Hypomagnesemia symptoms and causes – tables from [1, Slatoplosky, et al]
Magnesium supplements given orally during conditions of poor gastrointestinal absorption will be more likely to cause loose stools Magnesium ions can cause relaxation of the smooth muscles lining the intestines and watery bowel movements can occur – the common side effect is not similar to explosive diarrhea unless a very large dose is taken. Magnesium glycinate may be a better absorbed form. Lower more frequent doses are more likely to be absorbed well – 200 mg magnesium glycinate three times a day may result in more retention than 500 mg of a standard form two times a day. The RDA is lower and the UL – Upper Limit is a measly 325 mg but loose stools is really the only oral side effect. Intravenous use can be dangerous due to the rapid changes it can cause in the heart muscle that can trigger a stroke.Dosing Example for someone with a condition or medication that causes chronic wasting of magnesium stores:
“Maintenance therapy may require oral administration of Mg2+ oxide (400 mg twice daily or three times daily) for as long as the risk factors for Mg2+ deficiency exist. Oral Mg2+ gluconate (500 mg twice daily or three times daily) can also be used.” [1, p2293]
***This dosage is in reference to repletion needs for chronic magnesium deficiency typically due to decreased gastrointestinal absorption or increased renal losses.
Ideally our bodies expect a balance of magnesium in everything we eat and drink. Historically it was very rich in the water and soil and nature. An increase in insulin levels is the only main way the body can react to low magnesium levels. Historically an increased appetite would lead to increased magnesium levels because it was so common in the water and food supply. However it isn’t a primary fertilizer – the plants grow with minimal amounts and water softeners and bottling companies take it out along with the calcium and other ‘hard’ minerals. Our food supply and population is low in magnesium and when there is a high calcium intake the body loses more magnesium and preferentially absorbs the calcium. Calcium was never abundant directly in the soil and food supply – bird shells and tiny fish or animal bones would be rich sources and tiny amounts were available throughout the rest of the food and water supplies. Our bodies conserve calcium and waste magnesium because that is what used to work for us.Due to who knows what historical permutations, only sodium and potassium are officially considered electrolytes and have regulation standards for content in water supplies. The soil and everything consumed and drank was rich in magnesium ages ago as our bodies were adapting – before world flooding over the millennia washed nutrients to sea (brine pits are a source of many crucial nutrients and seaweed is a source of iodine because it filters it from the sea water – ocean vegetables for the next season are going to be contaminated from the nuclear accident). Electrolyte beverages in our current market rarely have magnesium – the Glaceau brand of Smart Water does.
“In general, Magnesium deficiency is the result of either gastrointestinal or renal losses. If no cause is readily apparent, then one can distinguish between gastrointestinal and renal losses by measuring the 24-H urinary MG²+ excretion or fractional excretion of Mg2+. The normal response of the kidney to Mg2+ depletion is to reduce Mg2+ excretion to low levels. The measurement of 24-H urinary Mg2+ excretion of more than 30 mg in a person with normal renal function and hypomagnesemia indicates renal Mg2+ wasting. If Mg2+ deficiency is suspected in the absence of hypomagnesemia, then one might consider evaluating the renal excretion of Mg2+ in response to an intravenous Mg2+ load. [20,21] this, however, is rarely done in clinical practice. In the presence of unexplained hypocalcemia or hypokalemia, a trial of Mg2+ administration is more commonly performed.” (Slatoplosky, et al, p2292 ) 
/Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./
“However, thiazides are now used in substantially smaller doses, and the term low-dose thiazide has become synonymous with hydrochlorothiazide at a dose of 12.5 to 25 mg per day (or the equivalent dose of another thiazide). Approximately 50% of patients will respond initially to these low doses. In the Systolic Hypertension in the Elderly Program (SHEP),34 chlorthalidone given at a dose of 12.5 mg per day controlled blood pressure, for several years, in more than 50% of patients. Increasing the dose of hydrochlorothiazide from 12.5 to 25 mg per day may result in a response in an additional 20% (approximately) of patients; at 50 mg per day, 80 to 90% of patients should have measurable decreases in blood pressure.35 Increased electrolyte losses at the higher doses of diuretics may preclude their routine use.”  (***diabetes after a year of use is also a risk)
- Bendroflumethiazide (Naturetin)
- Benzthiazide (Exna)
- Chlorothalidone (Hygroton, Thalitone)
- Chlorothiazide (Diurigen, Duril)
- Hydrochlorothiazide (Esidrix, Hydrodiuril, Hydro-Par, Microzide, Oretic)
- Hydroflumethiazide (Diucardin, Saluron)
- Indapamide (Lozol)
- Metolazone (Mykrox, Zaroxolyn, Diulo)
- Methychothiazide (Aquatensen, Enduron)
- Polythiazide (Renese)
- Quinethazone (Hydromax)
- Trichlormethiazide (Diurese, Metahydrin, Naqua)
Examples of loop diuretics include:
- Ethacrynic acid (Edecrin)
- Furosemide (Lasix)
- Torsemide (Demadex)
Healthline.com – Connect to Better Health
8. [icmr.nic.in/ijmr/2009/November/1128.pdf ] Tahmeed Ahmed, Sabuktagin Rahman & Alejandro Cravioto, Oedematous malnutrition, Indian J Med Res 130, November 2009, pp 651-654
Hyperaldosteronism may be occurring in edematous malnutrition:
Anti-diuretic factor in the urine of children with nutritional oedema: Nutritional oedema is associated with an increased secretion of an anti-diuretic substance (probably anti-diuretic hormone) which prevents the normal excretory response to water administration. Gopalan and Venkatachalam15 in a study furnished indirect proof of the effect of posture on the urinary response to water load in normal subjects and in cases of nutritional oedema. The normal subjects were found to excrete over 100 per cent of ingested water within 4 h of ingestion in the recumbent posture, while in the erect posture they excreted only 80 per cent. In case of nutritional oedema, the urinary excretion was found to be much lower than in the normal subjects in both recumbent and erect postures. The effect of dietary protein deficiency on the hepatic inactivation of ADH in rats has also been investigated. It was found that the rats maintained on low-protein, low-calorie diets showed a delayed and incomplete response to a water load, and that the livers of these animals showed a reduced capacity for inactivating ADH (Gopalan & Srikantia, unpublished).
Role of ferritin and aldosterone: Srikantia observed presence of ferritin in children with kwashiorkor16. With a view to reveal the precise role of ferritin in the pathogenesis of nutritional oedema, Gopalan and Srikantia17 investigated the sequence of changes occurring in induced protein and calorie under-nutrition with focus on oedema formation in monkeys. O n the basis of the findings, they suggested that calorie-protein undernutrition leads to structural and functional changes in the liver, further leading to defective inactivation of ADH. Active ferritin is released from damaged liver leading to increased secretion of ADH. The net result is water retention. Among other factors, aldosterone, the salt retaining hormone, which is known for influencing water metabolism by altering renal tubular reabsorption of sodium, is also known to be inactivated by the liver. Altered aldosterone metabolism has been reported in diseases of the liver. Associated hyperaldosteronism could account for the sodium retention18. In oedematous children aldosterone secretion becomes higher during loss of oedema19.
“In a clinical trial, the administration of N-acetylcysteine, a glutathione precursor, resulted in more rapid resolution of oedema in kwashiorkor31. These associations between oxidative stress and kwashiorkor indicate that antioxidant depletion may cause kwashiorkor which can therefore be prevented with antioxidant supplementation.”
Reduced production of sulfated glycosaminoglycans occurs in Zambian children with kwashiorkor but not marasmus also good –
10. Excerpt from wikipedia / Choreoathetosis
Choreia is characterized by brief, quasi-purposeful, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next.These ‘dance-like’ movements of choreia (from the same root word as “choreography”) often occur with athetosis, which adds twisting and writhing movements.Choreia can occur in a variety of conditions and disorders.
- Choreia is a primary feature of Huntington’s disease, a progressive neurological disorder.
- Twenty percent of children and adolescents with rheumatic fever develop Sydenham’s chorea as a complication.
- Choreia gravidarum is rare type of choreia which is a complication of pregnancy.
- Choreia may also be caused by drugs (levodopa, anti-convulsants, anti-psychotics), metabolic disorders, endocrine disorders, and vascular incidents.
- Ataxia telangiectasia
- Wilson’s disease, a genetic disorder that leads to toxic levels of copper in the body
- McLeod syndrome,is a genetic disorder that may affect the blood, brain, peripheral nerves, muscle and heart. Common features include peripheral neuropathy, cardiomyopathy and hemolytic anemia. Other features include limb chorea, facial tics, other oral movements (lip and tongue biting), seizures, a late-onset dementia and behavioral changes.
Aphasia is a total or partial loss of the ability to speak correctly or to understand or comprehend what is being said. It may be caused by brain injury or disease. It’s most often caused by a stroke that injures the brain’s language center, located on the left side of the brain in most people. Some people with aphasia recover quickly and completely after a stroke. Others may have permanent speech and language problems.
- Speech problems can range from trouble finding words to being unable to talk at all. Some stroke patients describe it as “having trouble getting words out.”
- Some people have problems understanding what others are saying or have trouble with reading, writing or math.
- In other cases, a person with aphasia may have trouble talking but can understand what others say perfectly.
13. Garrison M. Tong and Robert K. Rude, “Magnesium Deficiency in Critical Illness,” Journal of Intensive Care Medicine 20, no. 1 (January): 3 -17.
14. Satoru Torii et al., “Magnesium Deficiency Causes Loss of Response to Intermittent Hypoxia in Paraganglion Cells,” Journal of Biological Chemistry 284, no. 28 (July 10, 2009): 19077 -19089. (free article)[jbc.org/content/284/28/19077.full]
*** Magnesium deficiency is found to reduce the normal response to hypoxia (lack of oxygen) of increasing adrenal gland production of erthyopoietin and endothelial vascular growth factor. This could suggest fewer red blood cells and weaker capillary and blood vessel structure in the magnesium deficient individual with breathing issues or other reduced oxygen situations (smokers).
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Victoria Shanta-Retelny, RD, LD, The Magnesium-Diabetes Connection, Today’s Dietitian, Vol. 6, No. 11, p. 37, November 2004