Restless Legs Remedy (RLS): The Nervous System

inflammation is the cause of restless legs syndrome

alcohol

"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

aspartame

"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

"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

gluten

"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

salt

"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

sugar

"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