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Restoring the Wholeness In You
FenceDr Keith A Sarver DC, NRT
 
The Autonomic Nervous System

The Medulla or DiencephalonBelow the diencephalon are the midbrain (or mesencephalon) and the hindbrain (or rhombencephalon). The hindbrain consists of the pons (or metencephalon) and the medulla oblongata (or myelencephalon). These parts of the brain stem are characterized by three main features: (1) a roof plate superior to the cerebral aqueduct and fourth ventricle; (2) a central core of gray matter, known as the reticular formation; and (3) a massive basal collection of fibers descending from the cerebral cortex to the brain stem and spinal cord.

The roof plate of the midbrain is formed by two paired rounded eminences, the superior and inferior colliculi. The superior colliculus receives input from the retina and the visual cortex and participates in a variety of visual reflexes, particularly the tracking of objects in the contralateral visual field. The inferior colliculus receives both crossed and uncrossed auditory fibers and projects upon the medial geniculate body, the auditory relay nucleus of the thalamus (see above Diencephalon). In the hindbrain the roof plate is formed by the cerebellum and a membrane containing the choroid plexus of the fourth ventricle.

The reticular formation contains a core collection of cells of various sizes that project to the thalamus, the cerebellum, and the spinal cord. Surrounding this core are long ascending and descending tracts in which various cranial nerve nuclei are embedded.

Fibers derived from the cerebral cortex lie on or near the ventral surface of the midbrain, pons, and medulla. At the midbrain they gather into two bundles called the crura cerebri; from there they descend into the pons, where most terminate upon cell nuclei that project into the cerebellum. These constitute the corticopontine tract. The other major tract, called the corticospinal tract, forms the medullary pyramids before descending to the spinal cord.

The Midbrain

The midbrain contains the nuclear complex of the oculomotor nerve as well as the trochlear nucleus; these cranial nerves innervate muscles that move the eye and control the shape of the lens and the diameter of the pupil. In addition, between the midbrain reticular formation (known here as the tegmentum) and the crus cerebri is a large, pigmented structure called the substantia nigra. This nucleus consists of two parts, the pars reticulata and the pars compacta. Cells of the pars compacta contain the black pigment melanin; these synthesize dopamine and project to cells of either the caudate nucleus or the putamen but not to both. By exercising an inhibitory action on large aspiny cholinergic neurons in the neostriatum, the dopaminergic cells of the pars compacta influence the output of the neurotransmitter GABA from spiny striatal neurons. These spiny neurons in turn project to cells of the pars reticulata, which, by projecting fibers to the thalamus, are in effect part of the output system of the corpus striatum.

At the caudal midbrain, crossed fibers of the superior cerebellar peduncle (the major output system of the cerebellum) surround and partially terminate in a large, centrally located structure known as the red nucleus. Most crossed ascending fibers of this bundle project to thalamic nuclei, which have access to the primary motor cortex. A smaller number of fibers synapse on large cells in caudal regions of the red nucleus; these give rise to the crossed fibers of the rubrospinal tract (see below The spinal cord: Descending spinal tracts).

The Pons

Pons & Medulla, Anterior ViewThe pons consists of two parts: the tegmentum, a phylogenetically older part that contains the reticular formation; and the pontine nuclei, a larger part composed of masses of neurons that lie among large bundles of longitudinal and transverse fibers.

Fibers originating from neurons in all major lobes of the cerebral cortex terminate upon the pontine nuclei, which in turn project to the opposite cerebellar hemisphere. These massive crossed fibers form the middle cerebellar peduncle—in effect serving as the bridge that connects each cerebral hemisphere with the opposite half of the cerebellum.

The reticular formation in the pontine tegmentum contains multiple cell groups that exert facilitating influences upon motor function. It also contains the nuclei of several cranial nerves. The facial nerve and the two components of the vestibulocochlear nerve, for example, emerge from and enter the brain stem at the junction of the pons, medulla, and cerebellum. Motor nuclei for the trigeminal nerve lie in the upper pons. Located on the periphery of the pons are long ascending and descending tracts that connect the brain to the spinal cord.

Medulla oblongata

Medulla Oblongata, Anterior ViewThe medulla oblongata is closest to the spinal cord, and is involved with the regulation of heartbeat, breathing, vasoconstriction (blood pressure), and reflex centers for vomiting, coughing, sneezing, swallowing, and hiccuping.

It is the most caudal segment of the brain stem, and appears as a conical expansion of the spinal cord. Both the pons and the medulla are separated from the overlying cerebellum by the fourth ventricle, and cerebrospinal fluid entering the fourth ventricle from the cerebral aqueduct passes into the cisterna magna, a subarachnoid space surrounding the medulla and the cerebellum, via foramina in the lateral recesses and in the midline of the ventricle.

At the transition from the medulla to the spinal cord, there are two major decussations, or crossings, of nerve fibers. The corticospinal decussation is the site at which 90 percent of the fibers of the medullary pyramid cross and enter the dorsolateral funiculus of the spinal cord. Signals conveyed by this tract provide the basis for voluntary motor function on the opposite side of the body (see below The spinal cord: Descending spinal tracts). In the other decussation, sensory fibers ascending in the fasciculus gracilis and fasciculus cuneatus of the spinal cord terminate upon large nuclear masses on the dorsal surface of the medulla. Known as the nuclei gracilis and cuneatus, these masses give rise to fibers that decussate above the corticospinal tract and form a major ascending sensory pathway known as the medial lemniscus. Present at all brain-stem levels, the medial lemniscus projects upon the somesthetic relay nuclei of the thalamus.

The medulla contains nuclei associated with the hypoglossal, accessory, vagus, and glossopharyngeal cranial nerves. In addition, it contains portions of the vestibular nuclear complex, parts of the trigeminal nuclear complex concerned with pain and thermal sense, and solitary nuclei related to the vagus, glossopharyngeal, and facial nerves that subserve the sense of taste.

Of several medullary relay nuclei that project to the cerebellum via the inferior cerebellar peduncle, the largest is the inferior olive.

CerebellumThe cerebellum is the second largest part of the brain, after the cerebrum. It functions for muscle coordination and maintains normal muscle tone and posture. The cerebellum coordinates balance.

It overlies the posterior aspect of the pons and medulla and fills the greater part of the back portion of the skull. It consists of two paired lobes, or hemispheres, and a midline portion known as the vermis. Cerebellar cortex appears very different from cerebral cortex in that it consists of small, leaflike laminae, referred to as folia. Structurally the cerebellum consists of a three-layered, gray cellular mantle called the cerebellar cortex and a core of white matter containing four paired intrinsic (i.e., deep) nuclei, the dentate, globose, emboliform, and fastigial. Three paired fiber bundles—the superior, middle, and inferior peduncles—connect the cerebellum with the midbrain, pons, and medulla, respectively.

On an embryological basis the cerebellum can be divided into three parts: (1) the archicerebellum, related primarily to the vestibular system; (2) the paleocerebellum, or anterior lobe, concerned with control of muscle tone; and (3) the neocerebellum, known as the posterior lobe. Receiving input from the cerebral hemispheres via the middle cerebellar peduncle, the neocerebellum is the part most concerned with coordination of voluntary motor function.

The three layers of the cerebellar cortex are an outer synaptic layer (also called the molecular layer), an intermediate discharge layer (the Purkinje layer), and an inner receptive layer (the granular layer). Sensory input from all sorts of receptors are conveyed to specific regions of the receptive layer, which consists of enormous numbers of small nerve cells (hence the name granular) that project axons into the synaptic layer. There they excite the dendrites of the Purkinje cells, which in turn project axons to portions of the four intrinsic nuclei and upon dorsal portions of the lateral vestibular nucleus. Because most Purkinje cells are GABAergic and therefore exert strong inhibitory influences upon the cells that receive their terminals, all sensory input into the cerebellum results in inhibitory impulses being exerted upon the deep cerebellar nuclei and parts of the vestibular nucleus. Cells of all deep cerebellar nuclei, on the other hand, are excitatory (secreting the neurotransmitter glutamate) and project upon parts of the thalamus, red nucleus, vestibular nuclei, and reticular formation.

The cerebellum thus functions as a kind of computer, providing a quick and clear response to any set of sensory signals. It plays no role in sensory perception, but it exerts profound influences upon equilibrium, muscle tone, and the coordination of voluntary motor function. Lesions of the cerebellum produce a constellation of disturbances, including intention tremor, ataxia, hypotonus, easy fatigability, and disturbances of speech.

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 sugar's metabolic consequences from a variety of medical journals and other scientific publications.

  1. Sugar can suppress your immune system and impair your defenses against infectious disease.1,2

  2. Sugar upsets the mineral relationships in your body: causes chromium and copper deficiencies and interferes with absorption of calcium and magnesium. 3,4,5,6

  3. Sugar can cause can cause a rapid rise of adrenaline, hyperactivity, anxiety, difficulty concentrating, and crankiness in children.7,8

  4. Sugar can produce a significant rise in total cholesterol, triglycerides and bad cholesterol and a decrease in good cholesterol.9,10,11,12

  5. Sugar causes a loss of tissue elasticity and function.13

  6. Sugar feeds cancer cells and has been connected with the development of cancer of the breast, ovaries, prostate, rectum, pancreas, biliary tract, lung, gallbladder and stomach.14,15,16,17,18,19,20

  7. Sugar can increase fasting levels of glucose and can cause reactive hypoglycemia.21,22

  8. Sugar can weaken eyesight.23

  9. Sugar can cause many problems with the gastrointestinal tract including: an acidic digestive tract, indigestion, malabsorption in patients with functional bowel disease, increased risk of Crohn's disease, and ulcerative colitis.24,25,26,27,28

  10. Sugar can cause premature aging.29

  11. Sugar can lead to alcoholism.30

  12. Sugar can cause your saliva to become acidic, tooth decay, and periodontal disease.31,32,33

  13. Sugar contributes to obesity.34

  14. Sugar can cause autoimmune diseases such as: arthritis, asthma, multiple sclerosis.35,36,37

  15. Sugar greatly assists the uncontrolled growth of Candida Albicans (yeast infections)38

  16. Sugar can cause gallstones.39

  17. Sugar can cause appendicitis.40

  18. Sugar can cause hemorrhoids.41

  19. Sugar can cause varicose veins.42

  20. Sugar can elevate glucose and insulin responses in oral contraceptive users.43

  21. Sugar can contribute to osteoporosis.44

  22. Sugar can cause a decrease in your insulin sensitivity thereby causing an abnormally high insulin levels and eventually diabetes.45,46,47

  23. Sugar can lower your Vitamin E levels.48

  24. Sugar can increase your systolic blood pressure.49

  25. Sugar can cause drowsiness and decreased activity in children.50

  26. High sugar intake increases advanced glycation end products (AGEs)(Sugar molecules attaching to and thereby damaging proteins in the body).51

  27. Sugar can interfere with your absorption of protein.52

  28. Sugar causes food allergies.53

  29. Sugar can cause toxemia during pregnancy.54

  30. Sugar can contribute to eczema in children.55

  31. Sugar can cause atherosclerosis and cardiovascular disease.56,57

  32. Sugar can impair the structure of your DNA.58

  33. Sugar can change the structure of protein and cause a permanent alteration of the way the proteins act in your body.59,60

  34. Sugar can make your skin age by changing the structure of collagen.61

  35. Sugar can cause cataracts and nearsightedness.62,63

  36. Sugar can cause emphysema.64

  37. High sugar intake can impair the physiological homeostasis of many systems in your body.65

  38. Sugar lowers the ability of enzymes to function.66

  39. Sugar intake is higher in people with Parkinson's disease.67

  40. Sugar can increase the size of your liver by making your liver cells divide and it can increase the amount of liver fat.68,69

  41. Sugar can increase kidney size and produce pathological changes in the kidney such as the formation of kidney stones.70,71

  42. Sugar can damage your pancreas.72

  43. Sugar can increase your body's fluid retention.73

  44. Sugar is enemy #1 of your bowel movement.74

  45. Sugar can compromise the lining of your capillaries.75

  46. Sugar can make your tendons more brittle.76

  47. Sugar can cause headaches, including migraines.77

  48. Sugar can reduce the learning capacity, adversely affect school children's grades and cause learning disorders.78,79

  49. Sugar can cause an increase in delta, alpha, and theta brain waves which can alter your mind's ability to think clearly.80

  50. Sugar can cause depression.81

  51. Sugar can increase your risk of gout.82

  52. Sugar can increase your risk of Alzheimer's disease.83

  53. Sugar can cause hormonal imbalances such as: increasing estrogen in men, exacerbating PMS, and decreasing growth hormone.84,85,86,87

  54. Sugar can lead to dizziness.88

  55. Diets high in sugar will increase free radicals and oxidative stress.89

  56. High sucrose diets of subjects with peripheral vascular disease significantly increases platelet adhesion.90

  57. High sugar consumption of pregnant adolescents can lead to substantial decrease in gestation duration and is associated with a twofold increased risk for delivering a small-for-gestational-age (SGA) infant.91,92

  58. Sugar is an addictive substance.93

  59. Sugar can be intoxicating, similar to alcohol.94

  60. Sugar given to premature babies can affect the amount of carbon dioxide they produce.95

  61. Decrease in sugar intake can increase emotional stability.96

  62. Your body changes sugar into 2 to 5 times more fat in the bloodstream than it does starch.97

  63. The rapid absorption of sugar promotes excessive food intake in obese subjects.98

  64. Sugar can worsen the symptoms of children with attention deficit hyperactivity disorder (ADHD).99

  65. Sugar adversely affects urinary electrolyte composition.100

  66. Sugar can slow down the ability of your adrenal glands to function.101

  67. Sugar has the potential of inducing abnormal metabolic processes in a normal healthy individual and to promote chronic degenerative diseases.102

  68. I.V.s (intravenous feedings) of sugar water can cut off oxygen to your brain.103

  69. Sugar increases your risk of polio.104

  70. High sugar intake can cause epileptic seizures.105

  71. Sugar causes high blood pressure in obese people.106

  72. In intensive care units: Limiting sugar saves lives.107

  73. Sugar may induce cell death.108

  74. In juvenile rehabilitation camps, when children were put on a low sugar diet, there was a 44 percent drop in antisocial behavior.109

  75. Sugar dehydrates newborns.110

  76. Sugar can cause gum disease.111

References

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  2. Ringsdorf, W., Cheraskin, E. and Ramsay R. Sucrose, Neutrophilic Phagocytosis and Resistance to Disease, Dental Survey. 1976;52(12):46_48.

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

  4. Kozlovsky, A., et al. Effects of Diets High in Simple Sugars on Urinary Chromium Losses. Metabolism. June 1986;35:515_518.

  5. 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.

  6. Lemann, J. Evidence that Glucose Ingestion Inhibits Net Renal Tubular Reabsorption of Calcium and Magnesium. Journal of Clinical Nutrition. 1976 ;70:236_245.

  7. Goldman, J., et al. Behavioral Effects of Sucrose on Preschool Children. Journal of Abnormal Child Psychology.1986;14(4):565_577.

  8. 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.

  9. 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.

  10. Albrink, M. and 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. Med Hypotheses. Mar 1993;40(3):174-81.

  11. Reiser, S. Effects of Dietary Sugars on Metabolic Risk Factors Associated with Heart Disease. Nutritional Health. 1985;203_216.

  12. 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. 1996 Apr;19(4):390-3 R. Pamplona, M. .J., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses. 1990;40:174-181.

  13. Cerami, A., Vlassara, H., and Brownlee, M. "Glucose and Aging." Scientific American. May 1987:90. Lee, A. T. and Cerami, A. The Role of Glycation in Aging. Annals of the New York Academy of Science; 663:63-67.

  14. Takahashi, E., Tohoku University School of Medicine, Wholistic Health Digest. October 1982:41:00

  15. Quillin, Patrick, Cancer's Sweet Tooth, Nutrition Science News. Ap 2000 Rothkopf, M.. Nutrition. July/Aug 1990;6(4).

  16. 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.

  17. 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.

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

  19. De Stefani, E."Dietary Sugar and Lung Cancer: a Case control Study in Uruguay." Nutrition and Cancer. 1998;31(2):132_7.

  20. Cornee, J., et al. A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France. European Journal of Epidemiology 11 (1995):55-65.

  21. 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.

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

  23. Acta Ophthalmologica Scandinavica. Mar 2002;48;25. Taub, H. Ed. Sugar Weakens Eyesight, VM NEWSLETTER;May 1986:06:00

  24. Dufty.

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

  26. Cornee, J., et al. A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France, European Journal of Epidemiology. 1995;11

  27. Persson P. G., Ahlbom, A., and Hellers, G. Epidemiology. 1992;3:47-52.

  28. 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.

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

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

  31. Glinsmann, W., Irausquin, H., and Youngmee, K. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. Report of Sugars Task Force. 1986:39:00 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.

  32. Glinsmann, W., Irausquin, H., and K. Youngmee. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. Report of Sugars Task Force.1986;39:36_38.

  33. Appleton, N. New York: Healthy Bones. Avery Penguin Putnam:1989.

  34. Keen, H., et al. Nutrient Intake, Adiposity, and Diabetes. British Medical Journal. 1989; 1:00 655_658

  35. Darlington, L., Ramsey, N. W. and Mansfield, J. R. Placebo Controlled, Blind Study of Dietary Manipulation Therapy in Rheumatoid Arthritis, Lancet. Feb 1986;8475(1):236_238.

  36. 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.

  37. Erlander, S. The Cause and Cure of Multiple Sclerosis, The Disease to End Disease." Mar 3, 1979;1(3):59_63.

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

  39. Heaton, K. The Sweet Road to Gallstones. British Medical Journal. Apr 14, 1984; 288:00:00 1103_1104. Misciagna, G., et al. American Journal of Clinical Nutrition. 1999;69:120-126.

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

  41. Ibid.

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

  43. Behall, K. Influ ence of Estrogen Content of Oral Contraceptives and Consumption of Sucrose on Blood Parameters. Disease Abstracts International. 1982;431437.

  44. Tjäderhane, L. and Larmas, M. A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats. Journal of Nutrition. 1998:128:1807_1810.

  45. Beck, Nielsen H., Pedersen O., and Schwartz S. Effects of Diet on the Cellular Insulin Binding and the Insulin Sensitivity in Young Healthy Subjects. Diabetes. 1978;15:289_296 .

  46. Sucrose Induces Diabetes in Cat. Federal Protocol. 1974;6(97). diabetes

  47. Reiser, S., et al. Effects of Sugars on Indices on Glucose Tolerance in Humans. American Journal of Clinical Nutrition. 1986;43:151-159.

  48. Journal of Clinical Endocrinology and Metabolism. Aug 2000

  49. Hodges, R., and Rebello, T. Carbohydrates and Blood Pressure. Annals of Internal Medicine. 1983:98:838_841.

  50. Behar, D., et al. Sugar Challenge Testing with Children Considered Behaviorally Sugar Reactive. Nutritional Behavior. 1984;1:277_288.

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

  52. Simmons, J. Is The Sand of Time Sugar? LONGEVITY. June 1990:00:00 49_53.

  53. Appleton, N. New York: LICK THE SUGAR HABIT. Avery Penguin Putnam:1988. allergies

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

  55. Ibid. 132

  56. Pamplona, R., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses . 1990:00:00 174_181.

  57. Vaccaro O., Ruth, K. J. and Stamler J. Relationship of Postload Plasma Glucose to Mortality with 19 yr 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.

  58. 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.).

  59. Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology 1990:45(4):105_110.

  60. Cerami, A., Vlassara, H., and Brownlee, M. Glucose and Aging. Scientific American. May 1987:00:00 90

  61. 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_22.

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

  63. Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38. Milwakuee, WI

  64. Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology. 1990:45(4):105_110.

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

  66. Appleton, Nancy. New York; Lick the Sugar Habit. Avery Penguin Putnam, 1988 enzymes

  67. 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.

  68. Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38.

  69. Ibid.

  70. Yudkin, J., Kang, S. and Bruckdorfer, K. Effects of High Dietary Sugar. British Journal of Medicine. Nov 22, 1980;1396.

  71. Blacklock, N. J., Sucrose and Idiopathic Renal Stone. Nutrition and Health. 1987;5(1-2):9- Curhan, G., et al. Beverage Use and Risk for Kidney Stones in Women. Annals of Internal Medicine. 1998:28:534-340.

  72. Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38. Milwakuee, WI,:

  73. Ibid. fluid retention

  74. Ibid. bowel movement

  75. Ibid. compromise the lining of the capillaries

  76. Nash, J. Health Contenders. Essence. Jan 1992; 23:00 79_81.

  77. Grand, E. Food Allergies and Migraine.Lancet. 1979:1:955_959.

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

  79. 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.

  80. Christensen, L. The Role of Caffeine and Sugar in Depression. Nutrition Report. Mar 1991;9(3):17-24.

  81. Ibid,44

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

  83. Frey, J. Is There Sugar in the Alzheimer's 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.

  85. Yudkin, J and Eisa, O. Dietary Sucrose and Oestradiol Concentration in Young Men. Annals of Nutrition and Metabolism. 1988:32(2):53-55.

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

  87. Gardner, L. and 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.

  88. 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. 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

  92. Ibid.

  93. Sugar, White Flour Withdrawal Produces Chemical Response. The Addiction Letter. Jul 1992:04:00 Colantuoni, C., et al. Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence. Obes Res. Jun 2002 ;10(6):478-488. Annual Meeting of the American Psychological Society, Toronto, June 17, 2001 www.mercola.com/2001/jun/30/sugar.htm

  94. Ibid.

  95. Sunehag, A. L., et al. Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition Diabetes. 1999 ;48 7991_800.

  96. Christensen L., et al. Impact of A Dietary Change on Emotional Distress. Journal of Abnormal Psychology.1985;94(4):565_79.

  97. Nutrition Health Review. Fall 85 changes sugar into fat faster than fat

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

  99. Pediatrics Research. 1995;38(4):539-542. Berdonces, J. L. Attention Deficit and Infantile Hyperactivity. Rev Enferm. Jan 2001;4(1)11-4

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

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

  102. Fields, M. Journal of the American College of Nutrition. Aug 1998;17(4):317_321.

  103. 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.

  104. Sandler, Benjamin P. Diet Prevents Polio. Milwakuee, WI,:The Lee Foundation for for Nutritional Research, 1951

  105. Murphy, Patricia. The Role of Sugar in Epileptic Seizures. Townsend Letter for Doctors and Patients. May, 2001 Murphy Is Editor of Epilepsy Wellness Newsletter, 1462 West 5th Ave., Eugene, Oregon 97402

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Partial List of Conditions Related to Nutritional Deficiencies:
  • Allergies/Hay Fever
  • Ankle Swelling
  • Arthritis
  • Back Pain
  • Blood pressure
  • Bronchial Conditions
  • Colitis
  • Colon, Spastic
  • Constipation
  • Diabetes
  • Diarrhea
  • Diverticulitis
  • Dizziness (Vertigo)
  • Fatigue, Chronic
  • Feet, Cold or Burning
  • Gall Bladder Disorders
  • Gas
    		•
  • Glandular Troubles
  • Headaches
  • Heart, Fast “Nervous”
  • Insomnia
  • Joint Pain
  • Kidney Problems
  • Knee Pains,
  • Chronic Leg Pains
  • Leg Cramps, Tingling,
  • Liver Problems
  • Neuralgia
  • PMS
  • Prostate Trouble
  • Sciatica
  • Sinus Trouble
  • Thyroid Conditions
  • Ulcers—Stomach
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