Science > Diet and Health
The Magnesium Miracle
Laura:
I'd like to get some of this material here in the forum but can't do it right now. Can anyone else do it?
http://articles.a1supplements.com/supplements/vitamins-and-minerals/transdermal-magnesium-for-recovery-&-exercise/
http://george-eby-research.com/html/depression-anxiety.html
http://george-eby-research.com/html/mag-list.html
http://www.thewayup.com/newsletters/081501.htm
http://www.mgwater.com/
http://www.seekwellness.com/nutrition/celiac_disease.htm
http://www.mgwater.com/dur30.shtml
http://www.teachhealth.com/#stressscale
http://mgwater.com/listc.shtml#fm
Belibaste:
_http://articles.a1supplements.com/supplements/vitamins-and-minerals/transdermal-magnesium-for-recovery-&-exercise/
--- Quote ---Transdermal magnesium is a hard-core exercise recovery tool. Magnesium is a mineral used in and by, over 300 enzymes in the body. Magnesium has great benefit for bodybuilders and athletes. Here's how:
Atp And Phosphocreatine
ATP, which we all know is the molecular form of energy for the body, is only usable as an ATP/magnesium complex. Magnesium provides stability to ATP. Magnesium is also critical for the proper function of creatine kinase, an important enzyme that converts creatine into its storage form, phosphocreatine (also called creatine phosphate) and helps convert ADP( left over in the muscle after ATP is used for energy) and the stored phosphocreatine back into ATP for muscle contraction.
Since ATP must be bound to the magnesium to be available for use, without this ATP/Mg complex we would not be able to make proteins, RNA or DNA, nor would we be able to activate enzymes, transport minerals into and out of the cells, or phosphorylate proteins. We would not be able to do anything and we would die.
Protein Synthesis
Magnesium is necessary for protein synthesis at the ribosomal level. The ribosomes are the cellular organelles where proteins are synthesized. Magnesium "activates" the amino acids involved and allows the mRNA to attach to the ribosomes. Magnesium is also found in the nucleus of the cell and is essential for the stability of the nucleic acids RNA and DNA. If DNA and RNA structure do not remain stable you may have mutations in the codes and produce incorrect peptides are none at all during protein synthesis. Energy for the production of proteins must come from ATP as well. Without magnesium available in many areas of the cell, protein synthesis cannot occur.
Insulin Sensitivity
Many studies show a correlation between magnesium and insulin sensitivity. Low levels are associated with insulin insensitivity, type 2 diabetes, and syndrome X, although the exact mechanisms are still not clear. More studies are needed to clarify the mechanisms involved, but the relationship is there. Researchers strongly believe that increased magnesium levels, especially via trans-dermal methods, will increase insulin sensitivity.
Cellular Hydration
One should always maintain the correct ratio of magnesium and calcium. But that is very dependent on a number of factors that increase or decrease magnesium and calcium absorption and retention. Magnesium and Potassium are found in the intracellular fluid while calcium and sodium are found outside the cell. Normally you would want to consume a 2:1 ratio of calcium to magnesium, but due to the variables that affect their absorption and retention and the levels present in foods, it might be better to shoot for a ratio of 1:1.
Elevated magnesium and potassium levels inside the cell increase cellular hydration. Cellular hydration can be improved by many mechanisms and can help increase muscle torque as well as positively influence protein synthesis.
Muscle Tightness And Spasms
Magnesium must be present in the synaptic gap between neurons to control the rate of neuronal firing. Decreased magnesium will decrease the neural threshold making them fire to readily, even with a low stimulus. This leads to hyper excitability and hypersensitivity, often leading to anxiety. Epileptics often have a severe decrease of magnesium in the synapses of the CNS.
Vaso-Dilation And The Pump
Magnesium is thought to behave as a natural calcium channel blocker at the cellular level, thereby relaxing vascular tissue and increasing vasodilation independent of nitric oxide. Magnesium chloride can be used as a concentrated solution called magnesium oil. It is not really an oil, but due to the highly hygroscopic (water absorbing) nature of magnesium chloride, it has an oily feel at high concentrations. This magnesium oil can be massaged into the muscles to be worked just prior to exercise.
Many people have found that it has a local affect facilitating the pump and all the benefits that the pump provides. Some hard-core athletes have found a synergistic effect with NO boosters. The magnesium chloride will also have systemic effects as it is absorbed into the bloodstream. Some people may also add a small amount (one half to 1 teaspoon) to their workout drink or to their pre-workout stack.
MUSCLEFighting Pain
There are many mechanisms where transdermal magnesium can affect the sensation of pain, both direct and indirect. One direct method involves magnesium acting as a noncompetitive antagonist of the in NMDA (N-methyl-Daspartate) receptor, which is involved in the transmission of pain. This mechanism also gives magnesium anti-depressive and anxiolytic effects. There are numerous indirect ways that transdermal magnesium can affect pain as well.
Dhea,. Cortisol And Lactate
Dr. Norman Shealy, M.D. Ph.D. discovered that trans-dermal magnesium chloride increases the body's natural production of DHEA, and its metabolites, while oral supplementation and direct injections do not. Increased DHEA levels often lead to elevated testosterone levels. Transdermal magnesium has been linked to decreased plasma cortisol levels, but the exact mechanisms are unclear.
Elevated DHEA and decreased cortisol levels can have a number of positive effects in the body, especially as we age. According to James Thor, national director of Extreme Sports Medicine, increased amounts of magnesium are lost when a person is under stress, including exercise.
Transdermally absorbed magnesium promotes the release of lactic acid from muscle tissue. Dr. Mark Sircus, one of the leading experts on magnesium, says that transdermal magnesium therapy enhances recovery from athletic activity and injuries. We clearly need more studies to understand the mechanisms involved.
Recovery And Reduced Exercise Soreness
There are several theories addressing improved recovery and reduced muscle soreness from transdermal magnesium therapy. One theory for a proposed mechanism states that the decrease in plasma magnesium during exercise is due to a transient shift of magnesium from extracellular fluid to skeletal muscle tissue.
Following exercise, subjects demonstrated significantly increased levels of magnesium in skeletal muscle and a decrease of magnesium in plasma, erythrocytes and other tissue. Transdermal magnesium quickly replenished plasma magnesium preventing the subsequent shift back out skeletal muscle to replenish the plasma levels, thereby maintaining increased hydration and increase cellular volumization.
Maintaining cellular magnesium levels helps facilitate rapid restoration of the phosphocreatine and ATP levels, and the production of proteins by ribosomes allowing for improved recovery and tissue growth.
High intensity anaerobic exercise increases magnesium loss by inducing a transient increase in urinary excretion of magnesium due to metabolic acidosis and other mechanisms. Magnesium is lost in sweat as well. Only trans-dermal magnesium therapy (or direct injections), done within 12 to 24 hours (by soaking in a hot bathtub of magnesium chloride, with added transdermal antioxidants and anti-inflammatories) right before bedtime works best! This also promotes deep restful sleep.
Magnesium is involved in many other systems in the body and can help many degenerative painful conditions such as fibromyalgia, migraines, diabetes, cardio vascular problems, among other things.
Until recently most athletes, coaches and nutritionists thought that the best forms of magnesium supplementation were those chelated to an amino acid or Krebs cycle intermediate and absorbed through the G.I. tract.
Many new studies show that magnesium can be easily absorbed transdermally and rapidly replenish magnesium levels, quickly correcting diminished plasma and tissue levels. This allows for more rapid recovery after strenuous aerobic and anaerobic exercise.
Transdermal magnesium chloride therapy can maintain cardio respiratory efficiency, increase endurance performance, decrease oxygen consumption, increase work capacity, increase strength, energy, and muscle mass, decrease lactic acid and post exercise muscle soreness, increase insulin sensitivity and many other things!
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Belibaste:
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--- Quote ---Our topic is: MAGNIFICENT MAGNESIUM (Mg)
And you will soon know why. It is a supplement commonly prescribed by me because I often see deficiency conditions.
If you first like narrative explanations of a subject, you may want to skip the next section & return to it later. But if you want know whether you have low magnesium you may want to begin with this:
MAGNESIUM DEFICIENCY QUESTIONNAIRE
Circle each yes answer which is given a numerical value.
When you finish, total your score.
--With 30-50, you likely have low magnesium.
--Over 50 & you most certainly have low magnesium.
YES QUESTION...
2 Under excessive emotional stress
3 Irritable, or easily provoked to anger
2 Restless, or hyperactive
4 Easily startled by sounds or lights
2 Difficulty sleeping
3 Chronic headaches or migraines
2 Convulsions
3 Fine tremor or shakiness in your hands
3 Fine, barely noticeable muscle twitching around your eyes, facial muscles, or other muscles of your body
3 Muscle cramps
3 Muscle spasms in hands or feet
4 Gag or choke from spasms in your esophagus(food tube)
3 Have asthma or wheezing
2 Suffer from emphysema, chronic bronchitis, or shortness breath
5 Have osteoporosis
3 Have you ever had a kidney stone
2 Suffer from chronic kidney disease
4 Have diabetes
3 Have an overactive thyroid, or parathyroid gland
3 Have high blood pressure
4 Have mitral valve prolapse (“floppy heart valve”)
3 Have very fast heart beats, irregular heart beats, or arrhythmia
3 Take Digitalis (Digoxin)
5 Take any kind of diuretic
5 Recent radiation therapy or exposure
4 Have more than 7 alcohol drinks weekly
3 Have you ever had a drinking problem?
2 Have more than 3 servings of caffeine daily
2 Eat sugar containing food daily
2 Crave carbohydrates &/or chocolate
2 Crave salt
2 Eat a high processed food/ junk food diet
2 Eat a diet low in green, leafy vegetables, seeds, & fresh fruit
2 Eat a low protein diet
2 Pass undigested food or fat in your stools
3 Suffer from chronic intestinal disease, ulcerative colitis, Crohn’s, irritable bowel syndrome
3 Frequent diarrhea or constipation
3 Suffer from PMS or menstrual cramps
2 Pregnant or recently pregnant
4 In previous pregnancy had high blood pressure or pre-eclampsia
2 Chronic fatigue
2 Muscle weakness
2 Cold hands &/or feet
2 Numbness in face, hands, or feet
2 Persistent tingling in body
2 Chronic lack of interest, indifference, or apathy
2 Poor memory
2 Loss of concentration
3 Anxiety
2 Chronic depression for no apparent reason
2 Feelings of disorientation as to time or place
2 Feel your personality is stiff or mechanical
2 Hallucinations
2 Feel that people are trying to harm or persecute you
2 Face pale, puffy, or lacking in color
2 Loss of considerable sexual energy or vitality
2 Been told by your Dr that your blood calcium is low
3 Been told by your Dr that your blood potassium is low
2 Take Calcium supplements regularly without magnesium
2 Take iron or zinc supplements regularly without magnesium
2 Know chronic exposure to fluorides
3 Frequently use antibiotics, steroids, oral contraceptives, Indomethacin, Cisplatin, Amphotericin B, Cholestyramine, synthetic estrogens
<--- TOTAL ...
Subtract 15 from your score if you daily supplement at least 600 mg of magnesium.
WHAT ARE THE FUNCTIONS OF MAGNESIUM?
You can infer much of this by the questionnaire above, but let’s go into more detail.
The most known functions are the following:
1- MAINTAINS THE HEART MUSCLE & BLOOD VESSELS
Magnesium deficiency is associated with an increased incidence of atherosclerosis, high blood pressure, heart attacks, & strokes.
Interestingly, Mg mimics many of the activities associated with a variety of cardiovascular medications. It thins blood similarly to Coumadin. It blocks Calcium uptake similar to Calcium Channel Blocker. It acts as a potent vasodilator by relaxing blood vessels as do the Ace Inhibitors, such as Vasotec. It inhibits platelet aggregation as does aspirin. Magnesium maintains the balance of the clotting mechanisms. It also increases the oxygen in the heart by improving heart muscle contractility.
Fifteen percent of the population have what is called mitral valve prolapse ( a floppy heart valve). This is associated with an increased tendency to anxiety, an irregular or fast heart rate, palpitations, & in general a hyper-irritable heart muscle. Studies have shown 62% of these people are Mg deficient & symptoms can be prevented by Mg administration.
Unfortunately, some widely used cardiac medications such as digitalis & the diuretics increase urinary excretion of Mg & contribute to the deficiency states. Thus Mg is an important anti-arrhthymic agent in treating digitalis toxicity. It also helps in treating atrial tachycardia & ventricular tachycardia when used intravenously in these emergency conditions.
2- MAGNESIUM IS INTEGRAL TO BONE STRUCTURE
Sixty percent of the body’s Mg is in the bones. With osteoporosis, there is significant skeletal Mg depletion.
A common mistake which distresses me the is the recommendation by many Drs & the belief by many people that one need only supplement calcium to prevent or to treat osteoporosis. Not only is magnesium essential for bone formation, but calcium supplementation without magnesium will contribute to metabolic imbalances & bone loss.!!
Magnesium assists in the metabolism & uptake of calcium. Magnesium depletion promotes abnormal crystallization of calcium in soft tissues, such as kidney stones, gall stones, atheroslerosis, microcalcifications in the breast & other soft tissue. Magnesium can help dissolve calcium phosphate kidney stones, & may prevent the formation of calcium oxalate kidney stones. Natural estrogen helps move magnesium into the bones, while certain synthetic estrogens deplete bodily magnesium.
The parathyroid gland is adjacent to the thyroid & has a major function of regulating calcium metabolism. Magnesium synergizes the secretion of parathyroid hormone. Also a magnesium deficiency decreases the ability of the body to respond to parathyroid hormone. Magnesium deficiency associated with low blood calcium levels may create symptoms of parathyroid hormone deficiency.
This low calcium level will not respond to parathyroid hormone, to Vitamin D, or to calcium supplementation, but is only corrected with magnesium therapy.
Both Mg deficiency & Mg excess are detrimental to bones & extreme Mg excess contributes to a rare softness & deformity of the bones called osteomalacia, which is far less common than osteoporosis.
3- MAGNESIUM MAINTAINS NORMAL NERVE, BRAIN, & MUSCLE FUNCTION.
While 60% of the Mg is in the bones, the rest is primarily in the cells where it functions to regulate the transmission of impulses between brain cells, & from nerves to muscles & organs. It also maintains normal muscle function & contractility.
Since Mg regulates the irritability or sensitivity of the nerves & muscles, a deficiency leads to neuromuscular hyperexcitability which can be associated with muscle cramps, twitches, & tremors, tension, tightness, or soreness. It is also associated with various spasms, such as the bronchospasm of asthma, esophageal spasm ( a lump in the throat with difficulty swallowing), the vascular spasm of migraines some forms of hypertension, chest pain & other chronic pain syndromes, the urinary spasms with some forms of urinary problems & bedwetting, the spasms of premature labor & menstrual cramps, & of course the spasms of seizures. The excitability can also be associated with an easy startle response, noise & light sensitivity, numbness & tingling & strange body sensations.
Some of the most dramatic effects of Mg deficiency may occur in the central nervous system such as with the DT’s (delirium tremens) of alcoholism, general anxiety & irritability, nervousness, confusion, tantrums, insomnia, depression, The symptoms can even progress to the point of psychotic proportions. Studies have shown lower Mg in the blood of those with active schizophrenia than in those in remission.
4- MAGNESIUM IS A CO-FACTOR TO ACTIVATE & REGULATE OVER 300 ENZYMES SYSTEMS IN THE BODY RELATING TO LIFE SUPPORTING BIOCHEMICAL REACTIONS
It is integrally involved in the production of energy in the cells via a biochemical reaction called the Kreb’s Cycle. It participates in the formation of the energy reserve of the muscles ( called Cyclic AMP) Many of these functions take place in combination with pyridoxal 5 phosphate (the co-enzyme form of vitamin B6). Thus deficiency can be associated with fatigue & weakness.
Through its’ co-factor functions, Mg participates in the synthesis of protein, & genetic material such as DNA. It is a binding agent for the genetic material called messenger RNA. Thus a deficiency can lead to poor growth or genetic defects. A Study in the Journal Of The American Medical Association reported a70% lower incidence of mental retardation, & a 90% lower incidence of cerebral palsy in children of mothers supplemented with magnesium during pregnancy.
Magnesium works with vitamin C to build collagen. It assists with temperature regulation. Magnesium also supports the function of the pancreas.
5- MAGNESIUM IS CRITICAL IN GLUCOSE METABOLISM, TOGETHER WITH VITAMIN B1
It plays a role in the breakdown & digestion of sugars & fatty acids.
It helps to maintain normal levels of blood fats. Magnesium deficiency is especially associated with increased triglycerides & the insulin resistance known as Syndrome X. Insulin resistance can be reduced by taking Mg.
6- MAGNESIUM ACTS AS A BUFFERING AGENT TO REGULATE THE ACID/ALKALINE STATE OF THE BODY.
it regulates intracellular fluid & supports the cell membrane, including permeability.
7- MAGNESIUM IS A CHELATING & DETOXIFYING AGENT & WORKS TO MAINTAIN PROPER LIVER FUNCTION.
WHAT DEPLETES OR INTERFERES WITH MAGNESIUM?
High stress contributes to Mg deficiency which exacerbates anxiety, fear weakness & physical complaints, leading to more stress & a vicious cycle. The decreased oxygen in the tissues related to stress , tissue injury, & an acid condition cause Mg to move out of the cells into the blood plasma leading to intracellular deficiency.
Excess sugar, caffeine, carbohydrates, low dietary protein, prolonged fasting, general malnutrition, chronic diarrhea, vomiting, excess zinc, vitamin D & calcium contribute to Mg deficiency. Aluminum, fluoride, & phosphate interfere with absorption.
Excess alcohol deserves its’ own paragraph as it is a common cause of low Mg. Multiple mechanisms are at play. Often those who drink excessively eat less than optimal diets. Then the alcohol causes increased urinary loss of Mg & increased gastrointestinal losses of Mg. The acidotic & alkalotic shifting states which accompany high alcohol intake further deplete the Mg stores. Many of the physical & mental symptoms of alcoholism are related to depleted Mg.
Those with diabetes, chronic gastrointestinal disorders, an overactive thyroid or parathyroid gland, or in the last 6 months of pregnancy are particularly prone to low Mg. Radiation causes large losses of Mg & Mg has a radiation protective action. Since high dose Mg antagonizes thyroid, I use high doses as part of my natural for hyperthyroidism & avoid high doses when there is a problem with low thyroid function.
Diuretics are a major villain in both Mg & potassium depletion, causing loss of both in the urine.
Potassium is the most abundant intracellular mineral with Mg ranking second. Magnesium assists in the cellular uptake of potassium so a Mg deficiency can lead to decreased potassium in the cells. Forty two percent of those with low potassium also have low Mg & will not respond to the administration of potassium until Mg is added. Unfortunately, normal serum levels of Mg & potassium do not necessarily indicate normal intracellular levels.
Medium chain triglycerides & the milk sugar, lactose enhance Mg absorption.
Magnesium supplementation is indicated for those with:
* Anxiety/nervousness/panic
* Insomnia
* Depression
* Emotional overreactivity Irritability/anger
* Hyperactivity/restlessness/squirming
* Short attention span & learning disabilities
* Hypersensitivity to sound & pain
* High stress Fatigue Muscle pain, spasms & tension
* Tics & tremors
* Asthma
* High blood pressure
* Migraine or other headaches
* High sugar, alcohol or caffeine intake
* Constipation
* Rapid pulse
* Heart irregularities
* Mitral valve prolapse
* Those with low potassium (potassium supplemental therapy may be ineffective without concurrent magnesium)
SYMPTOMS OF MAGNESIUM DEFICIENCY BESIDES THOSE INFERRED FROM THE ABOVE LIST:
* Excessive perspiration
* Numbness & tingling
* Poor muscle coordination
* Increased startle response
* Decreased concentration & memory
* Confusion & disorientation
* Appetite loss
* Organic brain syndrome
* Kidney stones
HOW DO YOU MEASURE MAGNESIUM?
I am not thrilled with any of the available methods. Probably for blood tests, the Red Blood Cell Mg is the best. Urinary loss can be measured by a 24 hour urinary Mg level, but that doesn’t say much about what is I the cells. Though I may do the testing I prefer to make the decision based upon diet, symptoms, & medical history which suffices.
CAN YOU GET TOO MUCH MAGNESIUM?
Yes magnesium toxicity is possible, but not common & more likely to be associated with severe medical conditions such as liver or kidney failure. If one does not supplement beyond recommended dose should be no problem, but should not supplement if have the above conditions. Conversely mild kidney disorders contribute to Mg deficiency as one of the kidneys functions is to conserve Mg by reabsorbing it when needed rather than excreting it in the urine. With mild dysfunction there may be excess Mg loss in the urine & sometimes subsequent severe Mg deficiency symptoms.
The symptoms of Mg toxicity are a drop in blood pressure, skin flushing, nausea, vomiting, slowed heart beat & breathing, even leading to a coma or death in severe instances. The best treatment for this is intravenous Calcium which will antagonize the Mg & decrease the toxic effects.
WHAT FOODS ARE HIGHEST IN MAGNESIUM?
Listed in order of priority are re Mg content per 3 1/2 ounces: kelp, wheat bran, wheat germ, almonds, cashews, blackstrap molasses, brewer’s yeast, buckwheat, brazil nuts, dulse, filberts, peanuts, millet, wheat grain, pecans, walnuts, rye, tofu, beet greens, dry coconut, cooked soybeans, spinach, brown rice, dried figs, swiss chard, dried apricots, dates, collard leaves, shrimp, sweet corn, avocado, cheddar cheese, parsley, prunes, sunflower seeds, cooked beans, barley, dandelion greens, garlic, raisins, fresh green peas, potato with skin, crab, banana, sweet poet, blackberries, beets broccoli, cauliflower, carrots, celery, beef, asparagus.
WHAT ARE THE USUAL SUPPLEMENTAL DOSES?
Anywhere from 400 -2000 mg daily total in 2-3 divided doses depending upon symptoms & response. Magnesium is also quite laxative & this effect sometimes makes it difficult to take a high enough dose , so may do better with a time release form
Feel free to forward to anyone you feel would be interested.
Please tell me what you want to have in future newsletters.
Let us go about unselfishly scattering seeds of love, joy, peace, harmony, & healing.
Until then....
"Fear not to look upon the lovely truth in you."
Priscilla Slagle M.D.
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Belibaste:
_http://www.mgwater.com/dur30.shtml
--- Quote ---Mineral and Metal Neurotoxicology, ed. M. Yasui, M .J. Strong, K. Ota, & M. A. Verity, CRC Press: Boca Raton, New York, London, Tokyo, 1997
Chapter 20
Mechanisms of Action on the Nervous System in Magnesium Deficiency and Dementia
Jean Durlach and Pierre Bac
CONTENTS
20.1 Introduction
20.2 Mechanisms of Action of Magnesium Deficiency on the Nervous System
20.2.1 Electrophysiological Data
20.2.2 Biochemical Data
20.2.2.1 Factors Inducing NHE
20.2.2.2 NHE Compensatory Factors
20.2.3 Neuromuscular and Psychiatric Data
20.3 Magnesium Depletion and Dementias
20.3.1 Experimental Models of Mg Depletions
20.3.1.1 Neurological Degeneration Due to Al Load and Low Mg Intake
20.3.1.2 Mg Depletion Due to Kainic Acid Plus Mg Deficiency
20.3.2 Possible Links Between Dementias and Mg Depletion
20.4 Therapeutic Implications
20.4.1 Treatment of Magnesium Deficiency
20.4.2 Magnesium Therapy and Dementias
20.5 Conclusion
References
20.1 INTRODUCTION
Whatever the age, nervous forms of magnesium deficit represent the most commonly seen form in clinical practice.1 First of all, it seems very important to discriminate between the two types of magnesium deficit: magnesium deficiency and magnesium depletion. In the case of magnesium deficiency, the disorder corresponds to an insufficient magnesium intake: it merely requires oral physiological magnesium supplementation. In the case of magnesium depletion the disorder which induces magnesium deficit is related to a dysregulation of the control mechanisms of magnesium metabolism, either failure of the mechanisms which insure magnesium homeostasis or intervention of endogenous or iatrogenic perturbating factors of the magnesium status. Magnesium depletion requires more or less specific correction of its causal dysregulation.1 It should not be permitted today to extrapolate from physiological data observed in overt acute magnesium deficiency to physiological consequences of chronic magnesium deficiency. Although acute and chronic magnesium deficiencies are specifically reversible through oral magnesium supplementation with physiological doses, the experimental and clinical symptoms may differ. The typical pattern of chronic magnesium deficiency is latent whereas overt signs are observed in acute magnesium deficiency. The discrepancy between the patent and latent nervous forms of magnesium deficiency suggests that in the latent form there are compensatory factors which antagonize the nervous hyperexcitability observed in the overt form.
The aim of this review is to study:
1. The mechanisms of action of magnesium deficiency on the nervous system as demonstrated by
* Electrophysiological data testifying to diffuse nervous hyperexcitability (NHE)
* Biochemical data showing the mechanisms which may induce overt and latent NHE
* Neuromuscular and neurotic psychiatric data
2. The links between some types of magnesium depletions and dementias.
3. Therapeutical implications.
20.2 MECHANISMS OF ACTION OF MAGNESIUM DEFICIENCY ON THE NERVOUS SYSTEM
We will analyze the mechanisms of action of magnesium deficiency on the nervous system successively through electrophysiological, biochemical, and clinical data.
20.2.1 Electrophysiological Data
Experimental and clinical electrophysiological procedures allow us to neurophysiologically examine the effects of magnesium deficiency on the cortical, subcortical, and peripheral levels of the nervous system.
Standard electroencephalography (EEG) in humans exhibits "diffuse irritative tracings" without focal lesions or paroxysmal discharges. The recordings contain spikes, a pointed appearance of alpha and/or theta waves, which is facilitated more often by hyperventilation than by intermittent photic stimulation. The polygraphic study of afternoon sleep may complete the data of standard EEG: brevity of the time required to fall asleep, superficial character of the sleep, frequency of awakening, hypnoagnosia.1 The EEG in the magnesium-deficient rat (electrocorticography) allows us to make observations similar to those found in humans. Mg deficiency induces electrocorticographic alterations in the rat analogous with those seen in Mg deficiency in humans. Sleep quality analysis shows particularly similar alterations of the hypnograms.1,2
Electronystagmography shows functional impairment at the level of the second vestibulo-ocular motoneuron which becomes apparent mainly as the variable association of "paroxysmal ocular states", i.e., a sequence of repetitive ocular movements with vertical predominance over a period averaging 20 s, irregularity of evoked nystagmic responses, excessive bilateral labyrinthine reflex activity, oblique or rotary nystagmus, prolonged latency during pendular tests, and differences between pendular nystagmic responses with the eyes open and closed. Alterations in optokinetic tests confirm the importance of subcortical functional disturbances.1
Moreover, behavioral changes in the Mg-deficient rats are due to hyperexcitability which first arises in deeper structures -- in the whole limbic system and in the hippocampus, particularly -- and which secondarily becomes generalized by projecting on the neocortices. 3
Electromyography (EMG) shows peripheral NHE. A series of autorhythmic events is observed (singlets, multiplets, complex tonicoclonic activity) beating for more than 2 min during one (or several) of the three facilitations tests: tourniquet-induced ischemia lasting 10 min, a postischemic phase measured 10 min after removal of the tourniquet, and finally hyperventilation for a maximum of 5 min. A repetitive EMG, whatever the intensity, constitutes the principal neurophysiological mark of NHE due to Mg deficiency.1
Skin conductance reflex might appear attractive as an investigation tool of diffuse NHE due to Mg deficiency,4 but this procedure still requires further validation.
These neurophysiological procedures, mainly EEG, ENG, and EMG, allow us to examine the effects of Mg deficiency on the nervous system: Mg deficiency causes diffuse neuromuscular hyperexcitability operating from the center to the periphery. NHE affects the nervous system as a whole, but comparing the impairments in its various sectors is less important than determining the intra- or extracellular origin of NHE.1,5
The long duration of experimental Mg deficiency required to produce manifestations of NHE has led to the hypothesis of concurrent reduction of intracellular Mg which represents "the bulk" of the Mg pool. In Mg deficiency induced in young rats, there is a direct correlation between the severity of hyperexcitability and the decrease in the brain Mg level. Clinical evidence includes patients with Mg deficiency but without abnormalities of extracellular Mg, hypo- or normomagnesemia in the same patient at different times, and a reduction of the mean erythrocyte or lymphocyte Mg contents, two forms of intracellular Mg. This demonstrates the possible role of intracellular Mg in NHE due to Mg deficiency.
This NHE is not always accompanied by low levels of cerebral Mg: these are only observed in severe Mg deficiency in young rats. Usually, no changes have been found in brain Mg concentrations during the course of Mg deficiency in adult rats.5-7 It should be stressed that in Mg deficiency there exist complex mechanisms to maintain normal, and even increased, Mg concentration in the tissue which are of vital importance in brain, liver, and brown fat.5-8 With reduced plasma Mg levels, an extracellular origin of NHE due to Mg deficiency may intervene, but plasma normomagnesemia has also been observed with some Mg deficiencies.
An analysis of the relationship between extra- and intracellular concentrations, clinical findings, and electronystagmographic tracings have shown that more symptoms of NHE occur when Mg deficiency predominates in one of the intra- or extracellular compartments rather than when it affects both equally.1,5 This electroclinical observation highlights the importance of Mg distribution disturbances in the physiopathological consequences of Mg deficiency on the nervous system.
20.2.2 Biochemical Data
During Mg deficiency, a complex neuroendocrinometabolic and renal regulation may intervene for compensating its systemic effects. The role of the blood-brain barrier which attenuates the effect of the systemic regulating factors of Mg status and of the humoral consequences of decompensated Mg deficiency in the nervous system must not be overlooked. The biochemical factors capable of increasing nervous excitability are essentially local.1,5
20.2.2.1 Factors Inducing NHE
Extrapolating from data observed in vitro, in situ, or in other pharmacological manipulations to the physiological basis of an Mg deficiency simply due to insufficient intake1 remains a methodological error.
Pharmacological Mg excess causes some systemic reactions which are not the opposite of physiological effects of Mg. For example pharmacological load of Mg increases release of calcitonin and nitric oxide (NO).9,10 In contrast, physiological Mg supplementation, far from acting similarly, reduces high levels of calcitonin1 (as well as of calcitonin gene-related peptide11and of NO12 released in the case of Mg deficiency.
The great stability of brain Mg during Mg deficiency particularly disagrees with the very notion of extrapolating from in vitro or in situ, extra- or intracellular Mg data1,5 to in vivo physiological data. This leads to suggesting an updated scheme of the factors which cause NHE5: Mg deficiency would induce a diffuse NHE through a neuronal depolarization which derives from the sum of its direct cellular effects in the neural cells and from several mediated reactions.5
20.2.2.1.1 Direct Cellular Effects
Mg deficiency results in three basic effects: disturbances in cellular Ca distribution, decreased second messenger nucleotidic ratio,5 and increased susceptibility to peroxydation.12-14 Through membranous and postmembranous alterations, Mg deficiency brings about a cellular Ca load with subcellular distribution modifications.5 Mg deficiency reduces 3',5'-cyclic adenosine monophosphate (cAMP) concentration and increases 3',5'-cyclic guanosine monophosphate (cGMP) concentration, perhaps through inhibition of adenylate cyclase and activation of guanylate cyclase.5 Mg-deficient animals show an increased susceptibility to in vivo oxydative stress and the tissues of these animals are more susceptible to in vitro peroxydation, affecting lipid particularly.12-14 Protein oxydation in Mg-deficient rat brains occurs early. A significant increase of protein carbonyls is observed within 2 to 3 weeks of a Mg-deficient diet. These changes take place prior to any detectable tissue damage, dysfunction, or changes in cellular glutathione.15
Mg deficiency may increase formation of free radicals directly, but also indirectly through free-radical-triggered mechanisms.12 ,15
20.2.2.1.2 Mediated Local Effects
NHE due to Mg deficit is also linked to modifications in the turnover of various types of neurotransmitters: monoamines, amino acids, but also nitric oxide, neuropeptides, and cytokines.
Neurotransmitters - NHE due to Mg deficiency mainly depends on modifications in the turnover of several neuromediators and neuromodulators. They associate an increased turnover of the monoamines: serotonin (5HT), acetylcholine, catecholamines (dopamine and noradrenaline, mainly), and of excitatory amino acids (aspartic and glutamic acids, mainly) with a decreased turnover of inhibitory amino acids (γ-amino butyric acid and taurine, mainly).5 As a great number of in vitro studies on Mg and NMDA16 receptors have suggested that the latter had predominant and almost exclusive importance, their in vivo role has often been overestimated.2 If hyper NMDA receptivity enters into the mechanisms of NHE due to Mg deficiency as confirmed in vivo,17 a hyperreceptivity concerning other non-NMDA receptors of excitatory amino acids may also intervene.18 The genuine complexity of biology must not be disregarded just because the present trend is towards focusing on NMDA receptors at the expense of many other receptors.
Nitric oxide, peptides, and cytokines - An increased production of nitric oxide and of various inflammatory peptides - such as substance P, CGRP, and VIP - is observed in Mg-deficient rats. All these substances might directly intervene as neurotransmitters in the physiopathology of NHE due to Mg deficiency; but NO could also mediate an increase in cGMP whereas inflammatory neuropeptides might stimulate production of inflammatory cytokines and of free radicals.12-14 During the progression of Mg deficiency in a rodent model, dramatic increases of inflammatory cytokines were observed: interleukins 1 and 6 (IL1, IL6) and tumor necrosis factor (α(TNFα ). Increase of these various cytokines was neither concomitant nor constant, according to species and strains.12-14,19 So far, their importance in the physiopathology of NHE has not been clearly defined but we have observed with P. Maurois that audiogenic seizures in Mg-deficient mice might be correlated with possible TNFα release. According to the strains of mice, there is a parallelism between production of TNFα. induced by bacterial lipopolysaccharides and NHE. However, coexistence does not mean causality and further research focusing on the effects of specific TNFα antibody on the production of audiogenic seizures will be necessary. Opioid peptide activity could be reduced since, in the complex mechanisms of opioid action, Mg at the physiological level may be most often an agonist of δ, µ, and κ opioid receptors.5,20
The sum of these direct and mediated local factors may bring about overt NHE due to Mg deficiency. Frequency of latent forms of this NHE postulates the existence of local compensatory factors which may control NHE.5
20.2.2.2 NHE Compensatory Factors
The local compensatory factors instrumental in the latency of NHE due to Mg deficiency may also be direct and mediated.
20.2.2.2.1 Direct Compensatory Factors
Since Mg can more or less be replaced by a natural polyamine in many biochemical reactions, an "Mg-substitutive" increase in polyamines might decrease the direct cellular effects of Mg deficiency. This "Mg-vicariant" increase in polyamines may be a factor regulating the alterations of protein synthesis and particularly that of Ca2+ and Mg2+ binding proteins.5 Increased formation of free radicals may be antagonized by the cell antioxidant system: enzymes such as superoxide dismutase and glutathione peroxidase, antioxidant vitamins such as E, A, and C, selenium, and sulfur compounds such as glutathione and taurine.8, 14-18
20.2.2.2.2 Mediated Compensatory Factors
Some types of adenylate cyclase-receptors may contribute to a compensatory increase in the cAMP/cGMP ratio.5 The main compensatory factors are mediated by the increase of several physiological neuroprotective agents: inhibitory aminoacids1,5,10,21-23 and perhaps melatonin.24 The particular efficiency of N-acetyl-amino compounds such as Mg N-acetyl-amino taurinate and melatonin might depend on a decreased activity of the Mg-dependent N-acetyl-amino transferase in the nervous system (EC 2.3.1.5.).10,21-24 The main mediated compensatory factor is taurine (TA) with the help of its peptidic congener: γ-L-glutamyl taurine (GTA).5
When these direct and mediated compensatory factors are effective, NHE remains latent. It is patent when compensatory factors are insufficient. Their failure may depend on several reasons:
1 . Sufficient amounts of amino acids - precursors of neuromediators and neuromodulators - must be available in the nervous system. It is important to have qualitatively and quantitatively a sufficient protein intake and sufficient amino acid transport across the blood-brain barrier, eventually facilitated by a homeostatic reactive hyperinsulinism. Both may be lacking.
2. If a compensatory high release of cAMP counteracts the decrease of cAMP/cGMP ratio, it inhibits the TA biosynthesis through the reduction of cystine dioxygenase activity.
3. Efficient brain metabolism and, particularly enzymatic activity, is necessary. However, Mg deficiency frequently alters protein biosynthesis and induces enzymatic hypoactivity.
4. Finally, the number of excitatory factors appears larger than that of compensatory factors during Mg deficiency in the nervous system.5
However, one should not overlook the schematic nature of this general pattern which covers both a homogeneous explanation of the diffuse character of the symptomatic NHE due to Mg deficiency and the possibility of the Mg deficient latent form.
Because of the heterogenicity of NHE due to Mg deficiency, a special study of each parameter of this scheme in each brain area is necessary to obtain a better understanding of these complex phenomena.5
20.2.3 Neuromuscular and Psychiatric Data
NHE due to Mg deficiency results in a nonspecific clinical pattern which associates peripheral and autonomic neuromuscular signs and central or rather psychiatric symptoms. Neuromuscular disturbances include acroparesthesias, muscle fasciculations, cramps, and myalgias occurring more frequently than tetanoid or tetanic attacks, and various autonomic functional complaints such as cardiac palpitations, precordial pain, extrasystolae, Raynaud's syndrome, hepatobiliary dyskinesia, gastrointestinal cramps and spasms, and asthma-like dyspnea.
Psychiatric symptoms consist of anxiety, hyperemotionality, asthenia, headache, insomnia, dizziness, nervous fits, lipothymias, and sensations of a "lump in the throat" and of "blocked breathing". On encountering this nonspecific pattern, the signs of neuromuscular hyperexcitability are of much greater importance. Chvostek's sign must be sought systematically. The sign is positive in 85% of cases examined. Trousseau's sign, less sensitive than Chvostek's sign, is observed only in cases of obvious hyperexcitability. The hyperventilation test can complete the search for Chvostek's sign and may give greater sensitivity to the Trousseau's sign (Von Bonsdorff's test).
Neurophysiological tracings and routine Mg assessment (at least plasma and red blood cell Mg; if possible evaluation of Mg intake and daily magnesuria, calcemia, and calciuria) may complete the clinical examination. However, the diagnosis of Mg deficiency mainly requires an Mg oral loading test. The dose of Mg to be administered is 5 mg/kg/day for at least 1 month. At this physiological dose level, oral magnesium supplement is totally devoid of the pharmacodynamic effects of parenteral magnesium. Correction of symptoms by this oral Mg load constitutes the best proof that they were due to Mg deficiency and may represent the beginning of its treatment. 1,4,10
Psychiatric forms of Mg deficiency have been well identified. Personality disorders are of the neurotic type. For example the Minnesota Multiphasic Personality Inventory (MMPI) finds a direct correlation between the "neurotic triad" (hypochondria, depression, and hysteria) and the EMG marks of NHE due to Mg deficiency.1,4 With all the psychometric evaluations, and with the DSM III R interview particularly, the clinical pattern induced through Mg deficiency was always neurotic (for example: generalized anxiety, panic attack disorders, and depression) but never psychotic. Mg deficiency never induces dementia.1,4,25,26 Although a neurosis pattern due to Mg deficiency is frequently observed and simply cured through oral physiological supplementation, neuroses are preeminently conditioning factors for stress. Neuroses may therefore very frequently produce secondary Mg depletion. They require their own specific antineurotic treatment and not mere oral Mg physiological supplementation, but both genuine forms of neurosis due to primary neural Mg deficiency and Mg depletion secondary to a neurosis may exist. These two conditions may be concomitant and reinforce each other. In these stressful patients it may be difficult to establish the primacy of one or the other. In practice, physiological oral Mg supplements may be added to psychiatric treatments, at least at the start.1,10
It is imperative to emphasize that the nervous consequences of Mg deficiency remain functional with anatomical integrity for a long time. They are completely reversible since they can be restored to normal with simple oral physiological Mg supplementation,1,5,10 but it should also be pointed out that a prolongation of untreated chronic Mg deficiency can produce irreversible lesions1,5 with histological changes: morphological changes in the rat hippocampus, degeneration of the Purkinje cells, glial aberration of positive Gomori cells, and neurovasculitis. When Mg deficiency secondary to alcoholism was corrected, no alcoholic encephalopathy was observed within a period of 5 years.1,5 These processes could account for the clinical and paraclinical data that persist after treatment of NHE due to Mg deficiency.1,5 They are especially of concern during the early development of the nervous system. The constitutional characteristics of the nervous forms of primary chronic Mg deficiency could arise from undetected maternal Mg deficiency.1,5 An early maternal Mg deficiency could be the fountainhead of more severe impairments: sudden infant death syndrome8,28 some forms of infantile convulsions or psychiatric disturbances,1,5 and even in adults, cardiovascular diseases and noninsulin-dependent diabetes mellitus.28 The protocol of the multicenter trials of maternal Mg physiological supplementation should be followed not only on the mother, the fetus, and the neonate, but also on the child throughout life from infancy to older age.28
20.3 MAGNESIUM DEPLETION AND DEMENTIAS
Although Mg deficiency might not result in dementia, some types of Mg depletion can play a role in the physiopathology of several types of dementia.
20.3.1 Experimental Models of Mg Depletions
Various types of more or less severe Mg depletion are used: genetic models (in rats and mice) and acquired models: either secondary to an irreversible (or partially reversible) cause (such as traumatic brain injury) or reversible. In the latter case, the models associate a low Mg intake with diverse types of Mg stress.10,22,23 Two types of experimental Mg depletions will be highlighted because of their possible link with dementia.
20.3.1.1 Neurological Degeneration Due to Al Load and Low Mg Intake
Garden soil and drinking water in some Western Pacific areas with high incidence of amyotrophic lateral sclerosis and parkinsonism-dementia (ALS-PD) contain high concentrations of polluting metals such as Al, Fe, and Mn, and low concentrations of common metals such as Mg and Ca. Decreased exposure to traditional sources of foodstuffs and drinking water resulted in a dramatic decline in ALS-PD.
These data as well as the links between aluminum load, magnesium status, and dialysis encephalopathy -- more hypothetically, Alzheimer's disease -- highlight the interest of corresponding experimental studies. With a high Al diet alone, Al content in the nervous system in rats showed no difference with a control group although serum Al was high. No degenerative process was observed. However, with an insufficient intake of Mg the same Al load induced an increase in Al and Ca concentrations in the nervous system and neurodegeneration with precipitation of insoluble hydroxyapatites.28
20.3.1.2 Mg Depletion Due to Kainic Acid Plus Mg Deficiency
Hippocampal injury of ageing may originate from an increased calcium influx in pyramidal neurones resulting from the deleterious effects of increased release of excitatory aminoacids associated with a decrease of neuroprotective factors. Kainic acid acting through its specific receptors generates toxicity in the hippocampus, whereas Mg deficiency - a model of accelerated ageing - decreases Mg neuroprotection.23 In this model physiological Mg supplementation and pharmacological doses of Na acetyltaurinate were ineffective. On the other hand, Mg acetyltaurinate at pharmacological doses had preventive and curative effects in both the short and long terms.23
These two types of experimental Mg depletion models may be useful for screening various treatments of psychiatric disturbances possibly linked with Al load and ageing insults.21,23,29
20.3.2 Possible Links Between Dementias and Mg Depletion
Established links between some types of dementias and Mg depletion are presently scarce, but the experimental models of two types of Mg depletion, perhaps related to the physiopathology of some dementias, constitute promising tests for screening potentially efficient drugs both in these Mg depletions and in the related types of dementias.
20.4 THERAPEUTIC IMPLICATIONS
It seems obvious to contrast the specific, easy, and efficient treatment of the nervous form of Mg deficiency with the difficult problems set by the treatment of certain types of Mg depletion playing a possible role in the physiopathology of some dementias.
20.4.1 Treatment of Magnesium Deficiency
Physiological oral Mg supplementation (5 mg/kg/day) is simple and can be carried out in the diet or with Mg salts. To correct in vivo experimental or clinical Mg deficiency all Mg salts have a comparable bioavailability, but evidently their anions have their own importance. This treatment is totally atoxic since it palliates Mg deficiency by simply normalizing the Mg intake.1,10 It is able to cure all the functional symptoms of Mg deficiency: signs of neuromuscular hyperexcitability and psychiatric symptoms which frequently mimic a neurotic pattern. It prevents irreversible stigmata of NHE due to primary or secondary magnesium deficiency, alcoholic encephalopathy in chronic alcoholism particularly.1,5 It is necessary to highlight the curative and preventive importance of oral physiological maternal Mg supplementation, not only during pregnancy but also in the child throughout life from infancy to older age, to possibly prevent the so-called constitutional factor of neurolability, some cases of sudden infant death syndrome, infantile convulsions, or psychiatric diseases, and even in adult cardiovascular diseases and noninsulin-dependent diabetes mellitus.1,5,8,10,28
20.4.2 Magnesium Therapy and Dementias
With perhaps the one exception of the treatment of autism through very high pharmacological doses of vitamin B6 and high doses of Mg1,5,10,25,30 we cannot presently control the dysregulations of Mg status in Alzheimer's disease, dialysis encephalopathy, and ALS-PD. We can only advise some prophylactic measures. However, if an insufficient Mg intake (i.e., Mg deficiency) would add up to depletion cases, then an Mg deficit would be observed associating deficiency and depletion. The correction of Mg deficiency through simple oral supplementation therefore constitutes an adjuvant treatment of this possible component of Mg deficit.1,10
In some cases, the interest of pharmacological Mg therapy may be discussed. However, pharmacological Mg therapy may induce toxicity since it creates Mg overload. High oral doses of Mg (10 mg/kg/day) are advisable for chronic indications and the parenteral route is suitable for acute indications. Mg infusions can only be envisaged in intensive care units with careful monitoring of pulse, blood pressure, deep tendon reflexes, hourly diuresis, and electrocardiogram and respiratory recordings. It is presently difficult to evaluate the chronic toxicity of long-term high oral Mg doses: they may bring latent complications which may reduce life span.1,10 Neuromuscular hypoexcitability due to hypermagnesemia only occurs when plasma Mg is more than twice normal levels. The blood-brain barrier gives priority to the peripheral action of Mg overload.1,10 In vivo, this neuroprotection seems essentially indirect through the beneficial effects on antithrombotic platelet and endothelial functions and on vasospasm, mainly by acting as a calcium antagonist.1,9,10 Except for a pathological disruption of the blood-brain barrier, direct neuroprotection is observed with massively increased plasma Mg which cannot be practically carried out in human beings.10 In experimental models, the best protective effects with pharmacological doses of Mg were obtained with Mg acetyltaurinate, an Mg salt of the N-acetylamino-derived compound from taurine, the most neuroprotective inhibitory aminoacid.21,23 Further study should evaluate its clinical therapeutic effects.
20.5 CONCLUSION
Two different types of links between Mg deficit and the nervous system should be emphasized.
1 . NHE due to Mg deficiency with neuromuscular and psychiatric symptoms is well recognized nowadays. Induced by insufficient Mg intake, the primary or secondary acute or chronic nervous forms of Mg deficiency remain reversible over a long period by simply normalizing the Mg intake. Untreated chronic forms may however bring about irreversible organic disorders. The psychiatric forms of Mg deficiency may fit into a neurotic pattern, but never result in dementia.
2. In contrast, the relationships between some types of Mg depletion due to various dysregulations of Mg status and some dementias have not been clearly defined yet. However, some epidemiological, experimental and clinical data are promising and new paths remain open in this very interesting field of neuroscience research.
REFERENCES
1. Durlach J: Magnesium in clinical practice. London-Paris, John Libbey Eurotext, 1988, pp.360.
2. Depoortere H., Francon D., and Llopis J.: Effects of a magnesium deficient diet on sleep in rats. Neuropsychobiology, 1993; 27:237-245.
3. Goto Y, Nakamura M, Abe S, et al: Physiological correlates of abnormal behaviors in magnesium-deficient rats. Epilepsy Res., 1993; 15:81-89.
4. Sandrini G, Ruiz G, Alfonsi E, et al: Effects of Mg salt administration on skin conductance response in neuronal hyperexcitability syndrome. Magnesium Res., 1989; 1/2:122-123.
5. Durlach J, Poenaru S, Rouhani S, et at: The control of central neural hyperexcitability in magnesium deficiency. In: Nutrients and Brain Function, Ed., W.B. Essmann, Basel, Karger, 1987, pp 49-71.
6. Poenaru S, Aymard P, Durlach J, et al: Regional distribution of magnesium in normal and Mg deficient rats (abst.). Magnesium Res., 1991; 4:246.
7. Lerma A, Planells E, Aranda P, et al: Evolution of Mg deficiency in rats. Ann. Nutr. Metabol., 1993; 37:210-217.
8. Durlach J, Durlach V, Rayssiguier Y, et al: Magnesium and thermoregulation. I. Newborn and infant. Is sudden infant death syndrome a Mg-dependent disease of the transition from chemical to physical thermoregulation? Magnesium Res., 1991; 4:137-152.
9. Kemp PA, Gardiner SM, March JE, et at: Effects of N6-nitro-l arginine methyl ester on regional haemodynamic responses to MGSO4 in conscious rats. J. Pharmacol., 1994; 111:325-331.
10. Durlach J, Durlach V, Bac P, et al: Magnesium and therapeutics. Magnesium Res., 1994; 7:313-328.
11. Weglicki WB, Tong Mak I, and Phillips TM: Blockade of cardiac inflammation in Mg2+ deficiency by substance P receptors inhibition. Circ. Res., 1994; 74 1009-1013.
12. Rayssiguier Y, Mazur A, Gueux E, et al: Mg deficiency affects lipid metabolism and atherosclerosis processes by a mechanism involving inflammation and oxidative stress (abst.). Magnesium Res., 1994; 7 (Supp. 1): 46-47.
13. Rayssiguier Y, Gueux E, Bussière L, et al: Dietary Mg affects susceptibility of lipoproteins and tissue to peroxidation in rats. J. Am. Coll. Nutr., 1993; 12:133-137.
14. Rayssiguier Y, Durlach J, Gueux E, et al: Mg and ageing. I. Experimental data: importance of oxidative damage. Magnesium Res., 1993; 6:369-378.
15. Stafford RE, Mak IT, Kramer JH, et al: Protein oxidation in Mg deficient rat brains and kidneys. Biochem. Biophys. Res. Commun., 1993; 196:596-600.
16. Smalheiser NR and Swanson DR,: Assessing a gap in the biomedical literature: Mg deficiency and neurologic disease. Neurosci. Res. Commun., 1994; 15:1-9.
17. Nakamura M, Abe S, Goto Y, et al: in vivo assessment of prevention of white-noise-induced seizure in Mg-deficient rats by NMDA receptor blockers. Epilepsy Res., 1994; 17: 249-256.
18. Nakamura M, Abe S, and Akazawa K: AMPA - but not NMDA - receptor blocker NBQX prevents seizure induction in Mg-deficient rats. Magnesium Res., 1995; 8:55-56.
19. Rayssiguier Y, Malpuech C, Nowacki W, et al: Evaluation of the inflammatory state during Mg deficiency in the rat (abst.). Magnesium Res., 1994; 7 (Supp. 1): 51.
20. Benyhe S, Szucs M, Varga E, et al: Cation and guanine nucleotide effects on ligand bindings properties of mu and delta receptors in rat brain membranes. Acta Biochim. Biophys. Hung., 1989; 24:69-8 1.
21. Durlach J, Durlach V, Bac P, et al: Mg and ageing. II. Clinical data: aetiological mechanisms and physiopathological consequences of Mg deficit in the elderly. Magnesium Res., 1993; 6 374-394.
22. Bac P, Herrenknecht C, Binet P, et al: Audiogenic seizures in Mg-deficient mice: effects of Mg pyrrolidone-2carboxylate, Mg acetyltaurinate, Mg chloride and vitamin B6. Magnesium Res., 1993; 6:11-19.
23. Bac P, Herrenknecht C, Binet P, et al: Effects of various Mg salts on the action of systemic kainic acid in Mg deficient rats: a new model of accelerated hippocampal ageing-like injury? (abst.). Magnesium Res., 1993; 6:300-301.
24. Velloso A: Magnesium, free radicals and longevity. Magnesium Res., 1994; 7 (Supp. 1): 48.
25. Galland L: Magnesium, stress and neuropsychiatric disorders. Magnesium Trace Elem., 1991-1992; 10:287-301,
26. Kirov GK, Birch NJ, Steadman P, et al: Plasma Mg levels in a population of psychiatric patients: correlation with symptoms. Neuropsychobiology, 1994; 30:73-78.
27. Durlach J: Death from infancy to older age and marginal Mg deficiency. How long should follow-up of the consequences of undernutrition in pregnancy be continued? Magnesium Res., 1993; 6:297-298.
28. Mitani K: Relationship between neurological diseases due to Al load, especially amyotrophic lateral sclerosis and magnesium status. Magnesium Res., 1992; 5:203-213.
29. Durlach J: Magnesium depletion and pathogenesis of Alzheimer's disease. Magnesium Res., 1990; 3:217-218.
30. Tolbert L, Haigler T, Waits M, et al: Brief report: lack of response in an autistic population to a low dose clinical trial of pyridoxine plus magnesium. J. Autism Dev. Dis., 1993; 23:193-199.
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Belibaste:
_http://www.teachhealth.com/#stressscale
--- Quote ---Sample Chapters: Recognizing Stress
Which of these is stress?
* You receive a promotion at work.
* Your car has a flat tire.
* You go to a fun party that lasts till 2:00 a.m.
* Your dog gets sick.
* Your new bedroom set is being delivered.
* Your best friend and his wife come to stay at your house for a week.
* You get a bad case of hay fever.
* All of the above.
which are stress?
ALL OF THESE ARE STRESS
If you are used to thinking that stress is something that makes you worry, you have the wrong idea of stress. Stress is many different kinds of things: happy things, sad things, allergic things, physical things. Many people carry enormous stress loads and they do not even realize it!
WHAT IS STRESS?
We are all familiar with the word "stress". Stress is when you are worried about getting laid off your job, or worried about having enough money to pay your bills, or worried about your mother when the doctor says she may need an operation. In fact, to most of us, stress is synonymous with worry. If it is something that makes you worry, then it is stress.
Your body, however, has a much broader definition of stress. TO YOUR BODY, STRESS IS SYNONYMOUS WITH CHANGE. Anything that causes a change in your life causes stress. It doesn't matter if it is a "good" change, or a "bad" change, they are both stress. When you find your dream apartment and get ready to move, that is stress. If you break your leg, that is stress. Good or bad, if it is a CHANGE in your life, it is stress as far as your body is concerned.
Even IMAGINED CHANGE is stress. (Imagining changes is what we call "worrying".) If you fear that you will not have enough money to pay your rent, that is stress. If you worry that you may get fired, that is stress. If you think that you may receive a promotion at work, that is also stress (even though this would be a good change). Whether the event is good or bad, imagining changes in your life is stressful.
Anything that causes CHANGE IN YOUR DAILY ROUTINE is stressful.
Anything that causes CHANGE IN YOUR BODY HEALTH is stressful.
IMAGINED CHANGES are just as stressful as real changes.
Let us look at several types of stress -- ones that are so commonplace that you might not even realize that they are stressful.......
Emotional Stress
When arguments, disagreements, and conflicts cause CHANGES in your personal life -- that is stress.
Emotional Stress
Illness
Catching a cold, breaking an arm, a skin infection, a sore back, are all CHANGES in your body condition.
illness
Pushing Your Body Too Hard
A major source of stress is overdriving yourself. If you are working (or partying) 16 hours a day, you will have reducedyour available time for rest. Sooner or later, the energy drain on your system will cause the body to fall behind in its repair work. There will not be enough time or energy for the body to fix broken cells, or replace used up brain neurotransmitters. CHANGES will occur in your body's internal environment. You will "hit thewall," "run out of gas". If you continue, permanent damage may be done. The body's fight to stay healthy in the face of the increased energy that your are expending is major stress.
Environmental Factors
Very hot or very cold climates can be stressful. Very high altitude may be a stress. Toxins or poisons are a stress. Each of these factors threatens to cause CHANGES in your body's internal environment.
environmental toxins
The Special Case of Tobacco Use
Tobacco is a powerful toxin!! Smoking destroys cells that clean your trachea, bronchi, and lungs. Smoking causes emphysema and chronic bronchitis, which progress to slow suffocation. The carbon monoxide from cigarette smoking causes chronic carbon monoxide poisoning. Tobacco use damages the arteries in your body, causing insufficient blood supply to the brain, heart, and vital organs. Cigarette smoking increases the risk of cancer 50 fold.
Chewing tobacco or snuff is no safe haven. It also damages your arteries, and it carries the same cancer risk. (Cancers of the head and neck are particularly vicious, disfiguring, and deadly).
Poisoning the body with carbon monoxide, and causing the physical illnesses of emphysema, chronic bronchitis, cancer, and arterial damage, tobacco is a powerful source of added stress to one's life.
Hormonal Factors
PUBERTY
The vast hormonal changes of puberty are severe stressors. A person's body actually CHANGES shape, sexual organs begin to function, new hormones are released in large quantities. Puberty, as we all know, is very stressful.
PRE-MENSTRUAL SYNDROME
Once a woman passes puberty, her body is designed to function best in the presence of female hormones. For women past puberty, a lack of female hormones is a major stress on the body. Once a month, just prior to menstruation, a woman's hormone levels drop sharply. In many women, the stress of sharply falling hormones is enough to create a temporary OVERSTRESS. This temporary OVERSTRESS is popularly known as Pre MenstrualSyndrome (PMS).
POST-PARTUM
Following a pregnancy, hormone levels CHANGE dramatically. After a normal childbirth, or a miscarriage, some women may be thrown into OVERSTRESS by loss of the hormones of pregnancy.
MENOPAUSE
There is another time in a woman's life when hormone levels decline. This is the menopause. The decline in hormones during menopause is slow and steady. Nevertheless, this menopausal decline causes enough stress on the body to produce OVERSTRESS in many women.
Taking Responsibility for Another Person's Actions
When you take responsibility for another person's actions, CHANGES occur in your life over which you have little or no control. Taking responsibility for another person's actions is a major stressor.
Allergic Stress
Allergic reactions are a part of your body's natural defense mechanism. When confronted with a substance which your body considers toxic, your body will try to get rid of it, attack it, or somehow neutralize it. If it is something that lands in your nose, you might get a runny, sneezy nose. If it lands on your skin, you might get blistery skin. If you inhale it, you'll get wheezy lungs. If you eat it, you may break out in itchy red hives all over your body. Allergy is a definite stress, requiring large changes in energy expenditure on the part of your body's defense system to fight off what the body perceives as a dangerous attack by an outside toxin.
STRESS SCALE FOR ADULTS
In the following table you can look up representative changes in your life and see how much stress value each of these changes is adding to your life. NOTE ANY ITEM THAT YOU MAY HAVE EXPERIENCED IN THE LAST TWELVE MONTHS. Then, total up your score.
(Adapted from the "Social Readjustment Rating Scale" by Thomas Holmes and Richard Rahe. This scale was first published in the "Journal of Psychosomatic Research", Copyright 1967, vol.II p. 214. It is used by permission of Pergamon Press Ltd.)
STRESS
EVENT VALUE
DEATH OF SPOUSE 100
DIVORCE 60
MENOPAUSE 60
SEPARATION FROM LIVING PARTNER 60
JAIL TERM OR PROBATION 60
DEATH OF CLOSE FAMILY MEMBER OTHER THAN SPOUSE 60
SERIOUS PERSONAL INJURY OR ILLNESS 45
MARRIAGE OR ESTABLISHING LIFE PARTNERSHIP 45
FIRED AT WORK 45
MARITAL OR RELATIONSHIP RECONCILIATION 40
RETIREMENT 40
CHANGE IN HEALTH OF IMMEDIATE FAMILY MEMBER 40
WORK MORE THAN 40 HOURS PER WEEK 35
PREGNANCY OR CAUSING PREGNANCY 35
SEX DIFFICULTIES 35
GAIN OF NEW FAMILY MEMBER 35
BUSINESS OR WORK ROLE CHANGE 35
CHANGE IN FINANCIAL STATE 35
DEATH OF A CLOSE FRIEND (not a family member) 30
CHANGE IN NUMBER OF ARGUMENTS WITH SPOUSE OR LIFE PARTNER 30
MORTGAGE OR LOAN FOR A MAJOR PURPOSE 25
FORECLOSURE OF MORTGAGE OR LOAN 25
SLEEP LESS THAN 8 HOURS PER NIGHT 25
CHANGE IN RESPONSIBILITIES AT WORK 25
TROUBLE WITH IN-LAWS, OR WITH CHILDREN 25
OUTSTANDING PERSONAL ACHIEVEMENT 25
SPOUSE BEGINS OR STOPS WORK 20
BEGIN OR END SCHOOL 20
CHANGE IN LIVING CONDITIONS (visitors in the home, change in roommates, remodeling house) 20
CHANGE IN PERSONAL HABITS (diet, exercise, smoking, etc.) 20
CHRONIC ALLERGIES 20
TROUBLE WITH BOSS 20
CHANGE IN WORK HOURS OR CONDITIONS 15
MOVING TO NEW RESIDENCE 15
PRESENTLY IN PRE-MENSTRUAL PERIOD 15
CHANGE IN SCHOOLS 15
CHANGE IN RELIGIOUS ACTIVITIES 15
CHANGE IN SOCIAL ACTIVITIES (more or less than before) 15
MINOR FINANCIAL LOAN 10
CHANGE IN FREQUENCY OF FAMILY GET-TOGETHERS 10
VACATION 10
PRESENTLY IN WINTER HOLIDAY SEASON 10
MINOR VIOLATION OF THE LAW 5
TOTAL SCORE ___________________________ (See below for meaning of your Stress Score)
STRESS SCALE FOR YOUTH
STRESS
EVENT VALUE
DEATH OF SPOUSE, PARENT, BOYFRIEND/GIRLFRIEND 100
DIVORCE (of yourself or your parents) 65
PUBERTY 65
PREGNANCY (or causing pregnancy) 65
MARITAL SEPARATION OR BREAKUP WITH BOYFRIEND/GIRLFRIEND 60
JAIL TERM OR PROBATION 60
DEATH OF OTHER FAMILY MEMBER (other than spouse, parent or boyfriend/girlfriend) 60
BROKEN ENGAGEMENT 55
ENGAGEMENT 50
SERIOUS PERSONAL INJURY OR ILLNESS 45
MARRIAGE 45
ENTERING COLLEGE OR BEGINNING NEXT LEVEL OF SCHOOL (starting junior high or high school) 45
CHANGE IN INDEPENDENCE OR RESPONSIBILITY 45
ANY DRUG AND/OR ALCOHOL USE 45
FIRED AT WORK OR EXPELLED FROM SCHOOL 45
CHANGE IN ALCOHOL OR DRUG USE 45
RECONCILIATION WITH MATE, FAMILY OR BOYFRIEND/GIRLFRIEND (getting back together) 40
TROUBLE AT SCHOOL 40
SERIOUS HEALTH PROBLEM OF A FAMILY MEMBER 40
WORKING WHILE ATTENDING SCHOOL 35
WORKING MORE THAN 40 HOURS PER WEEK 35
CHANGING COURSE OF STUDY 35
CHANGE IN FREQUENCY OF DATING 35
SEXUAL ADJUSTMENT PROBLEMS (confusion of sexual identitity) 35
GAIN OF NEW FAMILY MEMBER (new baby born or parent remarries or adopts) 35
CHANGE IN WORK RESPONSIBILITIES 35
CHANGE IN FINANCIAL STATE 30
DEATH OF A CLOSE FRIEND (not a family member) 30
CHANGE TO A DIFFERENT KIND OF WORK 30
CHANGE IN NUMBER OF ARGUMENTS WITH MATE, FAMILY OR FRIENTS 30
SLEEP LESS THAN 8 HOURS PER NIGHT 25
TROUBLE WITH IN-LAWS OR BOYFRIEND'S OR GIRLFRIEND'S FAMILY 25
OUTSTANDING PERSONAL ACHIEVEMENT (awards, grades, etc.) 25
MATE OR PARENTS START OR STOP WORKING 20
BEGIN OR END SCHOOL 20
CHANGE IN LIVING CONDITIONS (visitors in the home, remodeling house, change in roommates) 20
CHANGE IN PERSONAL HABITS (start or stop a habit like smoking or dieting) 20
CHRONIC ALLERGIES 20
TROUBLE WITH THE BOSS 20
CHANGE IN WORK HOURS 15
CHANGE IN RESIDENCE 15
CHANGE TO A NEW SCHOOL (other than graduation) 10
PRESENTLY IN PRE-MENSTRUAL PERIOD 15
CHANGE IN RELIGIOUS ACTIVITY 15
GOING IN DEBT (you or your family) 10
CHANGE IN FREQUENCY OF FAMILY GATHERINGS 10
VACATION 10
PRESENTLY IN WINTER HOLIDAY SEASON 10
MINOR VIOLATION OF THE LAW 5
TOTAL SCORE _____________________________________
We have asked you to look at the last twelve months of changes in your life. This may surprise you. It is crucial to understand, however, that a major change in your life has effects that carry over for long periods of time. It is like dropping a rock into a pond. After the initial splash, you will experience ripples of stress. And these ripples may continue in your life for at least a year.
So, if you have experienced total stress within the last twelve months of 250 or greater, even with normal stress tolerance, you may be OVERSTRESSED. Persons with Low Stress Tolerance may be OVERSTRESSED at levels as low as 150.
OVERSTRESS will make you sick. Carrying too heavy a stress load is like running your car engine past the red line; or leaving your toaster stuck in the "on" position; or running a nuclear reactor past maximum permissible power. Sooner or later, something will break, burnup, or melt down.
What breaks depends on where the weak links are in your physical body. And this is largely an inherited characteristic.
Here are the common "weak links", and the symptoms of their malfunction
Brain OVERSTRESS
Fatigue, aches and pains, crying spells, depression, anxiety attacks, sleep disturbance.
Gastrointestinal Tract
Ulcer, cramps and diarrhea, colitis, irritable bowel.
Glandular System
Thyroid gland malfunction.
Cardiovascular
High blood pressure, heart attack, abnormal heart beat, stroke.
Skin
Itchy skin rashes.
Immune System
Decreased resistance to infections and neoplasm.
We have known for a long time that OVERSTRESS could cause physical damage to the gastrointestinal tract, glandular system, skin or cardiovascular system. But only recently have we learned that OVERSTRESS actually causes physical changes in the brain. One of the most exciting medical advances of our decade has been an understanding of how OVERSTRESS physically affects your brain. We now know that the fatigue, aches and pains, crying spells, depression, anxiety attacks and sleep disturbances of OVERSTRESS are caused by brain CHEMICAL MALFUNCTION.
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