens: After living in an overweight body, our gut microbes ENCOURAGE the body to regain the lost weight by storing more calories as fat – perhaps an evolutionary mechanism to help us survive in times of famine. About 95% of us who lose up to a tenth of our body weight gain it back within 12 months – along with some additional pounds. (Healy, 2016)
New research at the Weizmann Institute of Science in Israel demonstrated that the composition of the gut microbiome has a great influence on post-dieting weight regain. The research was done with mice but has clear implications for humans.
After the mice in the study gained and then lost weight, all their body systems fully returned to normal – except their gut microbiomes, which retained an abnormal ‘obese’ microbiome for about six months after they lost the weight.
In a series of experiments for the study, the researchers essentially created a yo-yo dieting situation for their mouse subjects by cycling them between diets of high-calorie feed, which made them obese, and healthy feed, on which they lost the weight in a month or so. But, when the mice were again fed the high-calorie feed, they often gained even more weight than they had before.
These yo-yo dieting mice also became less healthy than mice who had been overweight only once. The serial dieters had proportionately more body fat, higher cholesterol profiles, and more serious metabolic problems, such as insulin irregularities and glucose intolerance.
So what accounted for this extra weight gain and descent into poor metabolic health?
Even though it took a little over a month for a mouse to lose the weight it had gained on the high-calorie diet, it took another six months for the composition of its gut microbiome to return to its normal, pre-obesity state.
For about six months after losing weight, post-obese mice retained an abnormal “obese” microbiome.
Then, in another series of experiments, the scientists demonstrated that the gut microbiomes of obese mice became less able to utilize a class of important phytonutrients in their diet: flavonoids, the pigments that give plants their bright colors.
A flavonoid deficiency has a deleterious effect on the body’s energy-burning system: It creates brown fat, which converts calories to energy more efficiently. So a higher proportion of brown fat causes the body to uses up incoming calories more sparingly, storing what’s left over as more fat.
To counteract this deficit, the researchers fed some of the mice a daily flavonoid supplement in their drinking water during the post-dieting window, before their gut microbiomes returned to normal.
This worked! Compared with the yo-yo dieters who didn’t get the supplements, those who received the daily flavonoids burned up more calories when they were put back on a high-fat diet and regained less weight.
“We call this approach ‘post-biotic’ intervention. In contrast to probiotics, which introduce helpful microbes into the intestines, we are not introducing the microbes themselves but substances affected by the microbiome, which might prove to be more safe and effective.” (Weizmann, 2016)
Some tasty sources of flavonoids
FLAVONOIDS – THE GOOD NEWS
The article doesn’t identify the specific flavonoids these researchers used to protect the mice against post-dieting weight regain. Over 6,000 flavonoids have already been identified – one of the largest nutrient families known to science.
The large family of flavonoids provides us – and apparently mice – with many health benefits, including:
Inhibiting the destruction of collagen by white blood cells
Cardiovascular system support
Nervous system support
Help protect blood vessels from rupture and leakage
Enhancing the power of Vitamin C
Protecting cells from oxygen damage
– George Mateljan Foundation (2016) & NDhealthFACTS (2014)
You’ve probably heard the advice to “Eat the colors of the rainbow every day”. In part, this is to urge us to get adequate amounts of the various flavonoids we need to support good health.
Signs of flavonoid deficiency:
Frequent nose bleeds
Excessive swelling after injury
Frequent colds or infections
– NDhealthFACTS (2014)
DISCOVER WHAT MICROBES – HELPFUL AND PATHOLOGICAL – LIVE IN AND ON YOUR OWN BODY
uBiome, a biotechnology company based in San Francisco and a leader in microbial genomics, gives individuals and organizations access to technology to sequence their microbiomes, particularly gut flora, at a reasonable cost. It is a pioneer in the new era of microbiome-based precision medicine.
Take a look at the uBiome site for more information about who they are and the services they offer.
If you’d like to discover the make up of your own gut microbiome, you can get it sequenced by uBiome for $89.
If you want to discover even more about the microbes co-existing with you in and on your body, you can get five of your body’s important microbiomes sequenced: gut, mouth, nose, skin, and genital. uBiome is currently offering test kits for all five areas at the sale price of $89 instead of the usual $399.
Go to ubiome.com/explorer. Enter discount code 5FOR1BF16 at checkout to take advantage of the special 5-in-1 deal.
The results you’ll get from these tests will show how your microbiomes compare with the world’s largest human microbiome database.
uBIOME’S SMARTGUT™ KITS
To get even more detailed results that you and your doctor can use to identify specific pathogens and microbial imbalances in your gut that might be making you unwell, Ubiome also offers a SmartGut™ comprehensive screening test.
The SmartGut™ screening test can detect the micro-organisms associated with several common gut symptoms, including:
Crohn’s disease/Ulcerative Colitis
Irritable bowel syndrome (IBS)
Irritable bowel disease (IBD)
You can also sign up to receive an interesting and often amusing newsletter from Jessica Richman, one of uBiome’s co-founders, about every two weeks.
Many thanks to Zell Watson for bringing the Weizmann Institute article to my attention.
109. Sugar can slow down the ability of the adrenal glands to function.
110. Sugar has the potential of inducing abnormal metabolic processes in a normal healthy individual and to promote chronic degenerative diseases.
111.. IVs (intravenous feedings) of sugar water can cut off oxygen to the brain.
112. High sucrose intake could be an important risk factor in lung cancer.
113. Sugar increases the risk of polio.
114. High sugar intake can cause epileptic seizures.
115. Sugar causes high blood pressure in obese people.
116. In Intensive Care Units, limiting sugar saves lives.
117. Sugar may induce cell death.
118. Sugar can increase the amount of food that you eat.
119. In juvenile rehabilitation camps, when children were put on a low sugar diet, there was a 44% drop in antisocial behavior.
120. Sugar can lead to prostate cancer.
121. Sugar dehydrates newborns.
122. Sugar increases the estradiol in young men.
123. Sugar can cause low birth weight babies.
124. Greater consumption of refined sugar is associated with a worse outcome of schizophrenia
125. Sugar can raise homocysteine levels in the blood stream.
126. Sweet food items increase the risk of breast cancer.
127. Sugar is a risk factor in cancer of the small intestine.
128. Sugar may cause laryngeal cancer.
129. Sugar induces salt and water retention.
130. Sugar may contribute to mild memory loss.
131. As sugar increases in the diet of 10 years olds, there is a linear decrease in the intake of many essential nutrients.
132. Sugar can increase the total amount of food consumed.
133. Exposing a newborn to sugar results in a heightened preference for sucrose relative to water at 6 months and 2 years of age.
134. Sugar causes constipation.
135. Sugar causes varicose veins.
136. Sugar can cause brain decay in prediabetic and diabetic women.
137. Sugar can increase the risk of stomach cancer.
138. Sugar can cause metabolic syndrome.
139. Sugar ingestion by pregnant women increases neural tube defects in embryos.
140. Sugar can be a factor in asthma.
141. The higher the sugar consumption the more chances of getting irritable bowel syndrome.
142. Sugar could affect central reward systems.
143. Sugar can cause cancer of the rectum.
144. Sugar can cause endometrial cancer.
145. Sugar can cause renal (kidney) cell carcinoma.
146. Sugar can cause liver tumors.
Many thanks to Dr Beth Forgosh, of Discover Chiropractic of Soho, for bringing Dr Appleton’s list to my attention.
Note added to this post on 12/29/2014:
Suzette Lawrence, MSN, commented that Dr Appleton’s list, above, describes the effects of REFINED sugars:
“This is not the case for natural fruits sugars that are attached to the fiber in the fruit, known as levulose … if absorbed it occurs low in the intestines and is converted to glycogen in the liver and stored there as an emergency energy source. I agree that the SAD (Standard American Diet) beginning in infancy sets the stage for every disease, and some new ones. Think, GMO beet sugar … ”
Sugar, in all forms, is a simple carbohydrate that the body converts into glucose and uses for energy. But the effect on the body and your overall health depends on the type of sugar you’re eating, either natural or refined.
We wanted to explore the difference between these sugar types as a follow-up to our post about whether sugar drives the growth of cancer, which has received several comments. We again turned to Julie Baker, Clinical Oncology Dietitian at our hospital outside Atlanta, for her expertise on the issue.
Natural sugars are found in fruit as fructose and in dairy products, such as milk and cheese, as lactose. Foods with natural sugar have an important role in the diet of cancer patients and anyone trying to prevent cancer because they provide essential nutrients that keep the body healthy and help prevent disease.
Refined sugar comes from sugar cane or sugar beets, which are processed to extract the sugar. It is typically found as sucrose, which is the combination of glucose and fructose. We use white and brown sugars to sweeten cakes and cookies, coffee, cereal and even fruit. Food manufacturers add chemically produced sugar, typically high-fructose corn syrup, to foods and beverages, including crackers, flavored yogurt, tomato sauce and salad dressing. Low-fat foods are the worst offenders, as manufacturers use sugar to add flavor.
Most of the processed foods we eat add calories and sugar with little nutritional value. In contrast, fruit and unsweetened milk have vitamins and minerals. Milk also has protein and fruit has fiber, both of which keep you feeling full longer.
DR APPLETON’S REFERENCES
1. Sanchez, A., et al. Role of Sugars in Human Neutrophilic Phagocytosis, American Journal of Clinical Nutrition. Nov 1973;261:1180-1184.
Bernstein, J., et al. Depression of Lymphocyte Transformation Following Oral Glucose Ingestion. American Journal of Clinical Nutrition.1997;30:613.
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. Journal of Abnormal Child Psychology. 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, Postgraduate Medicine Journal. 1969;45:602-607.
5. Ringsdorf, W., Cheraskin, E. & Ramsay R. Sucrose,Neutrophilic Phagocytosis and Resistance to Disease, Dental Survey. 1976;52(12):46-48.
6. Cerami, A., Vlassara, H., & Brownlee, M. Glucose and Aging. Scientific American. May 1987:90.
Lee, A. T. & Cerami, A. The Role of Glycation in Aging. Annals of the New York Academy of Science. 663:63-67.
7. Albrink, M. & Ullrich I. H. Interaction of Dietary Sucrose and Fiber on Serum Lipids in Healthy Young Men Fed High Carbohydrate Diets. American Journal of Clinical Nutrition. 1986;43:419-428.
Pamplona, R., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses. Mar 1993;40(3):174-81.
8. Kozlovsky, A., et al. Effects of Diets High in Simple Sugars on Urinary Chromium Losses. Metabolism. June 1986;35:515-518.
9. Takahashi, E., Tohoku University School of Medicine, Holistic Health Digest. October 1982:41.
10. Kelsay, J., et al. Diets High in Glucose or Sucrose and Young Women. American Journal of Clinical Nutrition. 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. Human Nutrition Clinical Nutrition. 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, Journal of Clinical Nutrition. 1983;113:1335-1345.
12. Lemann, J. Evidence that Glucose Ingestion Inhibits Net Renal Tubular Reabsorption of Calcium and Magnesium. Journal Of Clinical Nutrition. 1976 ;70:236-245.
13. Acta Ophthalmologica Scandinavica. Mar 2002;48;25.
Taub, H. Ed. Sugar Weakens Eyesight, VM NEWSLETTER; May 1986:6
14. Sugar, White Flour Withdrawal Produces Chemical Response. The Addiction Letter. Jul 1992:4.
15. Dufty, William. Sugar Blues. (New York:Warner Books, 1975).
17. Jones, T. W., et al. Enhanced Adrenomedullary Response and Increased Susceptibility to Neuroglygopenia: Mechanisms Underlying the Adverse Effect of Sugar Ingestion in Children. Journal of Pediatrics. Feb 1995;126:171-7.
19. Lee, A. T. & Cerami A. The Role of Glycation in Aging.” Annals of the New York Academy of Science.1992;663:63-70.
20. Abrahamson, E. & Peget, A. Body, Mind and Sugar. (New York:Avon,1977.}
21. Glinsmann, W., Irausquin, H., & Youngmee, K. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. 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 Research. 1998; 32(2)107-12.
Riva Touger-Decker & Cor van Loveren, Sugars and Dental Caries. American Journal of Clinical Nutrition. Oct 2003; 78:881-892.
22. Keen, H., et al. Nutrient Intake, Adiposity, and Diabetes. British Medical Journal. 1989; 1: 655-658.
23. Tragnone, A. et al. Dietary Habits as Risk Factors for Inflammatory Bowel Disease. European Journal of Gastroenterological Hepatology. Jan 1995;7(1):47-51.
24. Yudkin, J. Sweet and Dangerous. (New York;Bantam Books:1974), 129.
25. Darlington, L., Ramsey, N. W. & Mansfield, J. R. 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. British Medical Journal. Apr 14, 1984; 288:1103-1104.
Misciagna, G., et al. American Journal of Clinical Nutrition. 1999;69:120-126.
29. Yudkin, J. Sugar Consumption and Myocardial Infarction. Lancet.Feb 6, 1971;1(7693):296-297.
Reiser, S. Effects of Dietary Sugars on Metabolic Risk Factors Associated with Heart Disease. Nutritional Health. 1985;203-216.
30. Cleave, T. The Saccharine Disease. (New Canaan, CT: Keats Publishing, 1974).
31. Erlander, S. The Cause and Cure of Multiple Sclerosis, The Disease to End Disease. Mar 3, 1979;1(3):59-63.
32. Cleave, T. The Saccharine Disease. (New Canaan, CT: Keats Publishing, 1974.)
33. Cleave, T. & Campbell, G. Diabetes, Coronary Thrombosis and the Saccharine Disease. (Bristol, England, John Wrightand Sons, 1960).
34. Behall, K. Influence of Estrogen Content of Oral Contraceptives and Consumption of Sucrose on Blood Parameters. Disease Abstracts International. 1982;431-437.
35. Glinsmann, W., Irausquin, H., & K. Youngmee. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. Report of Sugars Task Force. 1986;39:36_38.
36. Tjderhane, L. & Larmas, M. A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats. Journal of Nutrition. 1998:128:1807-1810.
37. Appleton, N. Healthy Bones. New York: Avery Penguin Putnam,1989.
38. Beck_Nielsen H., Pedersen O., & Schwartz S. Effects of Diet on the Cellular Insulin Binding and the Insulin Sensitivity in Young Healthy Subjects. Diabetes. 1978;15:289-296 .
39. Mohanty P. et al. Glucose Challenge Stimulates Reactive Oxygen Species (ROS) Generation by Leucocytes. Journal of Clinical Endocrinology and Metabolism. Aug 2000; 85(8):2970-2973.
40. Gardner, L. & Reiser, S. Effects of Dietary Carbohydrate on Fasting Levels of Human Growth Hormone and Cortisol. Proceedings of the Society for Experimental Biology and Medicine. 1982;169:36-40.
41. Reiser, S. Effects of Dietary Sugars on Metabolic Risk Factors Associated with Heart Disease. Nutritional Health. 1985;203:216.
42. Preuss, H. G. Sugar-Induced Blood Pressure Elevations Over the Lifespan of Three Substrains of Wistar Rats. Journal of the American College of Nutrition, 1998;17(1) 36-37.
43. Behar, D., et al. Sugar Challenge Testing with Children Considered Behaviorally Sugar Reactive. Nutritional Behavior. 1984;1:277-288.
44. Furth, A. & Harding, J. Why Sugar Is Bad For You. New Scientist. Sep 23, 1989;44.
45. Lee AT, & Cerami A. Role of Glycation in Aging. Annals of the New York Academy of Science. Nov 21,1992 ;663:63-70.
46. Appleton, N. Lick the Sugar Habit. (New York:Avery Penguin Putnam:1988).
47. Sucrose Induces Diabetes in Cats. Federal Protocol. 1974;6(97).
48. Cleave, T. The Saccharine Disease (New Canaan Ct: Keats Publishing, Inc., 1974).131.
49. Ibid. 132.
50. Vaccaro O., Ruth, K. J. & Stamler J. 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.
51. Lee, A. T. & 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.).
52. Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology. 1990:45(4 ):105-110.
53. Dyer, D. G., et al. “=Accumulation of Maillard Reaction Products in Skin Collagen in Diabetes and Aging. Journal of Clinical Investigation. 1993:93(6):421-422.
54. Veromann, S.et al. Dietary Sugar and Salt Represent Real Risk Factors for Cataract Development. Ophthalmologica. Jul-Aug 2003 ;217(4):302-307.
55. Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology. 1990:45(4):105-110.
56. Schmidt A.M. et al. Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis. Circular Research Archives. 1999 Mar 19;84(5):489-97.
57. Lewis, G. F. and Steiner, G. Acute Effects of Insulin in the Control of VLDL Production in Humans. Implications for Theinsulin-resistant State. Diabetes Care. 1996 Apr;19(4):390-3
R. Pamplona, M. .J., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses. 1990;40:174-181.
58. Ceriello, A. Oxidative Stress and Glycemic Regulation. Metabolism. Feb 2000;49(2 Suppl 1):27-29.
59. Appleton, Nancy. Lick the Sugar Habit. (New York:Avery Penguin Putnam, 1988).
60. 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., Vlassara, H., & Brownlee, M. Glucose and Aging. Scientific American. May 1987: 90.
62. Goulart, F. S. Are You Sugar Smart? American Fitness. Mar-Apr 1991: 34-38.
64. Yudkin, J., Kang, S. & Bruckdorfer, K. Effects of High Dietary Sugar. British Journal of Medicine. Nov 22, 1980;1396.
65. Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991: 34-38
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. Journal of the National Cancer Institute. Sep 4, 2002 ;94(17):1293-300.
73. Schauss, A. Diet, Crime and Delinquency. (Berkley Ca; Parker House, 1981).
74. Christensen, L. The Role of Caffeine and Sugar in Depression. Nutrition Report. Mar 1991;9(3):17-24.
76. Cornee, J., et al. A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France, European Journal of Epidemiology. 1995;11:55-65.
77. Yudkin, J. Sweet and Dangerous.(New York:Bantam Books,1974) 129.
78. Ibid, 44
79. Reiser, S., et al. Effects of Sugars on Indices on Glucose Tolerance in Humans. American Journal of Clinical Nutrition. 1986:43;151-159.
80. Reiser,S., et al. Effects of Sugars on Indices on Glucose Tolerance in Humans. American Journal of Clinical Nutrition. 1986;43:151-159.
81. Molteni, R, et al. A High-fat, Refined Sugar Diet Reduces Hippocampal Brain-derived Neurotrophic Factor, Neuronal Plasticity, and Learning. NeuroScience. 2002;112(4):803-814.
82. Monnier, V., Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology. 1990;45:105-111.
83. Frey, J. Is There Sugar in the Alzheimers Disease? Annales De Biologie Clinique. 2001; 59 (3):253-257.
84. Yudkin, J. Metabolic Changes Induced by Sugar in Relation to Coronary Heart Disease and Diabetes. Nutrition and Health. 1987;5(1-2):5-8.
86. 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. Annals of Internal Medicine. 1998:28:534-340.
87. Journal of Advanced Medicine. 1994;7(1):51-58.
89. Ceriello, A. Oxidative Stress and Glycemic Regulation. Metabolism. Feb 2000;49(2 Suppl 1):27-29.
90. Postgraduate Medicine. Sept 1969:45:602-07.
91. Moerman, C. J., et al. Dietary Sugar Intake in the Etiology of Biliary Tract Cancer. International Journal of Epidemiology. Ap 1993;2(2):207-214.
92. Quillin, Patrick, Cancer’s Sweet Tooth. Nutrition Science News. Apr 2000.
Rothkopf, M.. Nutrition. July/Aug 1990;6(4).
93. Lenders, C. M. Gestational Age and Infant Size at Birth Are Associated with Dietary Intake among Pregnant Adolescents. Journal of Nutrition. Jun 1997;1113-1117.
95. Bostick, R. M., 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.
97. Yudkin, J. & Eisa, O. Dietary Sucrose and Oestradiol Concentration in Young Men. Annals of Nutrition and Metabolism. 1988:32(2):53-55.
98. Lee, A. T. & Cerami A. The Role of Glycation in Aging. Annals of the New York Academy of Science. 1992; 663:63-70.
99. Moerman, C. et al. Dietary Sugar Intake in the Etiology of Gallbladder Tract Cancer. International Journal of Epidemiology. Apr 1993; 22(2):207-214.
100. Sugar, White Flour Withdrawal Produces Chemical Response. The Addiction Letter. Jul 1992:4.
Colantuoni, C., et al. Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence. Obesity Research. Jun 2002 ;10(6):478-488.
102. The Edell Health Letter. Sept 1991;7:1.
103. Sunehag, A. L., et al. Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition. Diabetes. 1999 ;48 7991-8000).
104. Christensen L. et al. Impact of A Dietary Change on Emotional Distress. Journal of Abnormal Psychology. 1985;94(4):565-79.
105. Nutrition Health Review. Fall 85. Sugar Changes into Fat Faster than Fat.
106. Ludwig, D. S., et al. High Glycemic Index Foods, Overeating and Obesity. Pediatrics. Mar 1999;103(3):26-32.
107. Girardi, N.L. Blunted Catecholamine Responses after Glucose Ingestion in Children with Attention Deficit Disorder. Pediatrics Research. 1995;38:539-542.
Berdonces, J. L. Attention Deficit and Infantile Hyperactivity. Rev Enferm. Jan 2001;4(1)11-4
108. Blacklock, N. J. Sucrose and Idiopathic Renal Stone. Nutrition Health. 1987;5(1 & 2):9-17.
109. Lechin, F., et al. Effects of an Oral Glucose Load on Plasma Neurotransmitters in Humans. Neurophychobiology. 1992;26(1-2):4-11.
110. Fields, M. Journal of the American College of Nutrition. Aug 1998;17(4):317-321.
111. Arieff, A. I. Veterans Administration Medical Center in San Francisco. San Jose Mercury. June 12/86. IVs of Sugar Water Can Cut Off Oxygen to the Brain.
112. De Stefani, E.Dietary Sugar and Lung Cancer: a Case Control Study in Uruguay. Nutrition and Cancer. 1998;31(2):132_7.
113. Sandler, Benjamin P. Diet Prevents Polio. Milwakuee, WI,:The Lee Foundation for for Nutritional Research, 1951.
114. Murphy, Patricia. The Role of Sugar in Epileptic Seizures. Townsend Letter for Doctors and Patients. May, 2001.
115. 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.
116. Christansen, D. Critical Care: Sugar Limit Saves Lives. Science News. June 30, 2001;159:404.
117. 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.
118. Allen S. Levine, Catherine M. Kotz, & Blake A. Gosnell . Sugars and Fats: The Neurobiology of Preference. Journal of Nutrition. 2003 133:831S-834S.
119. Schoenthaler, S. The Los Angeles Probation Department Diet-Behavior Program: An Empirical Analysis of Six Institutional Settings. International Journal of Biosocial Research. 5(2):88-89.
120. 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.
121. Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition. Diabetes. 1999 Apr;48(4):791-800.
122. Yudkin, J. and Eisa, O. Dietary Sucrose and Oestradiol Concentration in Young Men. Annals of Nutrition and Metabolism. 1988;32(2):53-5.
123. Lenders, C. M. Gestational Age and Infant Size at Birth Are Associated with Dietary Intake Among Pregnant Adolescents. Journal of Nutrition.128; 1998::807-1810.
124. Peet, M. International Variations in the Outcome of Schizophrenia and the Prevalence of Depression in Relation to National Dietary Practices: An Ecological
Analysis. British Journal of Psychiatry. 2004;184:404-408.
125. Fonseca, V. et al. Effects of a High-fat-sucrose Diet on Enzymes in Homosysteine Metabolism in the Rat. Metabolism. 200; 49:736-41.
126. 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.
127.Negri. E. et al. Risk Factors for Adenocarcinoma of the Small Intestine. International Journal of Cancer. 1999:82:I2:171-174.
128.Bosetti, C. et al. Food Groups and Laryngeal Cancer Risk: A Case-control Study from Italy and Switzerland. International Journal of Cancer, 2002:100(3): 355-358.
129. Shannon, M. An Empathetic Look at Overweight.CCL Family Foundation. Nov-Dec.1993. 20(3):3-5.
130. Harry G. Preuss, MD, of Georgetown University Medical School.
131. Health After 50. Johns Hopkins Medical Letter. May, 1994.
132. Allen, S. Sugars and Fats: The Neurobiology of Preference. Journal of Nutrition. 2003;133:831S-834S.
133. Booth, D.A.M. et al. Sweetness and Food Selection: Measurement of Sweeteners Effects on Acceptance. Sweetness. Dobbing, J., Ed., (London:Springer-Verlag, 1987).
134. Cleve, T.L On the Causation of Varicose Veins. Bristol, England, John Wright, 1960.
135. Cleve, T.L On the Causation of Varicose Veins. Bristol, England, John Wright, 1960.
136. Ket, Yaffe et al. Diabetes, Impaired Fasting Glucose and Development of Cognitive Impairment in Older Women. Neurology. 2004;63:658�663.
137. Chatenoud, Liliane et al. Refined-cereal Intake and Risk of Selected Cancers in Italy. American Journal of Clinical Nutrition, Dec 1999;70:1107-1110.
138. Yoo, Sunmi et al. Comparison of Dietary Intakes Associated with Metabolic Syndrome Risk Factors in Young Adults: the Bogalusa Heart Study. American Journal of Clinical Nutrition. 2004 Oct;80(4):841-848.
139. Shaw, Gary M. et al. Neural Tube Defects Associated with Maternal Periconceptional Dietary Intake of Simple Sugars and Glycemic Index. American Journal of Clinical Nutrition, Nov 2003;78:972-978.
140. Krilanovich, Nicholas J. Fructose Misuse, the Obesity Epidemic, the Special Problems of the Child, and a Call to Action American Journal of Clinical Nutrition, Nov 2004;80:1446-1447.
141.Jarnerot, G., Consumption of Refined Sugar by Patients with Crohn’s Disease, Ulcerative colitis, or Irritable Bowel Syndrome. Scandinavian Journal of Gastroenterology. 1983 Nov;18(8):999-1002.
142. Allen, S. Sugars and Fats: The Neurobiology of Preference. Journal of Nutrition.
143. De Stefani E, Mendilaharsu M, & Deneo-Pellegrini H. Sucrose as a Risk Factor for Cancer of the Colon and Rectum: a Case-control Study in Uruguay. International Journal of Cancer. 1998 Jan 5;75(1):40-4.
144. Levi F, Franceschi S, Negri E, & La Vecchia C. Dietary Factors and the Risk of Endometrial Cancer. Cancer. 1993 Jun 1;71(11):3575-3581.
145. Mellemgaard A. et al. Dietary Risk Factors for Renal Cell Carcinoma in Denmark. European Journal of Cancer. 1996 Apr;32A(4):673-82.
146. Rogers AE, Nields HM, & Newberne PM. Nutritional and Dietary Influences on Liver Tumorigenesis in Mice and Rats. Arch Toxicol Suppl. 1987;10:231-43. Review.
This is the Standard American Diet – aptly abbreviated as SAD – shown as a pie chart:
Here’s another way of looking at the Standard American Diet – as percentages of calories derived from plant, animal and processed foods:
And the SAD as represented in another pie chart – this one showing the number of calories we get from various sources:
No matter how the Standard American Diet is represented, it’s clearly bad news for our health.
The Standard American Diet is how the vast majority of Americans eat. It is characterized by high intake of sweets, animal products, cooking oils, high-fat and processed foods. People living on SAD have a higher incidence of heart disease and cancers. (Fuhrman, 2011) (Hardin, 2013 -a)
It is well known that factory farmed and processed foods are more likely to cause illness than organically grown, unprocessed foods. Yet 90 percent of the American food budget is spent on processed and fast foods. (Schlosser, 2001)
The Standard American Diet is high in refined sugars and red meat, both of which severely acidify the body, producing inflammation – the gateway to many serious ailments. An overly acidic diet is at the core of many symptoms such as fatigue, digestive imbalances, emotional imbalances and anxiety. Adding foods to our daily diet that alkalinize the blood, urine and saliva can help restore balance and health again. (Hardin, 2014 -a)
We all know that adult and childhood obesity has become a serious health issue in the US and elsewhere. Beginning in the 1950′s, when calorie-dense/nutrient poor foods and beverages started becoming standard fare in this country, the number of people consuming the Standard American Diet has steadily risen – much to the detriment of both our microbiota and our overall health. (Hardin, 2013 -c)
THE NITTY GRITTY ON CHICKEN MCNUGGETS
Chicken McNuggets, introduced by McDonald’s in 1983, consist of small pieces of processed chicken meat that have been battered and deep fried.
As of October 9, 2010, the ingredients in McDonald’s Chicken McNuggets within the United States are as follows (Wikipedia, 2014):
And … you can be sure the ingredients in Chicken McNuggets, their various sauces and the other items on the McDonald’s menu aren’t organic so you’re getting a good dose of genetically modified organisms with each serving.