Tag: calcification

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Calcium sparklets, TRPV channels and vanilla

     Calcium sparklets are not a good thing, not in excess at least. This is just a few interesting articles that have TRPV channels in common. The calcium channels cause problems in a variety of ways for some people. Identifying who is at risk for problems with fluid balance could help prevent the chronic degenerative changes that can result from electrolyte imbalance. (This post led to parts of this webpage: effectivecare.info/G3. Relaxation & Stress)
     I was amused when the search term ‘sparklets’ turned up something pertinent to my field of interest. TRPV channels and vanilloid receptors with overactive calcium flow can increase pain and other types of muscle and nerve signals.

Calcium sparklets are not a type of chewing gum. They are a sudden increase in flow of calcium through certain calcium channels in vascular tissue. A specific chemical trigger called protein kinase Calpha (PKCalpha) was found to signal L type calcium channels into increased calcium flow [3]. The sparklets occurred in diabetic vascular tissue following high blood sugar levels [2]. A cooperative action taking place with as few as three calcium channels needing to be open for maximal vasodilation to occur [1].
TRPV4 are a type of vanilloid receptor. Loss of function due to genetic difference has been associated with hyponatremia, low sodium blood levels. [6]

“TRPV4 is activated by hypotonicity in vitro, and perturbations of even a few mOsmol/kg H2O were sufficient to achieve this effect (5–7); such exquisite sensitivity closely parallels the in vivo mechanism whereby a change of only a few mOsmol/kg H2O influences release of arginine vasopressin. In rodents, TRPV4 is expressed in the blood–brain barrier-deficient central osmosensing nuclei (5, 35), and targeted deletion of the TRPV4 gene gives rise to aberrant osmoregulation in murine models (20, 21).” [6]

     Time to bake something with vanilla. The above paragraph’s reference to a blood-brain barrier deficiency having a genetic component suggests that susceptibility to headaches also could have a genetic component. The change in osmoregulation means that membranes could be more resistant to fluid and particles crossing or more open and barrierless (and  prone to get migraines). The problem could combine a deficiency in ability to transport needed nutrients into the cell with an increase in leakiness of important things out of or into the cell. The lack of nutrients like magnesium would further reduce the calcium channel blocking potential of the cell.
     So is vanilla something that some people genetically need more of? good question. And the bigger bell ringing loud was the risk of hyponatremia means that a low salt diet could lead to even lower levels of sodium in the blood.
     TRPV receptors have to do with pain control as well as flow of fluid and electrolytes (osmoregulation). Vanillin receptors can have a calming effect on the body and sooth pain. Baked goods with vanilla have a little extra besides love soothing the body. (So does hot pepper though – capsaicin).
 

Magnesium flow through the proton gates that the TRPV group of receptors control is what helps reduce  pain (when there is enough magnesium) and what causes pain signals when there isn’t enough to protect the cell interior from calcium entry. Calcium signals overwork, which leads to pain.
Calcium channel blocker medications are trying to close the gates and keep the calcium out – magnesium would be super delighted to do that if enough were being absorbed from the intestines (too full of calcium and active hormone D3).

     A study on the use of magnesium with opioid pain killers demonstrated the power of magnesium’s effect on for helping reduce diabetic pain. Diabetics normally do not find pain relief from opioids but when magnesium was given in advance the pain killer worked – and the pain killing effect continued for three days after the opioid medication effect would have worn off. The research discussion seemed to focus on using 30 mg with IVs of  morphine or other opioid and didn’t not address the fact that the 300 mg dose had reduced pain on its own, without opioid medication. [18]
 
  • by Sonkusare SK et al, Elementary Ca2+ signals through endothelial TRPV4 channels regulate vascular function. Science. 2012 May 4;336(6081):597-601. [ncbi.nlm.nih.gov/pubmed/22556255]
  • Calcium and diabetic vascular dysfunction, Focus on “Elevated Ca2+sparklet activity during acute hyperglycemia and diabetes in cerebral arterial smooth muscle cells,  by Katherine M. Dunn, KM and Mark T. Nelson (11/11/09 Am J Physiol Cell PhysiolFebruary 1, 2010 vol. 298 no. 2 C203-C205) “This report is also the first to describe a molecular mechanism by which hyperglycemia produces increased [Ca2+]i in VSM and suggests that this mechanism of Ca2+ sparklet activation may be uniquely initiated by hyperglycemia.”    [ajpcell.physiology.free article]
  • Article by Amberg GC et al “Calcium sparklets regulate local and global calcium in murine arterial smooth muscle” J Physiol. 2007 Feb 15;579(Pt 1):187-201. Epub 2006 Dec 7. [Free article]
  • The first three are from a search for ‘sparkles’ in pubmed, no sparkles-but autosuggester came up with ‘calcium sparklet’ and the whole list looks interesting: [ncbi.nlm.nih.gov/pubmed?term=calcium%20sparklet]-Truth can be stranger than fiction.

4. A different search ‘magnesium deficiency hyperglycemia‘ provided a summary worth reading :  Magnesium and Potassium in Lone Atrial Fibrillation, by Patrick Chambers, MD, pdf file: [afibbers.org/resources/PCmagnesium.pdf] *** this needs to be added to the IoM 1997 report on magnesium. Lefthandedness section near the bottom notes an increase calcium flow across cell membranes in left handers. A genetic difference that can lead to an increase in the isoprenoid pathway and inhibition of Na/K pumps in the membranes is suggested to occur in some left handed people. The difference can lead to an increased need for magnesium.

5. Reminder – vascular calcification is somewhat reversible and a simple way to start is to add less by limiting the amount of calcium taken in daily. Two servings a day of calcium rich foods is adequate for most people; there is also calcium in smaller amounts in many other foods too. Calcification of Soft Tissue, hardening organs and softening bones (post, 8/19/11 )

6. A loss-of-function nonsynonymous polymorphism in the osmoregulatory TRPV4 gene is associated with human hyponatremia, by Wei Tian, et al [pnas.org/content/early/2009/08/03/0904084106.full.pdf]

7. Physiology and Pharmacology of the Vanilloid Receptor, by Angel Messeguer, Rose Planells-Cases, and Anton Ferrer-Montiel (Curr. Neuropharmacol., 2006 January: 4(1) : 1-15) [link]

Excerpt:  In addition to the contribution of the vanilloid receptor as a target of the neurogenic inflammation underlying different diseases, TRPV1 is gaining interest for the treatment of neuropathic, postoperative and chronic pain and, recently, for the therapy of epithelial disorders. Thus, for instance, topical capsaicin or resiniferotoxin have been used in postherpetic neuralgia, diabetic neuropathy, postmastectomy pain and arthritis [64,103]. Recently, TRPV1 has been clearly validated as a key target for management of chronic pain in bone cancer [42]. As a result, the development of specific TRPV1 antagonists is a central focus of current drug discovery

***antagonist equals block – the vanilloid receptors are also involved in soothing – feed and educate the receptors because they all serve multiple purposes. Pain has a purpose – to signal that something is wrong. Masking pain with antagonists that deaden a function – to signal a problem – was a very disappointing climax to that paragraph. TRPV1 receptors and all the rest of the gang are very exciting – let’s not waste more money and time inventing synthetic antagonists to a message system that is very intertwined in controlling gates and flow of substance. the pain is there for a reason – starvation – lack of building blocks – lack of function.

8. More on vanilla from “Confessions of a Cardamom Addict” blogspot – blog part one–  –blog part two – ***These cover the history, processing, environmental concerns, major botanical varieties.

18(vit D bib.). [ncbi.nlm.nih.gov/pubmed/20081245] Magdalena Bujalska, Helena Makulska-Nowak, Stanis³aw W. Gumuka Magnesium ions and opioid agonistsin vincristine-induced neuropathy , Department of Pharmacodynamics, Medical University of Warsaw, Krakowskie Przedmieoecie 26/28, PL 00-927 Warszawa, Poland

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. Thanks.

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Calcification of the pineal gland – some statistics and sleep habits

Calcification of the pineal gland was found to be less prevalent in a study collecting data on a group of people of black ethnicity. The following link and article suggest that black people genetically may be less at risk for calcification of the pineal gland.(The pineal gland is important because of hormones like melatonin that it is involved in the production of and calcification reduces function and less melatonin means less quality sleep.I suggest that the research being reviewed may have been performed on a population that did not eat the same as now or as mixed and as similar to each other (black population differences from Caucasian is being discussed in the link.) The review article is suggesting the differing lab findings reflect actual structural or genetic differences but if an assumption that the populations were on similar nutrient ratios compared to now or to each other has been made then the correlation can not be used to draw such a conclusion.

The study in reference was from 1967 in a population with African ancestry. The diet in 1967 was less processed then and calcium fortified products may not have been as common as they are now.

I think reading and reviewing older studies is important but from a questioning perspective – what variables were in play at the time of the research study that may have changed. What differences between then and now may have changed the expected outcome?

There are some fundamental differences between different groups of people so it is certainly possible that the pineal gland has a few differences as well as the kidneys – but in 1974 the Black American group may not have been consuming the same typical diet as the Caucasian group. The blending of cultures and the fast food lifestyle wasn’t as prevalent or as inexpensive compared to home cooking as it is now. (It actually is fairly expensive to put a full meal together compared to buying a similar load of “calories,” not necessarily comparing any other nutrients. Fewer homes had single parents or two working parents compared  to now. I don’t have statistics on that but they may exist.).

The study and article are interesting but  I would like to see it repeated on a group of individuals today.
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PS: calcification is somewhat reversible and the first step is taking in less of it – how can the body ever hope to use up the stored up reserves if too much or even if adequate for maintenance levels are eaten daily – to de-calcify or to run out of reserved calcium we need to dip into the bank account and spend some of it. Some calcium is excreted by the kidneys daily, but just not as much as magnesium losses equal.

On today’s diet, I think people of black ancestry are likely to be just as much at risk of calcification of the pineal gland as anyone else.
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Excerpt from “Pineal Gland: A Cognitive Advantage for Africans”:
By Bernie Douglas (January 17, 2008) [link]

Racial differences have been noted in the rate of pineal calcification as seen in plain skull radiographs. In Caucasians, calcified pineal is visualized in about 50% of adult skull radiographs after the age of 40 years (Wurtman et al, 1964); other scholars argue that Caucasians, in general, may have rates of pineal gland calcification as high as ­60-80% (King, 2001). Murphy (1968) reported a radiological pineal calcification rate of 2% from Uganda, while Daramola and Olowu (1972) in Lagos, Nigeria found a rate of 5%. Adeloye and Felson (1974) found that calcified pineal was twice as common in White Americans as in Blacks in the same city, strengthening a suspicion that there may be a true racial difference with respect to this apparatus. In India a frequency of 13.6% was found (Pande et al, 1984). Calcified pineal gland is a common finding in plain skull radiographs and its value in identifying the midline is still complementary to modern neuroradiological imaging.

There is a surprising rarity of calcified pineal gland on skull roentgenograms in West Africans. Adeloye and Odeku (1967) working from a hospital where an average of about 2,000 skull roentgenographic examinations were done every year, encountered less than 10 cases of roentgenologically visible calcified pineal gland in the Neurosurgery unit during a period of 10 years. In the tasks of daily life, calcification in the pineal gland affects our brain’s ability to function. Calcification of the pineal gland is shown to be closely related to defective sense of direction (Bayliss et al, 1985). In a tricentre prospective study of 750 patients lateral skull radiographs showed that 394 had calcified pineal glands. Sense of direction was assessed by subjective questioning and objective testing and the results noted on a scale of 0-10 (where 10 equals perfect sense of direction). The average score for the 394 patients with pineal gland calcification was 3.7 (range 0-8), whereas the 356 patients without pineal gland calcification had an average score of 7.6 (range 2-10). This difference was highly significant (p less than 0.01) (Bayliss et al, 1985). Also, the effects of disturbed sleep and memory are well documented.

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[bonus link]on sleep personality types, “What’s Your Alarm Clock Personality?” by Sharon Tanenbaum, (11/16/11) on everydayhealth.com – not nutrition related as much as clues about how we tend to meet the day and how that might reflect on how we look forward to life – or sleep quality may have more to do with pillow softness – not sure.

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.
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Calcification of soft tissue – hardening organs and softening bone

     Vascular calcification is better known as atherosclerosis. Cholesterol plaques in blood vessels are generally a mixture of calcium with the fat. Calcification also occurs in arthritis as bone spurs and calcium can collect in organs and glands and impair their function. The pineal gland is very tiny and located within the brain. It it responsible for the melatonin hormone that helps us sleep. A calcified pineal gland no longer helps with sleep but the condition may be reversible by limiting intake of calcium and increasing intake of magnesium.     Reversing calcification may start with reducing calcium intake. The following article mentions a link between higher intake of calcium and worsening of coronary artery calcification and numbers of deaths within a group of end stage renal disease patients. Magnesium is wasted by healthy kidneys and little is recycled/reclaimed the way calcium and sodium are conserved by healthy kidneys – add end stage renal disease and magnesium is leaking out faster then intestinal absorption can occur even if the magnesium was in the food or drink or supplement.

Calcium can not make strong bones if nothing is keeping it from leaking out in response to the stress chemicals’ fight or flight messages. People suffer from osteoporosis and weak bones along with hardening of the arteries and organs –  excess calcium and vitamin D might be part of the problem. Too much active vitamin D can add to calcium imbalance because it signals the bones to let go of stored calcium and magnesium.

The minerals are also released during stress reactions in case there is a need to run from danger or heal a wound. White blood cells around wounds have the enzyme needed to activate vitamin D to the hormone form.

What do you know – it is important to mellow out and de-stress to help keep bone tissue hard and organ tissue soft.

  1. [jasn.asnjournals.org/content/15/12/2959.full] Vascular Calcification Mechanisms, by Cecilia M. Giachelli, doi: 10.1097/01.ASN.0000145894.57533.C4 JASN December 1, 2004 vol. 15 no. 12 2959-2964

“In a landmark study, Goodman et al. (24)  found that coronary artery calcification occurred in young patients with ESRD (end stage renal disease) decades before this pathology was observed in the normal population. Furthermore, progression of vascular calcification in this group was positively correlated with serum P levels, Ca x P, and daily intake of Ca (24).”

***Vascular calcification has been correlated to higher intakes of calcium and phosphorus in this research article. Cardiovascular deaths are common among end stage renal disease and/or diabetic patients – I suggest they should be limiting calcium and phosphorus and increasing their magnesium intake in order to reduce risks of calcium overload. In the average human the kidneys favor calcium absorption and retention and waste magnesium.
Over the course of mankind the body adapted to a food and water supply that was abundant in magnesium and limited in calcium content. Calcium is important for strong bones but only in combination with other nutrients. Vitamin K (brown rice, green leafy vegetables and good guy bacteria in our intestines are sources) is essential for blood clotting and for healthy bones. Strontium is a trace mineral that may be essential to healthy bones and of course magnesium is the trace mineral that helps keep calcium inside of the bone where it belongs. Excessive levels of active vitamin D tell the bone to release the stored minerals. Active vitamin D (a very strong steroid based hormone in actuality) can switch on and off 900+ genes.
The study found (unsurprisingly) that the end stage renal disease patients who were treated with the typical phosphate binding medications that contained calcium had 28% progression of calcification compared to the experimental group who were given a phosphate binding agent that didn’t contain calcium. [12]

Let’s keep the calcium in the bone tissue where it belongs.

The article Vascular Calcification Mechanisms [1] presents four potential ways the soft tissue calcification may develop.

“First, human and mouse genetic findings have determined that blood vessels normally express inhibitors of mineralization, such as pyrophosphate and matrix gla protein, respectively, and that lack of these molecules (“loss of inhibition”) leads to spontaneous vascular calcification and increased mortality (10,29).”

Second – genetic/phontypic changes leading to production of bone proteins within the blood vessel may occur (the blood vessel cell switches on bone cell mechanisms).

“Third, bone turnover leading to release of circulating nucleational complexes has been proposed to explain the link between vascular calcification and osteoporosis in postmenopausal women (41–43).”

“Fourth, cell death can provide phospholipid-rich membranous debris and apoptotic bodies that may serve to nucleate apatite, especially in diseases where necrosis and apoptosis are prevalent, such as atherosclerosis (34,44,45).”

*** Magnesium deficiency could effect the enzyme production necessary for producing the “inhibitors” of bone formation produced in functioning blood vessels. Magnesium is crucial to over 300 enzymes. It is also essential for the growth of healthy white blood cells. A plentiful supply of white blood cells would engulf waste products of apoptosis and the dead cell material wouldn’t be left messing up vessel walls. Chronic magnesium deficiency will promote bone turnover in order to access the stored magnesium found within. Long term kidney problems may be reducing the amount of magnesium that the body can retain and further through off the calcium/magnesium balance.
Chronically elevated active D would chronically cause demineralization of the bones and also might be switching on and off genes in areas of the body (blood vessels for example) that shouldn’t be forming bone tissue. I would be very curious what the end stage renal disease patients’ 1, 25 D levels (hormone) are compared to their 25 D levels (vitamin).  My 1, 25 D levels have been at the high end of normal and 25 D levels below normal (“deficient”) for five years of testing. I have been actively avoiding supplements and foods with vitamin D and much time in the sun during that time because I have found it reduces my symptoms of  muscle knots (fibromyalgia), I also have taken magnesium supplements regularly.
A 200-500 mg supplement taken along with food generally will not cause the smooth muscles of the intestines to relax into a sudden bowel movement. Magnesium supplements are non-toxic but if absorbed too rapidly can cause too much muscle relaxation in the bowels or heart. Fluttery weak heart beats may result if you hang out in an Epsom salt bath for a long time due to the relaxation of too many of the muscle fibers at the same time. Magnesium taken with food or in the glycinate form does’t seem to have the over relaxing effect on the bowels.
Magnesium helps keep the calcium in the bone and out of the soft tissue. Use the calcium channel blocker that Mother Nature provided – magnesium. Eat more nuts, beans, seeds, green leafy vegetables. and chocolate every day for strong bones and soft organs!
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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.

Reference List

From Vitamin D bibliography [link]:

10. Rutsch F, Ruf N, Vaingankar S, Toliat MR, Suk A, Hohne W, Schauer G, Lehmann M, Roscioli T, Schnabel D, Epplen JT, Knisely A, Superti-Furga A, McGill J, Filippone M, Sinaiko AR, Vallance H, Hinrichs B, Smith W, Ferre M, Terkeltaub R, Nurnberg P: Mutations in ENPP1 are associated with “idiopathic” infantile arterial calcification. Nat Genet 34: 379–381, 2003[CrossRef][Medline]
12. Sangiorgi G, Rumberger JA, Severson A, Edwards WD, Gregoire J, Fitzpatrick LA, Schwartz RS: Arterial calcification and not lumen stenosis is highly correlated with atherosclerotic plaque burden in humans: A histologic study of 723 coronary artery segments using nondecalcifying methodology. J Am Coll Cardiol 31: 126–133, 1998[Abstract/Free Full Text]

29. Luo G DP, McKee MD, Pinero GJ, Loyer E, Behringer RR, and Karsenty: G Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein. Nature 386(March 6): 78–81, 1997[CrossRef][Medline]

34. Tanimura A, McGregor DH, Anderson HC: Matrix vesicles in atherosclerotic calcification. Proc Soc Exp Biol Med 172: 173–177, 1983[CrossRef][Medline]

  1. Price PA, Caputo JM, Williamson MK: Bone origin of the serum complex of calcium, phosphate, fetuin, and matrix Gla protein: Biochemical evidence for the cancellous bone-remodeling compartment. J Bone Miner Res 17: 1171–1179, 2002[CrossRef][Medline]
  2. Price PA, Faus SA, Williamson MK: Bisphosphonates alendronate and ibandronate inhibit artery calcification at doses comparable to those that inhibit bone resorption. Arterioscler Thromb Vasc Biol 21: 817–824, 2001[Abstract/Free Full Text]
  3. Price PA, June HH, Buckley JR, Williamson MK: Osteoprotegerin inhibits artery calcification induced by warfarin and by vitamin D. Arterioscler Thromb Vasc Biol 21: 1610–1616, 2001[Abstract/Free Full Text]
  4. Proudfoot D, Skepper JN, Hegyi L, Bennett MR, Shanahan CM, Weissberg PL: Apoptosis regulates human vascular calcification in vitro: Evidence for initiation of vascular calcification by apoptotic bodies. Circ Res 87: 1055–1062, 2000[Abstract/Free Full Text]
  5. Schoen FJ, Tsao JW, Levy RJ: Calcification of bovine pericardium used in cardiac valve bioprostheses. Am J Pathol 123: 134–145, 1986[Abstract]
  • [ajsonline.org/cgi/content/full/305/6-8/661] Nita Sahai, Modeling apatite nucleation in the human body and in the geochemical environment American Journal of Science, Vol. 305, June/September/October 2005, P.661-672; doi:10.2475/ajs.305.6-8.661

“Magnesium inhibits nucleation by adsorbing faster than calcium, as an outer-sphere surface complex, at the active site.”

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Hypomagnesemia symptoms and causes list

Hypomagnesemia symptoms and causes – tables from [1, Slatoplosky, et al]

***This is an initial list of magnesium deficiency symptoms and causes. People with these conditions are at risk of chronic magnesium losses from bone stores and the resulting osteoporosis. Magnesium is used as a buffer by the kidneys and gastrointestinal tract when conditions are too acidic – frequently with our modern diet and beverages.

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.

Magnesium can also be absorbed through the skin from Epsom salt baths, foot soaks or skin creams that have had it added (a compounding pharmacist can make it if prescribed). [35 B, 36 B,37 B] Magnesium has been successfully used within emergency inhalers for asthma.
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Clinical consequences of hypomagnesemia     [tables from 1,Slatoplosky, et al] ***symptom list
Electrolyte abnormalities
                Hypokalemia
                Hypocalcemia
Neuromuscular
                Carpopedal spasm
                Tetany
                Muscle cramps
                Muscle fasciculations
Neurologic
                Vertigo                 / dizziness
                Nystagmus           /  involuntary eye movement
                Aphasia                /  loss of speech abilities, may be temporary [12]
                Hemiparesis
                Depression
                Delirium
                Choreoathetosis    [10]
Cardiovascular
                Ventricular arrhythmias
                Torsade de points
                Supraventricular tachycardia
                Enhanced sensitivity to digoxin
Causes of Magnesium deficiency    [1]
***triggers and conditions that lead to magnesium wasting that may be genetic, pharmaceutical side effect related or possibly preventable –ie quit drinking too much alcohol –also smoking [14] needs to be added to this list [Bruerger’s vasculitis] and proton pump inhibitors for some people.
Gastrointestinal
                Malnutrition
                Malabsorption
                Chronic diarrhea
                Primary infantile hypomagnesemia
                Nasogastric suction
                Intestinal fistula
Renal
                Congenital magnesium wasting
                Bartter syndrome
                Gitelman syndrome
                Postobstructive diuresis
                Diuretic phase of ATN         [11]
                Loop and thiazide diuretics   [3,4, 5,6]
                Cisplatin
                Aminoglycosides   [7-drug names, 9 – kwashiorkor reference]
                Pentamidine
                Foscarnet
                Cyclosporin A
                Tacrolimus
Endocrine
                Hyperparathyroidism
                Hyperthyroidism
SIADH
                Hyperaldosteronism    [8 – edematous malnutrition reference]
Redistribution
                Hungry bone syndrome
                Acute pancreatitis
                Blood transfusions
                Insulin treatment
Miscellaneous
                Diabetes                   [59]
                Chronic alcoholism

“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 ) [1]

/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./

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Bibliography
1.   1.   [jasn.asnjournals.org/content/20/11/2291.long]  Kevin J. Martin,  Esther A. González and Eduardo Slatopolsky, Clinical Consequences and Management of Hypomagnesemia,  doi: 10.1681/ASN.2007111194 (JASN November 1, 2009 vol. 20 no. 11 2291-2295)
3.       Michael E. Ernst and Marvin Moser, “Use of Diuretics in Patients with Hypertension,” New England Journal of Medicine 361, no. 22 (2009): 2153-2164.

“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.” [3]                      (***diabetes after a year of use is also a risk)

List of Thiazide and Thazide-like Diuretics (water pills) used in the Treatment of High Blood Pressure     4.   [infobloodpressure.com/drugs/thiazide-list.html ]
  • 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:

  • Bumetanide
  • Ethacrynic acid (Edecrin)
  • Furosemide (Lasix)
  • Torsemide (Demadex)
Aminoglycosides are a group of antibiotics including at least eight drugs: amikacin, gentamicin, kanamycin, neomycin, netilmicin, paromomycin, streptomycin, and tobramycin.
7. Read more on aminoglycoside antibiotics: [healthline.com/galecontent/aminoglycosides#ixzz1HdHbebJf]
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.”

9. [ajcn.org/content/89/2/592.long]
Reduced production of sulfated glycosaminoglycans occurs in Zambian children with kwashiorkor but not marasmus also good –

10. Excerpt from wikipedia / Choreoathetosis 
10. [en.wikipedia.org/wiki/Chorea_%28disease%29]

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.
11. Diseases of the kidney and urinary tract  By Robert W. Schrier  page 2303 hypophosphatemia, diuretic phase of ATN, acute tubule nephropathy

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.
Each person’s speech and language problem is unique. A language professional (speech therapist) can help set up a treatment plan and help others understand the needs of a person with aphasia.
For stroke information, call the American Stroke Association at 1-888-4-STROKE.
 
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).

15. “Possible Interactions with: Magnesium,” [umm.edu/altmed/articles/magnesium- 000968.htm.]

16. B Grimaldi, “The central role of magnesium deficiency in Tourette’s syndrome: causal relationships between magnesium deficiency, altered biochemical pathways and symptoms relating to Tourette’s syndrome and several reported comorbid conditions,” Medical Hypotheses 58, no. 1 (1, 2002): 47-60.

17. G Eby, “Rescue treatment and prevention of asthma using magnesium throat lozenges: Hypothesis for a mouth–lung biologically closed electric circuit☆,” Medical Hypotheses 67, no. 5 (2006): 1136-1141.

18. “Nut consumption and risk of coronary heart disease… [Curr Atheroscler Rep. 1999] – PubMed result,” [.ncbi.nlm.nih.gov/pubmed/11122711.]

19. “Magnesium deficiency and metabolic syndrome: stres… [Magnes Res. 2010] – PubMed result,” [ncbi.nlm.nih.gov/pubmed/20513641.]

20. “Magnesium and the inflammatory response: potential… [Arch Biochem Biophys. 2007] – PubMed result,” [ncbi.nlm.nih.gov/pubmed/16712775.]

21. “[Magnesium and inflammation: lessons from animal m… [Clin Calcium. 2005] – PubMed result,” [ncbi.nlm.nih.gov/pubmed/15692164]

22. P Chambers, “Lone atrial fibrillation: Pathologic or not?,” Medical Hypotheses 68, no. 2 (2007): 281-287.

23. “Complementary vascular-protective actions of magnesium and taurine: A rationale for magnesium taurate,” [medical-hypotheses.com/article/S0306-9877(96)90007-9/abstract.]

24. Abe E. Sahmoun and Brij B. Singh, “Does a higher ratio of serum calcium to magnesium increase the risk for postmenopausal breast cancer?,” Medical Hypotheses 75, no. 3 (9, 2010): 315-318.

25. “Epidemiological evidence associating dietary calci… [Am J Nephrol. 1986] – PubMed result,” [ncbi.nlm.nih.gov/pubmed/2950755.]

26. “High fructose consumption combined with low dietar… [Magnes Res. 2006] – PubMed result,” [ncbi.nlm.nih.gov/pubmed/17402291.]

[27. ..AppDataRoamingMozillaFirefoxProfiles5z5xh8vb.defaultzoterostorage4MGSRXSW9789241563550_eng.pdf ]  Cotruvo J, Bartram J, eds. Calcium and Magnesium in Drinking-water : Public health significance, Geneva, World Health Organization, 2009.

28. “Protein peroxidation, magnesium deficiency and fib… [Magnes Res. 1996] – PubMed result,” [ncbi.nlm.nih.gov/pubmed/9247880.]

29. E Planells et al., “Effect of magnesium deficiency on vitamin B2 and B6 status in the rat,” Journal of the American College of Nutrition 16, no. 4 (August 1997): 352-356.

30. Sivan Ben-Avraham et al., “Dietary strategies for patients with type 2 diabetes in the era of multi-approaches; review and results from the Dietary Intervention Randomized Controlled Trial (DIRECT),” Diabetes Research and Clinical Practice 86 Suppl 1 (December 2009): S41-48.

31. “Utility of magnesium as antiarrhythmic agent reviewed. – Health & Medicine Week | HighBeam Research – FREE trial,” [highbeam.com/doc/1G1-121345520.html.]

32. Barbara Chipperfield and JohnR. Chipperfield, “Relation of Myocardial Metal Concentrations to Water Hardness and Death-Rates from Ishchaemic Heart Disease,” The Lancet 314, no. 8145 (October 6, 1979): 709-712.

33. Barbara Chipperfield et al., “Magnesium and Potassium Content of Normal He3art Muscle in Areas of Hard and Soft Water,” The Lancet 307, no. 7951 (January 17, 1976): 121-122.

34. “Regulation of Contraction in Striated Muscle — Gordon et al. 80 (2): 853 — Physiological Reviews,” [physrev.physiology.org/cgi/content/full/80/2/853.]

35. “Potassium, calcium, magnesium, and sodium levels i… [Clin Lab. 2010] – PubMed result,” [ncbi.nlm.nih.gov/pubmed/21086788. ]

36. “Magnesium: Its proven and potential clinical significance.(Statistical Data Included) – Southern Medical Journal | HighBeam Research – FREE trial,” [highbeam.com/doc/1G1-82553295.html#.]

37. “Magnesium Treatment for Sudden Hearing Loss – The Annals of Otology, Rhinology & Laryngology | HighBeam Research – FREE trial,”[highbeam.com/doc/1P3-679636211.html#.]

39. “Magnesium supplementation decreases oxidative stress in diabetic rats. – Biotech Week | HighBeam Research – FREE trial,” [highbeam.com/doc/1G1-104471960.html#.]

40. “Magnesium requirement of kittens is increased by high dietary calcium – The Journal of Nutrition | HighBeam Research – FREE trial,”[highbeam.com/doc/1P3-37651279.html#.]

41. Daniel G. Chausow et al., “Experimentally-induced magnesium deficiency in growing kittens,” Nutrition Research 6, no. 4 (April 1986): 459-468.

42. Yuhei Kawano et al., “Effects of Magnesium Supplementation in Hypertensive Patients : Assessment by Office, Home, and Ambulatory Blood Pressures,” Hypertension 32, no. 2 (August 1, 1998): 260-265.

43. Robert E. Kleiger et al., “Effects of chronic depletion of potassium and magnesium upon the action of acetylstrophanthidin on the heart,” The American Journal of Cardiology 17, no. 4 (April 1966): 520-527.

44. Andrew D Hershey, “Current approaches to the diagnosis and management of paediatric migraine,” The Lancet Neurology 9, no. 2 (2, 2010): 190-204.

45. A M Gordon and E B Ridgway, “Cross-bridges affect both TnC structure and calcium affinity in muscle fibers,” Advances in Experimental Medicine and Biology 332 (1993): 183-192; discussion 192-194.

46. Karin Ladefoged and Kikki Hagen, “Correlation between concentrations of magnesium, zinc, and potassium in plasma, erythrocytes and muscles,” Clinica Chimica Acta 177, no. 2 (October 14, 1988): 157-166.

47. “Common genetic variants of the ion channel transient receptor potential membrane melastatin 6 and 7 ( TRPM6 and TRPM7 ), magnesium intake, and risk of type 2 diabetes in women.(Research article)(Report) – BMC Medical Genetics | HighBeam Research – FREE trial,”[.highbeam.com/doc/1G1-193482837.html#.]

48. M Fu et al., “Association between Unhealthful Eating Patterns and Unfavorable Overall School Performance in Children,” Journal of the American Dietetic Association 107, no. 11 (11, 2007): 1935-1943.

49. “Antenatal magnesium treatment and neonatal illness severity as measured by the Score for Neonatal Acute Physiology (SNAP) – Journal of Maternal – Fetal & Neonatal Medicine | HighBeam Research – FREE trial,”[.highbeam.com/doc/1P3-856244151.html#.]

50. “Acid-Base Status Affects Renal Magnesium Losses in Healthy, Elderly Persons1 – The Journal of Nutrition | HighBeam Research – FREE trial,” [highbeam.com/doc/1P3-1123831511.html#.]

51. “Ancient Minerals Launches Comprehensive Online Magnesium Health Resource. – PRWeb Newswire | HighBeam Research – FREE trial,”[.highbeam.com/doc/1G1-241203537.html#.]

52. K Michaelsen, “Inadequate Supplies of Potassium and Magnesium in Relief Food? Implications and Countermeasures,” The Lancet 329, no. 8547 (6, 1987): 1421-1423.

53. “High Dietary Intake of Magnesium May Decrease Risk of Colorectal Cancer in Japanese Men1,2 – The Journal of Nutrition | HighBeam Research – FREE trial,”[highbeam.com/doc/1P3-1998563311.html.]

54. “Magnesium – The Clinical Advisor : For Nurse Practitioners | HighBeam Research – FREE trial,” [highbeam.com/doc/1P3-2195246591.html.]

55. “Magnesium prevents chemotherapy side effects.(Editorial)(Report) – Townsend Letter | HighBeam Research – FREE trial,”[highbeam.com/doc/1G1-206620332.html#.

56. J Caddell, “Magnesium Deprivation in Sudden Unexpected Infant Death,” The Lancet 300, no. 7771 (8, 1972): 258-262.

57. “Magnesium builds bones in pre-pubertal and adolescent girls.(ABSTRACTS OF INTEREST)(Clinical report) – Original Internist | HighBeam Research – FREE trial,” [highbeam.com/doc/1G1-166995340.html#.]

58. J D Potter, S P Robertson, and J D Johnson, “Magnesium and the regulation of muscle contraction,” Federation Proceedings 40, no. 12 (October 1981): 2653-2656.

[59.  todaysdietitian.com/newarchives/td_1104p37.shtml]

Victoria Shanta-Retelny, RD, LD, The Magnesium-Diabetes Connection, Today’s Dietitian, Vol. 6, No. 11, p. 37, November 2004

 

Magnesium references From Bibliography for Dietitian Recommends Stop Vitamin D and Calcium ASAP 
8B. http://www.ijkd.org/index.php/ijkd/article/view/140 Assadi, F., Hypomagnesemia, An Evidence-Based Approach to Clinical Cases, (Iranian Journal of Kidney Diseases, Vol 4, No 1 (2010)
18 B. http://www.ncbi.nlm.nih.gov/pubmed/20081245 Magdalena Bujalska, Helena Makulska-Nowak, Stanis³aw W. Gumuka Magnesium ions and opioid agonistsin vincristine-induced neuropathy , Department of Pharmacodynamics, Medical University of Warsaw, Krakowskie Przedmieoecie 26/28, PL 00-927 Warszawa, Poland
19 B. Magnesium: an emerging drug in anaesthesia, , Editorial I, M. F. M. James, British Journal of Anaesthesia, 103 (4): 465-7 (2009) DOI:10.1093/bja/aep242
23 B. http://www.ncbi.nlm.nih.gov/pubmed/17823441 Dai Q, Shrubsole MJ, Ness RM, Schlundt D, Cai Q, Smalley WE, Li M, Shyr Y, Zheng W., The relation of magnesium and calcium intakes and a genetic polymorphism in the magnesium transporter to colorectal neoplasia risk. ( Am J Clin Nutr. 2007 Sep;86(3):743-51)
24 B. Joan L Caddell, Geriatric cachexia: a role for magnesium deficiency as well as for cytokines?, Letter to the Editor, , (Am J Clin Nutr 2000;;71:844-53. pp 851-853)
25 B. Carl J Johnson, M.D., Donald R. Peterson, M.D., Elizabeth K. Smith, PhD, Myocardial tissue concentrations of magnesium and potassium in men dying suddenly from ischemic heart disease, (Am J Clin Nutr 32: MAY 1979, pp 967-970)
29 B. Geeta Sharma and Charles f Stevens, A mutation that alters magnesium block of N-methyl-D-aspartate receptor channels, Pub: Proceedings of the National Academy of Sciences of The United States 93.n17 (August 20, 1996): pp9259+. InfoTrac General Science Collection.
30 B. Beasley R, Aldington S, Magnesium in the treatment of asthma..Medical Research Institute of New Zealand, Wellington, New Zealand., Richard.Beasley@mrinz.ac.nz, Curr Opin Allergy Clin Immunol. 2007 Feb;7(1):107-1
32 B. Maged M. Costantine, MD, Steven J. Weiner, MS, Effects of Antenatal exposure to Magnesium Sulfate on Neuroprotection and Mortality in Preterm Infants: A Meta Analysis, Obstet Gynecol. 2009 August; 114(2 Pt 1): 354-364 DOI:10.1097/AOG0b013e3181ae98c2
33 B. Burton M. Altura, Bella T. Altura and Anthony Carella., Magnesium deficiency-induced spasms of umbilical vessels: relation to preeclampsia, hypertension, growth retardation. Pub:Science, 221 (July 22, 1983): pp376(2)
34 B. Burton M. Altura, Bella T. Altura, Asefa Gebrewold, Harmut Ising and Theo Gunther, Magnesium deficiency and hypertension: correlation between magnesium-deficient diets and microcirculatory changes in situ.,. Pub: Science, 223.(March 23, 1984): pp1315(3).
37 B. [ahavaus.com/site/dead_sea_wonders.html] Line of skin care products containing magnesium.
42 B. Magnesium intake from food and supplements is associated with bone mineral density in healthy older white subjects. (elderly health), Kathryn M. Ryder, Ronald I Shorr, Andrew J. Bush, Tamara Harris, Katie Stone and Frances A Tylavsky. Journal of the American Geriatrics Society, 53.11 (Nove 2005): p1875-1881. Academic One File. Web. 13 Dec. 2010
43 B. DASH Diet May Cut Heart Disease Risk, – source John Hopkins Medicine, Today’s Dietitian, Vol . 12, No. 10, Oct. 2010, p 25
44 B. Christine Feillet-Coudray, Charles Coudray, Zjean-Claude Tressol, Denise Pepin, Andrzej Mazur, Steven A Abrams, Exchangeable magnesium pool masses in healthy women: effects of magnesium supplementation, Yves Rayssiguier, Am J Clin Nutr 2002;75;72-8
45 B. [.highbeam.com/doc/1P3-2180507851.html] “Researchers Identify Protein that Regulates Magnesium and Can Restart Stem Cells.” Targeted News Service. Targeted News Service LLC. 2010. HighBeam Research. 16 Feb. 2011 . “An international team led by researchers at the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School has published new findings that demonstrate how a specific protein controls the body’s ability to balance magnesium levels. Magnesium is an essential element for good health and is critical to more than 300 biochemical reactions that occur in the body. “Currently more than half of the US population does not consume an adequate amount of magnesium in their diet,” said Alexey G. Ryazanov, Ph.D., one of the study’s authors and a professor of pharmacology and member of The Cancer Institute of New Jersey at UMDNJ-Robert Wood Johnson Medical School. “Magnesium deficiency may be associated with many medical disorders including hypertension, atherosclerosis, anxiety, asthma and a host of other disorders.” “The team of researchers from the United States, France and Poland demonstrated for the first time that a protein called TRPM7 plays a key role in the maintenance of magnesium homeostasis (balance within the body) and is essential for proliferation of embryonic stem cells.”
77 B. Neuromed Phamaceuticals and Merck and Co., Inc. Announce Agreement for Novel N-type Calcium channel Compounds, from Business Wire, March 20, 2006, High Beam Research – **Neuromed is a pharmaceutical company focusing on calcium channel blockers. “blocking pain signaling through the N-type calcium channel is a novel approach for the treatment of pain” said Christopher Gallen,MD, PhD, President and Chief Executive Officer of Neuromed. **Providing adequate magnesium would be a less novel way to block nerve pain caused by overexcitation by excess calcium. Citation #9 demonstrated that diabetic neuropathy pain could be reduced by magnesium injection alone – why bother with the opioid or the synthetic calcium channel blocker. They are an expensive and dangerous class of pharmaceuticals that would be pretty much not necessary if we weren’t being drained of magnesium reserves by excessive calcium and acidity intakes.
95 B [also 3/PPI article].     [jasn.asnjournals.org/content/20/11/2291.long]  Kevin J. Martin,  Esther A. González and Eduardo Slatopolsky, Clinical Consequences and Management of Hypomagnesemia,  doi: 10.1681/ASN.2007111194 (JASN November 1, 2009 vol. 20 no. 11 2291-2295)
96 B.    [.ncbi.nlm.nih.gov/pmc/articles/PMC2639130/?tool=pubmed] Karl T. Weber, William B. Weglicki, and Robert U. Simpson, Macro- and micronutrient dyshomeostasis in the adverse structural remodelling of myocardium,  (Cardiovasc Res. 2009 February 15; 81(3): 500–508.) Published online 2008 October 3. doi: [10.1093/cvr/cvn261].