Even in the nervous system of a single species such as humans, hundreds of different types of neurons exist, with a wide variety of morphologies and functions. These include sensory neurons that transmute physical stimuli such as light and sound into neural signals, and motor neurons that transmute neural signals into activation of mucles or glands; however in many species the great majority of neurons receive all of their input from other neurons and send their output to other neurons.
Kandel ER, Schwartz JH, Jessel TM, ed (2000). "Ch. 2: Nerve cells and behavior". Principles of Neural Science. McGraw-Hill Professional. ISBN 9780838577011.
Finger S (2001). "Ch. 1: The brain in antiquity". Origins of neuroscience: a history of explorations into brain function. Oxford Univ. Press. ISBN 9780195146943.
Sakarya O, Armstrong KA, Adamska M, et al. (2007). "A post-synaptic scaffold at the origin of the animal kingdom". PLoS ONE 2 (6): e506. doi:10.1371/journal.pone.0000506. PMID 17551586.
Ruppert EE, Fox RS, Barnes RD (2004). Invertebrate Zoology (7 ed.). Brooks / Cole. pp. 111-124. ISBN 0030259827.
Kandel ER, Schwartz JH, Jessel TM, ed (2000). "Ch. 4: The cytology of neurons". Principles of Neural Science. McGraw-Hill Professional. ISBN 9780838577011
Some research suggests that restless legs syndrome may be due to nerve impairment in the spinal cord. It had been thought that such abnormalities were likely to originate from nerve pathways in the lower spine. However, some patients with RLS commonly have symptoms in the arms suggesting that the upper spine may be involved as well. One 2001 study suggested that in patients with RLS and PLMD there is an abnormal over-excitable response along the entire spinal cord, which is triggered by sleep-related factors.
Other research suggests that neurologic abnormalities involved with RLS and PLMD originate in the brain. A variety of studies support the hypothesis that an imbalance in neurotransmitters (chemical messengers in the brain), notably dopamine and serotonin, may play a part in RLS. Dopamine and serotonin unleash an array of nerve impulses that affect muscle movement.
Some experts suggest that RLS, particularly if it occurs in older adults, may be a form of neuropathy, which is an abnormality in the nervous system outside the spine and brain. Nevertheless, there is no evidence of a causal relationship.
Electromyography and nerve conduction studies may be recommended to measure electrical activity in muscles and nerves, and Doppler sonography may be used to evaluate muscle activity in the legs. Such tests can document any accompanying damage or disease in nerves and nerve roots (such as peripheral neuropathy and radiculopathy) or other leg-related movement disorders.
"Restless Legs Syndrome and Related Disorders - Causes." ChronicPainConnection.com www.healthcentral.com/ency/408/guides/000095_2.html
Bliwise DL, Freeman A, Ingram CD, Rye DB, Chakravorty S, Watts RL. "Randomized, double-blind, placebo-controlled, short-term trial of ropinirole in restless legs syndrome." Sleep Med. 2005;6(2):141-147.
Desautels A, Turecki G, Montplaisir J, Xiong L, Walters AS, Ehrenberg BL, et al. "Restless legs syndrome: confirmation of linkage to chromosome 12q, genetic heterogeneity, and evidence of complexity." Arch Neurol. 2005;62(4):591-596.
Kotagal S, Silber MH. "Childhood-onset restless legs syndrome." Ann Neurol. 2004;56(6):803-807.
"Restless Legs Syndrome Fact Sheet." National Institute of Neurological Disorders and Stroke www.ninds.nih.gov/disorders/restless_legs/detail_restless_legs.htm
"Inflammation is a key component of host defence responses to peripheral inflammation and injury, but it is now also recognized as a major contributor to diverse, acute and chronic central nervous system (CNS) disorders."
Stuart M. Allan and Nancy J. Rothwell, "Inflammation in central nervous system injury." Philos Trans R Soc Lond B Biol Sci. 2003 October 29; 358(1438): 1669-1677. doi: 10.1098/rstb.2003.1358. PMCID: PMC1693261
"One promising lead was provided two years ago, when it was discovered that there is a connection between inflammation and the involuntary nervous system."
Claude Libert, "Inflammation: A nervous connection." Nature 421, 328-329 (23 January 2003) doi:10.1038/421328a
"In conclusion, the nervous system is broadly involved in immune modulation. In this context, the spinal cord appears to participate as an important relay station for propagating information from the periphery to supraspinal centres, from where efferent pathways maintaining inflammation-related body homeostasis are being regulated. In addition, spinal reflexes, either dorsal root reflexes or sympathetic reflexes, can influence inflammation more directly."
Dr. Michael Boettger, "Influences of the nervous system on inflammation." SciTopics (March 17, 2011). www.scitopics.com/Influences_of_the_nervous_system_on_inflammation.html
"Our findings are consistent with the hypothesis that inflammation and inadequate antioxidant defenses are associated with accelerated decline of nerve conduction velocity over the aging process."
Angelo Di Iorio, Antonio Cherubini, Stefano Volpato, Eleonora Sparvieri, Fulvio Lauretani, Claudio Franceschi, Umberto Senin, Giuseppe Abate, Roberto Paganelli, Antonio Martin, Cristina Andres-Lacueva and Luigi Ferruccidi, "Markers of inflammation, Vitamin E and peripheral nervous system function." Neurobiol Aging. 2006 September; 27(9): 1280-1288. doi: 10.1016/j.neurobiolaging.2005.07.004.
"Inflammation associated with the activation of microglial cells is an important factor that appears to contribute to tissue damage and disability in many of the important neurodegenerative disorders. By decreasing this inflammatory response, tissue loss after injury can be reduced. Thus, what we found in this study has important potential therapeutic implications for the treatment of a number of important neurological disorders," says the study's senior investigator, Alan I. Faden, M.D., a professor of neuroscience and director of the Laboratory for the Study of Central Nervous System Injury."
Karen Mallet, "Novel Mechanism To Reduce Nervous System Inflammation Identified By Researchers." Georgetown University Medical Center (Press Release, Sep 15, 2011). explore.georgetown.edu/news/?ID=36563&PageTemplateID=295
"The Neuroinflammation Research Lab consists of a group of investigators dedicated to the study of the biology and treatment of destructive inflammatory mechanisms in the brain, particularly as they relate to neurodegenerative disorders such as Alzheimer's disease. The lab conducts studies that range from molecular biology to treatment trials in humans."
"Research Overview." Neuroinflammation Research Laboratory: Mount Sinai School of Medicine, New York, NY www.mssm.edu/research/labs/neuroinflammation-research-laboratory
"Previous studies have indicated that the central nervous system (CNS) can potentially regulate immune function and inflammation in peripheral tissue. Furthermore, p38 is activated in the CNS in response to pain. Armed with this knowledge, Firestein and colleagues ran a series of tests to determine whether and how p38 within the central nervous system regulates inflammation in a rat model of rheumatoid arthritis."
"Central Nervous System Regulation of Inflammation." Arthritis Foundation www.arthritis.org/central-nervous-system-inflammation.php
Boyle DL, Jones TL, Hammaker D, et al. "Regulation of peripheral inflammation by spinal p38 MAP kinase in rats." PLoS Medicine 2006; 3:e338.
VITAMINS AND SUPPLEMENTS
"Lecithin acts like motor oil for your nervous system, keeping everything firing away smoothly and efficiently. It contains phosphatidylcholine (PC), which is broken down into choline and then acetylcholine, a nerve chemical which is key for brain function. Lecithin is also uniquely suited for supporting the nervous system. In fact, after strenuous exercise, choline levels drop in the body, and this drop is linked to fatigue. The lower choline levels result in lower acetylcholine, which means nerve impulses (the messengers that tell your muscles when to work) travel slower, leading to slower reaction times and even more fatigue."
"Lecithin: Nonessential Micronutrient." Nutritional Supplements Knowledgebase www.nutros.com/nsr-02039.html
Niederau, C., et al., "Polyunsaturated Phosphatidyl-Choline and Interferon Alpha for Treatment of Chronic Hepatitis B and C: A Multi-Center, Randomized, Double-Blind, Placebo-Controlled Trial," Hepatogastroenterology 45.21 (1998) : 797-804.
"Lecithin helps the body digest and utilize the fats and oils that are critical in maintaining efficient brain and nerve function. Perhaps the greatest recent discovery is the use of lecithin to activate a sluggish mind and improve memory by providing the body with the ingredients necessary to produce the vital neurotransmitter acetylcholine. This is the neurotransmitter that is responsible for memory storage and retrieval and the effectiveness of nerve signals in many areas of the brain. Your brain, if dried and analyzed, would show a composition of about 30% of lecithin."
Dianne Craft, MA, CNHP, "Improving Your Memory With Lecithin." Child Diagnostics www.diannecraft.com/article-010.htm
"There is evidence that bipolar disorder is associated with reduced choline in the central nervous system. Supplementing with lecithin has been shown to result in significant improvement and stabilization of mood during hypermanic phases; however it has also been reported to depress mood, so its use for mood disorders should be monitored by a qualified health practitioner."
Dr. Melina Roberts,ND, "Lecithin." alive #311, Calgary Centre for Naturopathic Medicine (September 2011). www.calgarynaturopathic.com/Resources/Articles/Lecithin.aspx
"Omega-6 and omega-3 PUFA are important structural components of cell membranes. When incorporated into phospholipids, they affect cell membrane properties such as fluidity, flexibility, permeability and the activity of membrane bound enzymes. DHA is selectively incorporated into retinal cell membranes and postsynaptic neuronal cell membranes, suggesting it plays important roles in vision and nervous system function."
Jane Higdon, Ph.D. "Essential Fatty Acids." Linus Pauling Institute, Oregon State University (2005). lpi.oregonstate.edu/infocenter/othernuts/omega3fa
Stillwell W. Wassall Sr. "Docosahexaenoic acid: membrane properties of a unique fatty acid. Chem Phys Lipids." 2003;126(1):1-27.
"Omega-3 fatty acids have been the subject of volumes of international research, the results of which indicate these substances may have therapeutic value in a number of medical conditions. An emerging area of research is examining the neurobehavioral aspects of omega-3 fatty acids (alpha-linolenic, eicosapentaenoic, docosahexaenoic) and the critical role of these essential fats in the functioning of the central nervous system."
Alan C. Logan, "Neurobehavioral aspects of omega-3 fatty acids: possible mechanisms and therapeutic value in major depression." Altern Med Rev 2003;8(4):410-425.
"The omega-3 essential fatty acids commonly found in fatty fish and algae help animals avoid sensory overload, according to research published by the American Psychological Association. The finding connects low omega-3s to the information-processing problems found in people with schizophrenia; bipolar, obsessive-compulsive, and attention-deficit hyperactivity disorders; Huntington's disease; and other afflictions of the nervous system."
"New Study Links DHA Type of Omega-3 to Better Nervous-System Function." ScienceDaily (Dec. 19, 2011).
Fedorova et al. "Deficit in prepulse inhibition in mice caused by dietary n-3 fatty acid deficiency." Behavioral Neuroscience, 2011; 123 (6): 1218 DOI: 10.1037/a0017446
vitamin b3 (niacin)
"Niacin helps keep your nervous system, digestive system, skin, hair and eyes healthy."
Mayo Clinic Staff, "Niacin to boost your HDL, 'good,' cholesterol." Mayo Foundation for Medical Education and Research www.mayoclinic.com/health/niacin/CL00036
"Participation of nicotinic acid and its derivates in the functioning of nervous system is considered basing on the data from literature. It is supposed that the favourable therapeutic effects of nicotinamide, nicotinic acid and their active biological form--NAD are realized due to the mechanisms of their functioning in the nervous system, for treating schizophrenia, epilepsy and other diseases of the nervous system."
PK Parkhomets, TM Kuchmerovskaia, GV Donchenko, GV Chichkovskaia and AP Klimenko, "Role of nicotinic acid and its derivatives in disorders of nervous system function." Ukr Biokhim Zh. 1995 Jul-Aug;67(4):3-11. PMID: 8553469
"Niacin helps to maintain the central nervous system and is also effective in improving circulation and reducing cholesterol levels in the blood."
"Vitamin B3 (Niacin)." Diet and Fitness Today www.dietandfitnesstoday.com/niacin.php
vitamin b6 (pyridoxine hydrochloride)
"The role of vitamin B6 in our nervous system is very broad, and involves many aspects of neurological activity. One aspect focuses on the creation of an important group of messaging molecules called amines. The nervous system relies on formation of these molecules for transmission of messages from one nerve to the next. (The molecules can be classified as "neurotransmitters" for this reason.) Amines are one type of neurotransmitter in the nervous system. They are often made from parts of protein called amino acids, and the key nutrient for making this process happen is vitamin B6. Some of the amine-derived neurotransmitters that require vitamin B6 for their production include serotonin, melatonin, epinephrine, norepinephrine, and GABA. The key role of vitamin B6 in the nervous system also results in many nerve-related symptoms when B6 is deficient. These symptoms can include convulsions and seizures in the case of severe deficiency. The critical role of vitamin B6 in the formation of red blood cells means that B6 deficiency can also result in symptoms of anemia, malaise, and fatigue. When anemia is exclusively related to B6 deficiency, it is usually classified as hypochromic, microcytic (pernicious) anemia."
"Vitamin B6." The George Mateljan Foundation www.whfoods.com/genpage.php?tname=nutrient&dbid=108
"Vitamin B6, also known as pyridoxine hydrochloride, is essential for the metabolism of protein by the body, and the proper functioning of the nervous system and the immune system. It is also involved in the synthesis of hormones and red blood cells."
"Vitamin B6." BBC News: Medical notes (June 8, 1998).
"The nervous and immune systems need vitamin B6 to function efficiently."
Gerster H. The importance of vitamin B6 for development of the infant. Human medical and animal experiment studies. Z Ernahrungswiss 1996; 35:309-17. Bender DA. Novel functions of vitamin B6. Proc Nutr Soc 1994; 53:625-30.
Chandra R and Sudhakaran L. Regulation of immune responses by Vitamin B6. NY Acad Sci 1990; 585:404-423.
Trakatellis A, Dimitriadou A, Trakatelli M. Pyridoxine deficiency: New approaches in immunosuppression and chemotherapy. Postgrad Med J 1997; 73:617-22.
vitamin b11 (folic acid)
"Folic acid supplementation has proved to be extremely effective in reducing the occurrence of neural tube defects (NTDs) and other congenital abnormalities in humans, suggesting that folic acid can modulate key mechanisms for growth and differentiation in the central nervous system (CNS). To our knowledge, this is the first time that folic acid supplementation is shown to enhance repair processes in the adult CNS."
Bermans J. Iskandar, MD, Aaron Nelson, BS, Daniel Resnick, MD, JH Pate Skene, PhD, Peng Gao, PhD, Chenara Johnson, BS, Thomas D. Cook, PhD, and Nithya Hariharan, MD, "Folic Acid Supplementation Enhances Repair of the Adult Central Nervous System." Ann Neurol 2004;56:221-227
"Folates and vitamin B12 have fundamental roles in CNS function at all ages, especially the methionine-synthase mediated conversion of homocysteine to methionine, which is essential for nucleotide synthesis and genomic and non-genomic methylation. Folic acid and vitamin B12 may have roles in the prevention of disorders of CNS development, mood disorders, and dementias, including Alzheimer's disease and vascular dementia in elderly people."
E. Reynolds, "Vitamin B12, folic acid, and the nervous system." Lancet Neurol. 2006 Nov;5(11):949-60. PMID: 17052662
"Beginning in the early 1980's, researchers began to successfully use folic acid supplementation to reduce the risk of nervous system problems in newborn infants."
"Folate." The George Mateljan Foundation www.whfoods.com/genpage.php?tname=nutrient&dbid=63
vitamin b12 (cobalamin)
"Vitamin B12, also called cobalamin, is a water soluble vitamin with a key role in the normal functioning of the brain and nervous system, and for the formation of blood."
"Vitamin B12." Wikipedia en.wikipedia.org/wiki/Vitamin_B12
"Vitamin B12 is essential for the nervous system, which is why a deficiency can also cause inflammation of the nerves (neuritis) and dementia (mental deterioration)."
Dr. Patrick Davey and Dr. Rachel Green, "Anaemia due to vitamin B12 deficiency - (pernicious anaemia)" NetDoctor.co.uk www.netdoctor.co.uk/diseases/facts/anaemiab12.htm
"Although there is much to be learned, it is now clear that a normally functioning cobalamin-dependent methyl transferase is required for development and function of the human brain."
Charles A. Hall, "Function of vitamin B12 in the central nervous system as revealed by congenital defects." American Journal of Hematology Volume 34 Issue 2, Pages 121 - 127 (11 Jul 2006). 10.1002/ajh.2830340208
vitamin c (ascorbic acid)
"Vitamin C may help lower high blood pressure by calming an overactive central nervous system, new Italian research suggests. Using intravenously delivered vitamin C, "our study demonstrated for the first time in humans that we can reduce sympathetic nervous system overactivity, and consequently blood pressure, (by) targeting oxidative stress," said study lead author Dr. Rosa Maria Bruno from the University of Pisa."
Alan Mozes, "Vitamin C Might Help Lower Hypertension." HealthDay News (September 19, 2011). www.washingtonpost.com/wp-dyn/content/article/2011/09/19/AR2011091901851.html
"Ascorbic acid is needed in in vitro studies for proper myelination of axons (in cultures containing serum). Recently, in a mouse model for CMT1A it has been shown that ascorbic acid improves the CMT1A phenotype. Mice (2-4 months old) treated with ascorbic acid once a week during three months showed an increase in the percentage of myelinating nerve fibers and showed better results in locomotor tests."
C. Verhamme, MD, M. Vermeulen, MD, PhD, F. Baas, MD, PhD, R. de Haan, MD, PhD, M. de Visser, MD, PhD and I. N van Schaik, MD, PhD, "Ascorbic Acid Treatment in CMT1A Trial (AATIC)." Academic Medical Center, university of Amsterdam, ClinicalTrials.gov identifier: NCT00271635 (Jan. 23, 2006).
"Vitamin C helps the immune system to fight against foreign invaders and tumour cells. Vitamin C also supports the cardiovascular system by facilitating the metabolism of fats and protecting tissues from free radical damages, and it assists the nervous system by converting certain amino acids into neurotransmitters (Schectman et al., 1991). Vitamin C contributes to a variety of other biochemical functions. These include the biosynthesis of the amino acid carnitine and the catecholamine that regulate the nervous system. It also helps the body to absorb iron and to break down histamine, the inflammatory component of many allergic reactions."
Maria Cioroi, "Study on l-ascorbic acid contents from exotic fruits." Cercetari Agronomice ??n Moldova, Anul XXXX , Vol. 1 (129) / 2007.
"Vitamin E is essential for normal neurological function. It is the major lipid-soluble, chain-breaking antioxidant in the body, protecting the integrity of membranes by inhibiting lipid peroxidation. Mostly on the basis of symptoms of primary vitamin E deficiency, it has been demonstrated that vitamin E has a central role in maintaining neurological structure and function."
Chandan K. Sen, Savita Khanna and Sshwati Roy, "Tocotrienol: The natural vitamin E to defend the nervous system?" Annals of the New York Academy of Sciences 2004, vol. 1031, pp. 127-142 ISSN 0077-8923 CODEN ANYAA9
"Our findings in chronic vitamin E deficiency indicate that (a) in addition to the degeneration of central extensions of sensory neurons, their peripheral axons are also affected, (b) the distribution of lesions is similar to those seen in distal axonopathies or a 'dying back' process."
J. Towfighi, "Effects of chronic vitamin E deficiency on the nervous system of the rat." Acta Neuropathologica, Volume 54, Number 4 / December, 1981 Pages 261-267 10.1007/BF00696998 ISSN 0001-6322
"A second area of focus for vitamin E deficiency symptoms is called peripheral neuropathy. This area focuses on nervous system problems in the arms, hands, legs, and feet. Pain, tingling, and loss of sensation in these extremities have been associated with vitamin E deficiency."
"vitamin E." The George Mateljan Foundation www.whfoods.com/genpage.php?tname=nutrient&dbid=111
"The most important thing that calcium does in the human body is provide the means for electrical impulses to travel along nerves. Calcium is what the nervous system of our body uses to conduct electricity. This is why the most common symptoms of parathyroid disease and high calcium levels are related to the nervous system (depression, weakness, tiredness, etc.)."
"Introduction to Parathyroid Glands." Norman Parathyroid Center (March 26, 2011). www.parathyroid.com/parathyroid.htm
"Among the many calcium-binding proteins in the nervous system, parvalbumin, calbindin-D28K and calretinin are particularly striking in their abundance and in the specificity of their distribution. They can be found in different subsets of neurons in many brain regions. Although it is not yet known whether they play a 'triggering' role like calmodulin, or merely act as buffers to modulate cytosolic calcium transients, they are valuable markers of neuronal subpopulations for anatomical and developmental studies."
KG Baimbridge, MR Celio and JH Rogers, "Calcium-binding proteins in the nervous system." Trends Neurosci (1992) 15: 303-8.
"These results indicate that in the rat spinal cord and brain stem Ca(V)1.3 is probably a common calcium channel used by many kinds of neurons to facilitate the neuronal information processing via certain intracellular mechanisms, for instance, PICs."
N. Sukiasyan, H. Hultborn and M. Zhang, "Distribution of calcium channel Ca(V)1.3 immunoreactivity in the rat spinal cord and brain stem. Neuroscience (2011) 0:
"Iron deficiency anemia has long been thought to have effects on the central nervous system (CNS). Finding direct evidence of this in human infants, however, has been challenging. This study shows that iron deficiency anemia in 6-mo-old infants is associated with adverse effects on at least one aspect of CNS development and suggests the fruitfulness of studying other processes that are rapidly myelinating during the first 2 y of life."
M. Roncagliolo, M. Garrido, T. Walter, P. Peirano and B. Lozoff, "Evidence of altered central nervous system development in infants with iron deficiency anemia at 6 mo: delayed maturation of auditory brainstem responses." American Journal of Clinical Nutrition, Vol 68, 683-690
"Iron is one of few metal ions whose role in the central nervous system has received little attention, even though it is important in many enzymatic, metabolic and structural processes. The brain is rich in iron, and iron is the most likely initiator of free oxygen radicals generation. Recent investigations have reported that iron-generated free radicals play an important role in the pathogenesis of many neurological disorders. Experimental studies have shown that iron chelators and free-radical scavengers may have an important therapeutic potential in the future trends of treatment."
M. Tynecka, "The role of iron in the pathology of nervous system." Neurol Neurochir Pol. 1995 May-Jun;29(3):409-17.
"In conclusion, the present study demonstrates an altered autonomic balance in patients with true iron deficiency anemia."
Mehmet Yokusoglu, Oral Nevruz, Oben Baysan, Mehmet Uzun, Sait Demirkol, Ferit Avcu, Cem Koz, Turker Cetin, Adnan Hasimi, Ali Ugur Ural and Ersoy Isik, "The Altered Autonomic Nervous System Activity in Iron Deficiency Anemia." The Tohoku Journal of Experimental Medicine Vol. 212 (2007), No. 4 pp.397-402
With magnesium deficiency, the central nervous system is markedly affected. Symptoms include insomnia, anxiety, hyperactivity and restlessness with constant movement, panic attacks, agoraphobia, and premenstrual irritability. Magnesium deficiency symptoms involving the peripheral nervous system include numbness, tingling, and other abnormal sensations, such as zips, zaps and vibratory sensations.
Michael Schachter M.D., "The Importance of Magnesium to Human Nutrition." HealthWorld Online www.healthy.net/scr/article.aspx?Id=541
"Taking advantage of new advances in electronic measuring techniques, the scientists studied the electrical conduction of currents by the nerves. Their most important finding was that while calcium is the prime conductor of these minute electrical currents, it is magnesium that maintains normal levels of calcium in the system. How does magnesium regulate calcium levels? Inside the body, these two minerals are positively charged. When they come into contact with negatively charged particles, an electrical current is formed. It is believed that fatty acids comprising the major portion of nerve tissue are negatively charged. It is for this reason, then, that calcium and magnesium supplies must be constantly renewed; without them, the flow of current by the nerves cannot be maintained. Magnesium works in other ways to preserve the health of the nervous system. By the twentieth century, doctors had learned that magnesium injections exert a depressant effect upon the nerves. In fact, one of the early uses of the mineral was to induce sleep. It is significant that hibernating animals have very high magnesium levels. Magnesium has also been shown effective in controlling convulsions, in pregnant women, epileptic seizures, and "the shakes" in alcoholics."
J.I. Rodale, "Magnesium, The Nutrient That Could Change Your Life." Pyramid Prevention, New York, NY (1968)
Richard D. Penn and Werner R. Loewenstein, "Uncoupling of a Nerve Cell Membrane Junction by Calcium-Ion Removal." Science 7 January 1966: Vol. 151. no. 3706, pp. 88 - 89 DOI: 10.1126/science.151.3706.88
"Ionic magnesium (Mg(2+)) depletion has long been known to cause hyperexcitability with convulsive seizures in rodents, effects that have been reversed by treatment with magnesium (Mg). This open study indicates that hyperexcitable children have low ERC-Mg with normal serum Mg(2+) values, and that Mg(2+)/vitamin B6 supplementation can restore normal ERC-Mg levels and improve their abnormal behavior."
M. Mousain-Bosc, M. Roche, J. Rapin and JP Bali, "Magnesium VitB6 intake reduces central nervous system hyperexcitability in children." J Am Coll Nutr. 2004 Oct;23(5):545S-548S. PMID: 15466962
"Potassium, calcium and magnesium are three inorganic ions that occur in significant quantity in extracellular fluid of the mammalian brain and have powerful effects on the functioning of nervous tissue. Due to the recent developement of postassium-selective microelectrodes there has been a new surge of interest in the functional significance of potassium distribution in the nervous system."
GG Somjen, "Extracellular Potassium in the Mammalian Central Nervous System." Annual Review of Physiology Vol. 41: 159-177 (October 1979) doi:10.1146/annurev.ph.41.030179.001111
"Neurons communicate or send impulses through an action potential., This takes place from the dendrite and all the way to the axon ends. An action potential is a change of voltage within the axon. In other words, the negative state off the inner axon turns positive when the impulses comes by. This happens by the use of a sodium and potassium pump. Sodium [Na] surrounds the axon with a positive charge, while the potassium [K] is within the axon. As an impulse enters at the axon hillock, the sodium, potassium pump puts positive sodium into the axon while it puts negative potassium out of the axon. As more sodium enters the potential of the impulse changes from -70 mV to +30 mV, (a difference of 100 mV) This change is called an action potential. The sodium, potassium pump works furiously to pass the impulse through the axon. As the impulse leaves the axon, it is reverted to a normal state which is called the resting potential. At the end of the axon, the impulse or stimulus enters the synapses and is called a post synaptic potential. From here, the impulse is transferred into neurotransmitters, some of which are chemicals called epinephrine and dopamine. These neurotransmitters flow into the fluid filled gap called the synaptic cleft and enter the dendrites. And, again, the process is repeated."
"The Nervous System." Oracle ThinkQuest Education Foundation library.thinkquest.org/2935/Natures_Best/Nat_Best_Low_Level/Nervous_page.L.html
"The rapid accommodation of leech neurons is based primarily on an increased potassium conductance. The possibility is considered that concentration changes like those produced experimentally may occur naturally, affecting integrative processes in the central nervous system."
W. R. Schlue, "Sensory neurons in leech central nervous system: changes in potassium conductance an excitation threshold." J Neurophysiol 39: 1184-1192, 1976; 0022-3077/76
"Zinc is essential to the structure and function of myriad proteins, including regulatory, structural and enzymatic. It is estimated that up to 1% of the human genome codes for zinc finger proteins. In the central nervous system, zinc has an additional role as a neurosecretory product or cofactor. In this role, zinc is highly concentrated in the synaptic vesicles of a specific contingent of neurons, called "zinc-containing" neurons."
Christopher J. Frederickson, Sang Won Suh, David Silva, Cathy J. Frederickson and Richard B. Thompson, "Importance of Zinc in the Central Nervous System: The Zinc-Containing Neuron." (Journal of Nutrition. 2000;130:1471S-1483S.)
"Numerous syndromes associated with zinc deficiency, including immune and nervous system abnormalities, have been described in infants, adolescents, and the elderly. Although the antioxidant properties of zinc were first demonstrated in vitro, there is also clear evidence that zinc functions as an antioxidant in the body. One area of growing interest is the role of zinc as an antioxidant in the central nervous system (CNS), particularly the brain. Compared to other soft tissues, the human brain contains significant amounts of zinc."
Mark A. Levy, Ph.D.and Tammy M. Bray, Ph.D., "The Antioxidant Function of Dietary Zinc and Protection Against Neural Disorders." Linus Pauling Institute: Oregon State University (2003).
"Maternal serum zinc concentrations were estimated during 244 normal pregnancies and 15 abnormal pregnancies. The serum zinc concentrations were lower in the anencephalic pregnancies than in the normal control subjects. The serum zinc levels in women whose pregnancies terminated in a spontaneous abortion were normal. There was no variation of serum zinc level with gestational age between 15 to 18 weeks in normal pregnancies."
PK Buamah, M. Russell, G. Bates, A. Milford Ward and AW Skillen, "Maternal zinc status: a determination of central nervous system malformation." BJOG: An International Journal of Obstetrics & Gynaecology Volume 91 Issue 8, Pages 788 - 790 (23 Aug 2005). 10.1111/j.1471-0528.1984.tb04851.x
butcher's broom (ruscus aculeatus)
"CONCLUSION: With proven phlebotherapeutic properties, including vasoconstrictive action and venotonic properties, Ruscus aculeatus shows great promise for ameliorating the symptoms of Chronic orthostatic hypotension and improving the quality of life for large groups in the population. It clearly deserves to be the object of wider research and study as a treatment for chronic orthostatic hypotension."
DA Redman, "Ruscus aculeatus (butcher's broom) as a potential treatment for orthostatic hypotension, with a case report." J Altern Complement Med. 2000 Dec;6(6):539-49. PMID: 11152059
cayenne pepper (capsicum annuum)
"When used topically, the active component capsaicin has been reported to be useful in alleviating pain associated with arthritis and a number of other conditions. Scientists think this pain-relief activity is linked to the stimulation of nerves that further stimulate the body's own natural pain relief mechanisms."
"Cayenne." Natural Health Information On Demand articles.directorym.com/Cayenne-a853087.html
BM Magnusson, "Effects of Topical Application of Capsaicin to Human Skin: A Comparison of Effects Evaluated by Visual Assessment, Sensation Registration, Skin Blood Flow and Cutaneous Impedance Measurements." Acta Derm Venereol. Mar1996;76(2):129-32.
Rains C, et al. "Topical Capsaicin. A Review of Its Pharmacological Properties and Therapeutic Potential in Post-herpetic Neuralgia, Diabetic Neuropathy and Osteoarthritis." Drugs Aging. Oct1995;7(4):317-28.
P. Anand, "Capsaicin and menthol in the treatment of itch and pain: recently cloned receptors provide the key." Gut. Sep2003;52(9):1233-5.
Purkiss JR, et al. "Capsaicin Stimulates Release of Substance P from Dorsal Root Danglion Neurons Via Two Distinct Mechanisms." Biochem Soc Trans. Aug1997;25(3):542S.
"Cayenne regulates the flow of blood from the head to the feet so that the pressure is equalized; it influences the heart immediately, then gradually extends its effects to the arteries, capillaries, and nerves (the frequency of the pulse is not increased, but is given more vigor).
"Health Benefits of Cayenne Pepper." CayennePepper.info www.cayennepepper.info/health-benefits-of-cayenne-pepper.html
"Capsaicin is being studied as an effective treatment for sensory nerve fiber disorders, including pain associated with arthritis, psoriasis, and diabetic neuropathy."
"Cayenne Pepper." The George Mateljan Foundation www.whfoods.com/genpage.php?tname=foodspice&dbid=140
"In the central nervous system of rats, curcumin exerts a protective effect against neurodegeneration. Possible mechanisms of neuroprotection exerted by curcumin include inhibition of glutamate-mediated excytotoxicity, antioxidant activity, and induction of chaperone proteins. Indeed, in cultured neurons, treatment with curcumin reduced cell demise mediated by glutamate-induced Ca(2+) influx and caspase-3 activation. The possible use of curcumin as a neuroprotective drug is of potentially enormous importance; indeed neurodegenerative diseases such as AD affect millions of people world-wide and are becoming a dramatic health emergency in developed countries."
S. Salvioli, E. Sikora, EL Cooper and C. Franceschi, "Curcumin and the Nervous System: A More Sensitive Target is Neuroprotection." eCAM 2007 4(2):181-190; doi:10.1093/ecam/nem043
Frank B, Gupta S. A review of antioxidants and Alzheimer's disease. Ann Clin Psychiatry ( 2005;) 17:: 269-86.
Bala K, Tripathy BC, Sharma D. Neuroprotective and Anti-ageing Effects of Curcumin in Aged Rat Brain Regions. Biogerontology ( 2006;) 7:: 81-9.
Yazawa K, Kihara T, Shen H, Shimmyo Y, Niidome T, Sugimoto H. Distinct mechanisms underlie distinct polyphenol-induced neuroprotection. FEBS Lett ( 2006;) 580:: 6623-8.
"Gliomas are the most common and lethal primary tumors of the central nervous system (CNS). Despite current rigorous treatment protocols, effect of chemotherapy has failed to improve patient outcome significantly. The results demonstrate that curcumin exerts inhibitory action on glioma cell growth and proliferation via induction of cell cycle arrest instead of induction of apoptosis in a p53-dependent manner, and ING4 possibly is in part involved in the signal pathways."
Enyu Liu, Jing Wu, Weidong Cao, Jianning Zhang, Weiping Liu, Xiaofan Jiang and Xiang Zhang, "Curcumin induces G2/M cell cycle arrest in a p53-dependent manner and upregulates ING4 expression in human glioma." Journal of Neuro-Oncology Volume 85, Number 3 / December, 2007 Pages 263-270, ISSN 0167-594X (Print) 1573-7373, DOI 10.1007/s11060-007-9421-4
"A prayer was answered the day I emailed Dr. Cole. His team at UCLA has developed a formulation of "Optimized Curcumin" that works more like a drug with "super bio-availability." UCLA's Curcumin was not only crossing into the blood stream it was crossing through the blood brain barrier (BBB). The BBB is a membranic structure in the central nervous system (CNS) that restricts the passage of various chemical substances and things like bacteria between the bloodstream and the neural tissue itself, while still allowing the passage of substances like oxygen that is essential to metabolic function."
Chris Hempel, "The "Real Curcumin" for Treating Alzheimer's, Parkinson's and Other Brain Diseases." (September 28, 2011). Addi & Cassi Fund addiandcassi.com/the-real-curcumin-for-treating-alzheimer's-parkinson's-and-other-brain-disease
devil's claw (harpagophytum)
"Western use falls in line with the traditional African applications, but it is also used as supportive therapy for degenerative disorders of the CNS (central nervous system). The herb is sold today in pharmacies and health food stores as a remedy for arthritis and rheumatism."
"Devil's CLaw." Innvista www.innvista.com/health/herbs/devilscl.htm
"It would appear that H. procumbens secondary root aqueous extract (HPE) produces its anticonvulsant activity by enhancing GABAergic neurotransmission and/or facilitating GABAergic action in the brain. In general, the average onset of convulsion was delayed, while the average duration of convulsion was markedly reduced. The plant's extract also depressed the central nervous system (CNS). It is, therefore, thought that the anticonvulsant property of the herb may be linked, at least in part, to its ability to depress the central nervous system."
IM Mahomed and JA Ojewole, "Anticonvulsant activity of Harpagophytum procumbens DC [Pedaliaceae] secondary root aqueous extract in mice." Brain Res Bull. 2006 Mar 15;69(1):57-62. Epub 2005 Nov 15. PMID: 16464685
"Researchers postulate that Devil's Claw has an effect on sensory and vascular muscular response, reducing muscle stiffness without acting on the central nervous system (Gobel et al 2001)."
Todd Caldecott, "Devil's Claw." toddcaldecott.com (2011). www.toddcaldecott.com/devils_claw.html
Gobel H, Heinze A, Ingwersen M, Niederberger U, Gerber D, Schmerz. 2001. Effects of Harpagophytum procumbens LI 174 (devil's claw) on sensory, motor und vascular muscle reagibility in the treatment of unspecific back pain. Neurologisch-verhaltensmedizinische. Feb;15(1):10-8
"Ginkgo is one of the herbs with documented antioxidant properties. Studies in France have shown ginkgo to be very effective in protecting the lipid (fat) portion of cellular membranes from free radical damage. If one considers that the brain cells contain the highest content of unsaturated fats (lipids) of any cells in the body, this protective action further supports ginkgo's benefits for the central nervous system. Free radical damage in the rain and nervous system is widely postulated to be a major cause of accelerated aging."
Donald J. Brown N.D. "Ginkgo biloba- Old and New." Let's Live magazine (April 1992). www.ginkgocostcompare.com/ginkgo_article1.cfm
"Ginkgo has marked effects on neurophysiology, but it also seems to concentrate in the vascular and endocrine systems that strongly affect the function of the nervous system."
David L. Hoffmann B.Sc. (Hons), M.N.I.M.H. "Ginkgo and Alzheimer's Disease." healthy.net www.healthy.net/scr/article.aspx?Id=1324
Funfgeld, E.W. (Ed.). Rokan, "Ginkgo biloba. Recent Results in Pharmacology and Clinic." Springer-Verlag, Berlin 1988
"Extracts of Ginkgo biloba (EGb) are among the most prescribed drugs in France and Germany. EGb is claimed to be effective in peripheral arterial disorders and in "cerebral insufficiency." The mechanism of action is not yet well understood. Three of the ingredients of the extract have been isolated and found to be pharmacologically active, but which one alone or in combination is responsible for clinical effects is unknown. it was established that the electrophysiological effects of EGb in CNS are similar to those of well-known cognitive activators such as "nootropics" as well as tacrine, the only marketed "antidementia" drug currently available in the United States."
TM Itil, E. Eralp, E. Tsambis, KZ Itil and U. Stein, "Central Nervous System Effects of Ginkgo Biloba, a Plant Extract." Am J Ther. 1996 Jan;3(1):63-73. PMID: 11856998
skullcap (scutellaria lateriflora)
"The phytochemistry and biological activity of Scutellaria lateriflora L. (American skullcap) which has been traditionally used as a sedative and to treat various nervous disorders such as anxiety was studied. In vivo animal behaviour trials were performed to test anxiolytic effects in rats orally administered S. laterifolia extracts. Significant increases in the number of entries into the center of an "open-field arena"; number of unprotected head dips, number of entries and the length of time spent on the open arms of the Elevated Plus-Maze were found. The identification and quantification of the flavonoid, baicalin in a 50% EtOH extract (40 mg/g) and its aglycone baicalein in a 95% EtOH extract (33 mg/g), as well as the amino acids GABA in H2O and EtOH extracts (-1.6 mg/g) and glutamine in a H2O extract (31 mg/g), was performed using HPLC. These compounds may play a role in anxiolytic activity since baicalin and baicalein are known to bind to the benzodiazepine site of the GABAA receptor and since GABA is the main inhibitory neurotransmitter."
R. Awad, "Phytochemical and biological analysis of Skullcap ( L.): A medicinal plant with anxiolytic properties." Phytomedicine, Volume 10, Issue 8, Pages 640-649
"Traditionally, skullcap is known to be an effective stimulant for the nervous organization, as the herb contains high value ingredients for a sound nervous system. The herb is particularly effective in helping as well as escalating the nervous system when a person undergoes mental and physical stress and strain. In fact, skullcap is a time tested medicine for all kinds of disturbed mental state, be it tension, anxiety, insomnia, neurasthenia, panic, headaches, fatigue, depression as well as melancholy."
"Skullcap." herbs2000.com www.herbs2000.com/herbs/herbs_skullcap.htm
"Rats that received a weak solution of the three herbal fluid extracts of Scutellaria lateriflora (Skullcap), Gelsemium sempervirens (Gelsemium) and Datura stramonium (Jimson Weed) displayed no seizures during treatment while all the other groups were not seizure-free. However, when this treatment was removed, the rats in this group displayed numbers of spontaneous seizures comparable to the controls. Although there is no proof that herbal remedies can control limbic or temporal lobe epilepsy, the results of this experiment strongly suggest that the appropriate combination of herbal compounds may be helpful as adjunctive interventions."
Oksana Peredery and Michael A. Persinger, "Herbal treatment following post-seizure induction in rat by lithium pilocarpine: Scutellaria lateriflora (Skullcap), Gelsemium sempervirens (Gelsemium) and Datura stramonium (Jimson Weed) may prevent development of spontaneous seizures." Phytotherapy Research, Volume 18 Issue 9, Pages 700 - 705 (11 Oct 2004). DOI: 10.1002/ptr.1511
st. john's wort (hypericum perforatum)
"This Hypericum perforatum extract is therapeutically equivalent to imipramine in treating mild to moderate depression, but patients tolerate hypericum better."
Helmut Woelk, "Comparison of St John's wort and imipramine for treating depression: randomised controlled trial." BMJ 2000;321(7260):536 (2 September), doi:10.1136/bmj.321.7260.536
"A meta-analysis assessing 23 of the double-blind trials was published recently,5 and will not be replicated in this article. In summary, most patients in the reports had mild to moderately severe depression. (In mild depression the patient is distressed by depressive symptoms but will probably be able to perform most activities; symptoms are more numerous and intense when depression is of moderate severity, and the patient is likely to have significant difficulty in continuing with ordinary activities.) Three trials included patients with severe depression. Most trials lasted four to eight weeks. Across all reports, 50%-80% of patients improved with SJW, a rate similar to that achieved with conventional antidepressants."
Joseph M. Rey and Garry Walter, "Hypericum perforatum (St John's wort) in depression: pest or blessing?" The Medical Journal of Australia (1998).
Linde K, Ramirez G, Mulrow CD, et al. "St. John's wort for depression: an overview and meta-analysis of randomised clinical trials." BMJ 1996; 313: 253-258.
World Health Organization. "The ICD-10 classification of mental and behavioral disorders. Clinical descriptions and diagnostic guidelines." Geneva: World Health Organization, 1992; 121-122.
"St John's Wort is a persistent, gentle nerve tonic, boosting the whole Nervous System when taken regularly over an extended period of 3-6 months. If long-term stress has led to nervous exhaustion, St John's Wort will often help, slowly but surely, to building the energy level back up towards normal. It is superior to anti-depressive drugs, which tend to weaken the body."
"St. John's Wort." Alternative Health Zine (2011).www.alternative-healthzine.com/html/0300_2.html
A possible mechanism by which a valerian extract may cause sedation is by increasing the amount of gamma aminobutyric acid (GABA, an inhibitory neurotransmitter) available in the synaptic cleft. Results from an in vitro study using synaptosomes suggest that a valerian extract may cause GABA to be released from brain nerve endings and then block GABA from being taken back into nerve cells
"Valerian." Office of Dietary Supplements: National Institutes of Health (2011). ods.od.nih.gov/factsheets/Valerian.asp
Santos MS, Ferreira F, Cunha AP, Carvalho AP, Macedo T: "An aqueous extract of valerian influences the transport of GABA in synaptosomes." Planta Medica 60: 278-279, 1994.
"The objective of this study is to show better improvement of sleep quality when treating non-organic insomniacs with extractum Valerianae radix siccum instead of oxazepam (a drug which is a benzodiazepine derivative). The study showed no differences in the efficacy for valerian and oxazepam. Because of the more favourable adverse effect profile of valerian compared to oxazepam, this hypothesis should be analysed confirmatorily in an equivalence study."
"Efficacy and tolerability of Baldrian versus oxazepam in non-organic and non-psychiatric insomniacs: a randomised, double-blind, clinical, comparative study." Forsch Komplementarmed Klass Naturheilkd. 2000 Apr;7(2):79-84. PMID: 10899744
"Over the past several decades, valerian has undergone rather extensive chemical, pharmacological, and clinical studies. Its aqueous extract has been found to be mostly responsible for its sleep-inducing effect, while the volatile oil (mainly valerenic acid) and the valepotriates (through their degradation products) are major contributors to its sedative effects. Current data also indicate the valepotriates to be responsible for the antianxiety or tranquilizing effect of valerian. No serious toxic side effects associated with the clinical use of valerian have been reported."
Dennis V. C. Awang and Albert Y. Leung, "Encyclopedia of Dietary Supplements: Valerian." Informa Healthcare, (Feb 22, 2005). ISBN: 0824755049 DOI: 10.1081/E-EDS-120022131
"One mapped brain activity with functional MRI and found that stimulating an acupuncture point on the little toe, used for eye disorders, triggers activity in the brain's visual cortex. "There is no question it is working through the nervous system," says Zang- Hee Cho, the study author and a radiologist at the University of California- Irvine. Other research suggests that acupuncture may trigger the release of endorphins, the body's natural painkillers, and other brain chemicals. That effect might explain how acupuncture fights nausea, say researchers in the JAMA chemotherapy trial. And Arthur Margolin of Yale University School of Medicine, an author of the August addiction study, says acupuncture activates the "parasympathetic" part of the nervous system, which has a calming effect that reduces cravings."
Stacey Schultz, "Acupuncture Can Work: It's not just wishful thinking." U.S. News & World Report (Dec 19, 2000).
"An interesting study performed in China reveals that in 324 acupuncture points observed, 99% of the points are within 0.5 mm away from nerves, 96% are closely related to superficial nerves in the skin, and 86% are near an artery. This study points to a close correlation between acupuncture points and the nervous system."
Helen C. Ly, "Acupuncture and Chronic Pain." Vanderbilt University Psychology Health Page www.vanderbilt.edu/ans/psychology/health_psychology/Acupuncture.htm
"As far as we know, this is the first scientific report which shows distinctly that acupuncture is transmitted directly by the nervous system and the performance of analgesic acupuncture requires an intact nervous system. The more distal the acupuncture treatment is given upon the nerve, the greater the degree of analgesia is afforded."
B. Levy and T. Matsumoto, "Pathophysiology of acupuncture: nervous system transmission." Am Surg. 1975 Jun;41(6):378-84. PMID: 164810
"Subjects who participated in the yoga course demonstrated significant decreases in self-reported symptoms of depression and trait anxiety. These effects emerged by the middle of the yoga course and were maintained by the end. Changes also were observed in acute mood, with subjects reporting decreased levels of negative mood and fatigue following yoga classes. Finally, there was a trend for higher morning cortisol levels in the yoga group by the end of the yoga course, compared to controls."
A. Woolery, H. Myers, B. Sternlieb and L. Zeltzer, "A yoga intervention for young adults with elevated symptoms of depression." Altern Ther Health Med. 2004 Mar-Apr;10(2):60-3. PMID: 15055096
"Yogic relaxation and bio-feedback techniques were used in the treatment of 20 patients with hypertension. As a result, antihypertensive therapy was stopped altogether in 5 patients and reduced by 33-60% in a further 7 patients. Blood-pressure control was better in 4 other patients, while 4 patients did not respond to therapy. Of these 4 patients, at least 1 had derived indirect benefit by the relief of migraine and depression. The results of this study promise a useful new approach to the treatment of hypertension."
CH Patel, "Yoga and bio-feedback In the Management of Hypertension." The Lancet, Volume 302, Issue 7837, Pages 1053-1055 doi:10.1016/S0140-6736(73)92660-3
"Subjects with MS participating in either a 6-month yoga class or exercise class showed significant improvement in measures of fatigue compared to a waiting-list control group."
B. S. Oken, MD, S. Kishiyama, MA, D. Zajdel, D. Bourdette, MD, J. Carlsen, AB, M. Haas, DC MA, C. Hugos, MS PT, D. F. Kraemer, PhD, J. Lawrence, BS and M. Mass, MD, "Randomized controlled trial of yoga and exercise in multiple sclerosis." Neurology 2004;62:2058-2064
"When people drink alcohol, it's absorbed into their bloodstream. From there, it affects the central nervous system (the brain and spinal cord), which controls virtually all body functions. Because experts now know that the human brain is still developing during our teens, scientists are researching the effects drinking alcohol can have on the teen brain."
"Alcohol." TeensHealth kidshealth.org/teen/drug_alcohol/alcohol/alcohol.html
"Because alcohol is highly neurotoxic, as we've said before, it leads to damage of the brain and nervous system. Over time it can cause cognitive deficits, or loss of mental abilities in areas such as memory, concentration, motor control and ability to learn. However, there is some hope now that those precious brain-cells are not lost for ever. Researchers at Stanford University have found that after at least six months of sobriety, the brain damage caused by alcohol's toxicity does in fact repair itself. They concluded that the mental abilities of their study group of long-term alcoholics, who had all been sober for between six months and thirteen years, were now the same as their control group who had not been alcoholics. The only capability that had not been recovered was spatial awareness."
"Abstinence reduces alcohol damage to brain & nervous system." Bright Eye Counselling www.brighteyecounselling.co.uk/alcohol-drugs/abstinence-reduce-alcohol-brain-damage
"Researchers now know that alcohol can change gene expression in the brain, and that these changes are likely responsible for many of the 'symptoms' of addiction, such as tolerance, physical dependence, and craving, as well as the 'consequences' of alcoholism, such as brain damage."
Indiana University School of Medicine, "Alcohol's effects on gene expression in the central nervous system." BiologyNews.net www.biologynews.net/archives/2005/02/15/alcohols_effects_on_gene_expression_in_the_central_nervous_system.html
"It is suggested that its use as an artificial sweetener for soft drinks may cause human neurochemical changes that could have functional or behavioral consequences. The results show that, if aspartame-containing beverages are consumed with normal dietary carbohydrates, the effect of aspartame on brain composition is enhanced."
Richard J. Wurtman, "Neurochemical changes following high-dose aspartame with dietary carbohydrates." New-Engl-J-Med. Boston : Massachusetts Medical Society. Aug 18, 1983. v. 309 (7) p. 429-430. charts.
"Compared to other environmental factors putatively linked to brain tumors, the artificial sweetener aspartame is a promising candidate to explain the recent increase in incidence and degree of malignancy of brain tumors. Evidence potentially implicating aspartame includes an early animal study revealing an exceedingly high incidence of brain tumors in aspartame-fed rats compared to no brain tumors in concurrent controls, the recent finding that the aspartame molecule has mutagenic potential, and the close temporal association."
John W. Oney, MD, Nuri B. Farber, Edward Spitznagel and Lee N. Robins, "Increasing Brain Tumor Rates: Is There a Link to Aspartame?" Journal of Neuropathology & Experimental Neurology November 1996 - Volume 55 - Issue 11
"Aspartame (ASM), an artificial sweetener, was shown to dose dependently increase 45Ca influx into and lactate dehydrogenase (LDH) leakage from murine brain cell cultures. Astrocytes were more resistant than neurones to the effects of ASM. LDH leakage, a sign of severe cell damage, was observed at 1 mM concentrations of ASM after 22 h. Cerebral astrocytes on the other hand were more resistant and showed morphological changes, increased calcium influx and LDH leakage first at 5 mM concentrations of ASM."
U. Sonnewald, G. Unsgard and SB Petersen, "Effects of aspartame on 45Ca influx and LDH leakage from nerve cells in culture." Neuropharmacology and Neurotoxicology, January 1995 - Volume 6 - Issue 2
"Caffeine belongs to the xanthine chemical group. Adenosine is a naturally occurring xanthine in the brain that is used as a neurotransmitter at some synapses. One effect of caffeine is to interfere with adenosine at multiple sites in the brain including the reticular formation."
Eric H. Chudler, Ph.D. "Effects of Caffeine on the Nervous System." Neuroscience For Kids faculty.washington.edu/chudler/caff.html
"Three main mechanisms of action of caffeine on the central nervous system have been described. Mobilization of intracellular calcium and inhibition of specific phosphodiesterases only occur at high non-physiological concentrations of caffeine. The only likely mechanism of action of the methylxanthine is the antagonism at the level of adenosine receptors. Caffeine increases energy metabolism throughout the brain but decreases at the same time cerebral blood flow, inducing a relative brain hypoperfusion. Caffeine activates noradrenaline neurons and seems to affect the local release of dopamine. Many of the alerting effects of caffeine may be related to the action of the methylxanthine on serotonin neurons. The methylxanthine induces dose-response increases in locomotor activity in animals. Its psychostimulant action on man is, however, often subtle and not very easy to detect. The effects of caffeine on learning, memory, performance and coordination are rather related to the methylxanthine action on arousal, vigilance and fatigue. Caffeine exerts obvious effects on anxiety and sleep which vary according to individual sensitivity to the methylxanthine. However, children in general do not appear more sensitive to methylxanthine effects than adults."
A. Nehlig, JL Daval and G. Debry, "Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects." Brain Res Brain Res Rev. 1992 May-Aug;17(2):139-70. PMID: 1356551
"Because caffeine is primarily an antagonist of the central nervous system's receptors for the neurotransmitter adenosine, the bodies of individuals that regularly consume caffeine adapt to the continuous presence of the drug by substantially increasing the number of adenosine receptors in the central nervous system. First, the stimulatory effects of caffeine are substantially reduced, a phenomenon known as a tolerance adaptation. Second, because these adaptive responses to caffeine make individuals much more sensitive to adenosine, a reduction in caffeine intake will effectively increase the normal physiological effects of adenosine, resulting in unwelcome withdrawal symptoms in tolerant users."
Holtzman SG, Mante S, Minneman KP "Role of adenosine receptors in caffeine tolerance". J. Pharmacol. Exp. Ther. 256 (1): 62???8. (1991). PMID 1846425
"Some examiners claim that ataxia is one of the most common disorders produced by gluten in relationship to our nervous system. Poor coordination and clumsiness does occur with gluten intolerance and affects children as well as adults. But how does gluten cause our brains to function improperly and cause this imbalance? Evidence suggests that it is all due to the immune system's reaction to gluten itself. In your cerebellum (a part of the brain that plays an important role in the integration of sensation and control of movement), there are special cells called Purkinje cells. These cells are found in your cerebellum and are the main components of the "balancing center." In patients with gluten sensitivity, it has been shown that these individuals have antibodies against these Purkinje cells. The antibodies made against gluten (anti-gliadin antibodies) cross-react against these Purkinje cells. What this means is that in a person who is genetically at-risk for gluten sensitivity, gluten induces an immune attack against the protein gliadin, and this antibody not only attacks gliadin, but also attacks tissues far away from the intestines. In this case, through the bloodstream, these antibodies travel to the cerebellum and attack the Purkinje cells. As these cells become inflamed from the immune attack, the ability to coordinate all the "balance information" is impaired. Symptoms of poor balance and coordination then result."
"How Gluten Creates Problems in the Nervous System." The Gluten Doctors (Aug 21, 2011). glutendoctors.blogspot.com/2011/08/how-gluten-creates-problems-in-nervous.html
"One idea is that antibodies generated by food proteins or peptides can attack the brain. This immune mistake is generally known as molecular mimicry. A second idea is that gluten proteins or peptides generated from them during digestion can act directly on the brain. A third idea is that your brain is affected by immune responses in other parts of your body. All immune activity sends signals to the brain to change behavior and to recruit a range of defensive responses. Disturbances to brain function vary from routine effects such as sleepiness, fogginess, and brief episodes of confusion to symptoms of major mental or neurological illness. For example, people with celiac disease suffer for many years before the diagnosis is made. They often state that they never feel well. Most of these patients will report episodes of fatigue with cognitive dysfunction; difficulty concentrating, mental "fogginess", recent memory dropouts. They complain of mood liability and are often tearful and irritable. They return to normal when they no longer eat problem foods."
Stephen Gislason MD, "Gluten Problems and Solutions." Alpha Education Books Rev. 2011
"Celiac disease is a digestive condition triggered by consumption of the protein gluten, which is found in bread, pasta, cookies, pizza crust and many other foods containing wheat, barley or rye. If you have celiac disease and eat foods containing gluten, an immune reaction occurs in your small intestine, causing damage to the surface of your small intestine and an inability to absorb certain nutrients. Eventually, the decreased absorption of nutrients (malabsorption) that occurs with celiac disease can cause vitamin deficiencies that deprive your brain, peripheral nervous system, bones, liver and other organs of vital nourishment. This can lead to other illnesses and stunted growth in children."
Mayo CliniC Staff, "Celiac disease." Mayo Clinic services www.mayoclinic.com/health/celiac-disease/DS00319
monosodium glutamate (msg)
"Early on (in the 50s) studies reported significant issues relating to the exposure of mammals to MSG. If neonatal rats were given a single exposure to MSG, the neurons in the inner layer of their retina were killed. It was also reported that certain parts of their brains were injured as well (the hypothalamus). When considering various findings of MSG exposure in the rat, remember that humans are some 5-6 times more sensitive to MSG than rats."
Nika, "Monosodium Glutamate: Bad for your brain, your figure, and your health." Nikas Culinaria Blog (Feb 21, 2007). nikas-culinaria.com/2007/02/21/monosodium-glutamate-bad-for-your-brain-your-figure-and-your-health
"Lucas DR, Newhouse JP. The toxic effect of sodium-L-glutamate on the inner layers of the retina." AMA Arch Ophthalmol. 1957;58(2):193-201.
"Work by Lemkey-Johnston and Reynolds published in 1974 included an extensive review of the data on brain lesions in mice. They confirmed the phenomenon of monosodium glutamate induced neurotoxicity; described the sequence of the lesions; and emphasized the critical aspects of species variation, developmental age, route of administration, time of examination of brain material after insult, and thoroughness of tissue sampling methods. A review of monosodium glutamate induced neurotoxicity, published by Olney in 1976, mentioned species (immature mice, rats, rabbits, guinea pigs, chicks, and rhesus monkeys) demonstrating monosodium glutamate induced neurotoxicity, and efficiency of both oral and subcutaneous administration of monosodium glutamate in producing acute neuronal necrosis; discussed the nature and extent of the damage done by monosodium glutamate administration and the impact of monosodium glutamate administration to monosodium glutamate levels in both brain and blood; and discussed the similar neurotoxic effects of a variety of acidic structural analogues."
Adrienne Samuels, Ph.D, "Monosodium Glutamate and the Central Nervous System." truthinlabeling.org www.truthinlabeling.org/Proof_BrainLesions_CNS.html
Lemkey-Johnston, N, Reynolds WA. "Nature and extent of brain lesions in mice related to ingestion of monosodium glutamate: a light and electron microscope study." J Neuropath Exp Neurol. 1974;33(1):74-97.
Olney JW. "Brain damage and oral intake of certain amino acids." In: Levi G, Battistin L, Lajtha A, eds.Transport Phenomena in the Nervous System: Physiological and Pathological Aspects. New York: Plenum Press; 1976.
"Albino mice injected with monosodium glutamate developed brain lesions in the arcuate nucleus of the hypothalamus."
Edward A. Arees and Jean Mayer, "Monosodium Glutamate-Induced Brain Lesions: Electron Microscopic Examination." Science 30 October 1970: Vol. 170. no. 3957, pp. 549 - 550 DOI: 10.1126/science.170.3957.549
"High salt intake is associated with significantly increased risk of stroke and total cardiovascular disease."
Strazzullo P, D'Elia L, Kandala NB, Cappuccio FP (2011). "Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies". BMJ 339: b4567. doi:10.1136/bmj.b4567. PMID 19934192
"To examine the mechanisms underlying the sensitivity to sodium intake in a subset of patients with essential hypertension, we studied the effects of different sodium intake (10, 100, 200 mEq/day) on blood pressure, the function of the renin-angiotensin-aldosterone system, and on blood levels of catecholamines in 20 patients with essential hypertension and 10 normal subjects. Plasma norepinephrine (NE) levels were not significantly different between normal subjects or hypertensive patients while on low sodium intake. But during high sodium intake, they decreased significantly (P less than 0.05) in normal subjects (from 22 +/- 3.4 to 12 +/- 2.3 ng/dl) and in salt-resistant patients (from 17 +/- 4.5 to 13 +/- 2.4 ng/dl) but not in salt-sensitive patients (from 20 +/- 1.9 to 22 +/- 3.2 ng/dl). Furthermore, the majority of salt-sensitive patients displayed inappropriately high plasma NE in relation to their urine excretion of sodium during high sodium intake. Finally, the increments in plasma NE after 5 min of standing were significantly greater in salt-sensitive patients than they were in salt-resistant patients and normal subjects during both low or high sodium intake. These data indicate that a subset of patients with essential hypertension may have impaired suppressibility of plasma NE during high sodium intake, which suggests hyperactivity of the sympathetic nervous system in these patients. These aberrations may be responsible for the increase in MBP in the salt-sensitive patients during high sodium intake."
VM Campese, MS Romoff, D. Levitan, Y. Saglikes, RM Friedler and SG Massry, "Abnormal relationship between sodium intake and sympathetic nervous system activity in salt-sensitive patients with essential hypertension." Kidney Int. 1982 Feb;21(2):371-8.
"Americans eat about 1 1/2 teaspoons of salt daily, more than double what they need for good health and enough to increase the risk of high blood pressure, strokes and other problems. Most of that sodium doesn't come from the table salt shaker; it's hidden inside common processed foods and restaurant meals. The American Medical Association has said 150,000 lives a year could be saved by cutting in half sodium levels in processed and restaurant food."
Lauran Neergaard, "Too much salt: Report urges FDA to force rollback." Associated Press (Apr 20, 2011). abcnews.go.com/Entertainment/wireStory?id=10427996
"Dr. Martin classified refined sugar as a poison because it has been depleted of its life forces, vitamins and minerals. "What is left consists of pure, refined carbohydrates. The body cannot utilize this refined starch and carbohydrate unless the depleted proteins, vitamins and minerals are present. Nature supplies these elements in each plant in quantities sufficient to metabolize the carbohydrate in that particular plant. There is no excess for other added carbohydrates. Incomplete carbohydrate metabolism results in the formation of 'toxic metabolite' such as pyruvic acid and abnormal sugars containing five carbon atoms. Pyruvic acid accumulates in the brain and nervous system and the abnormal sugars in the red blood cells."
William Duffy, "Refined Sugar - The Sweetest poison of All..." Sugar Blues, Grand Central Publishing (March 17, 1986). ISBN-10: 0446343129
"Processed sugar has many harmful effects throughout the body and can cause major imbalances in the organ systems. You could say that sugar tends to throw off the homeostatic balance of the whole body by increasing the production of adrenaline by many times. In essence, sugar stimulates the nervous system by inducing a flight or fight response."
Anandmurti Gurumaa "Sugar - The Sweet Assassin!" Gurumaa.com www.gurumaa.com/content/sugar-the-sweet-assassin.html
"It is well known that too much sugar causes tooth decay, but might it also cause "brain decay?" Recent research suggests that it just might. With the growing epidemic of obesity in the US, the number of people with diabetes is also increasing. Diabetes is due to the body's inability to maintain a constant level of sugar in the blood, as it should. Over time, this results in problems in many parts of the body, including the kidneys, heart, muscles, nerves and brain."
Janet Jankowiak, MD, "Too much sugar may cause 'brain decay.'" Neurology 2004;63:E9-E10
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