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Our Tarot Reader On The Antagonistic Effects Of Magnesium On Calcium

Discussion in 'Magnesium' started by Amazoniac, Nov 1, 2017.

  1. haidut

    haidut Member

    Mar 18, 2013
    USA / Europe
    When I used it as supplement, I make magnesium bicarbonate. It seems to be the least irritating and never causes laxative effect for me.
  2. robknob

    robknob Member

    Feb 1, 2016
    St Louis
    It would be interesting to compare to sodium bicarb, but I find the taste of that stuff apPauling, Linus (Is that a good quip?). I think I remember a few others on the forum had similar misgivings avec mag bicarb. Ive been taking mag citrate w/ no sides, but looking at malate now thanks to your suggestion. The only acetate I could find on ebay was a lab chemical named magnesium acetate tetrahydrate, any info on that is welcome.
  3. robknob

    robknob Member

    Feb 1, 2016
    St Louis
    On Mag acetate tetrahydrate:


    "Magnesium acetate tetrahydrate is a hydrated form of anhydrous magnesium acetate salt with the chemical formula of Mg(CH3COO)2 • 4H2O. As a salt form of magnesium, magnesium acetateis one of the bioavailable forms of magnesium and forms a very water soluble compound. Magnesium is an essential element and second most abundant cation in the body that plays a key role in maintaining normal cellular function such as production of ATP and efficient enzyme activity. Magnesium acetate tetrahydrate can be used as an electrolyte supplementation or a reagent in molecular biology experiments."
  4. OP

    Amazoniac Member

    Sep 10, 2014
    - Albion's magnesium malate provide two magnesium atoms per molecule, which minimizes the acid exposure a bit.

    - The only trouble with magnesium gluconate is that it would be hard to fit into a capsule, other than that I'm not aware of downsides.
    I don't think you can't fake reviews any further than that, but I'm posting just to show how little magnesium you'll get per capsule.

    - paymanz trained the forum during a bootcamp on magnesium acetate preparation from its hydroxide. I'm not sure if some is left unreacted, and vinegar is more than just acetic acid, so you'll be getting unnecessary stuff along. But there's an advantage which is knowing how much acid you're ingesting when you prepare it on your own. There should be videos on Youtube if you search for "magnesium hydroxide" and "acetic acid"; or "milk of magnesia" and "vinegar".
  5. OP

    Amazoniac Member

    Sep 10, 2014
    I was thinking that when magnesium is combined with organic acids, there's a possibility that they could enhance the absorption of contaminants. I already posted that malic acid can chelate aluminium, but the reaction can occur before digestion, picking up metals and shoving them inside. If I'm not wrong, I think I read some concerns about this elsewhere. Perhaps the same thing can occur with lead:

    Influence of dietary factors on the gastrointestinal absorption of lead - ScienceDirect

    "Sodium citrate and citric acid are added to many kinds of foods for a variety of reasons (Furia, 1968). Citrate also occurs naturally in foods and plays a role in several biochemical systems. In this investigation, it was found that both sodium citrate and orange juice, a source of citric acid, increased GI absorption of lead. It is common knowledge that lead poisoning can occur as a result of storing acidic beverages in pottery coated with lead-containing glazes (Klein et al., 1970). The enhancement of lead absorption by sodium citrate and orange juice should be distinguished from the ability of acidic solutions to leach lead from lead-containing pottery glazes. Both factors may contribute to the health hazards associated with the storage of acidic fruit juices in improperly glazed vessels."
    Nutrition of lead - ScienceDirect

    "Since all soil contains lead, there is no lead-free food; a natural level of lead exists in food according to natural levels in the soil. The main source of contamination of soil is aerial deposition, the aspect which has received the greatest attention in recent years being the emissions of motor vehicles derived from the use of leaded fuels. Other sources, such as mining, may also contribute to lead in the atmosphere, lead levels in soil and air being highest in areas of high industrialization (Schulter and Egan. 1976; Underwood, 1971)."

    "Lead paint on walls, woodwork and toys, lead glazes on ceramics, and pewter containers may all contribute to the total lead intake and to the possibility of lead poisoning (Arrow, 1976). Infants and children between the ages of 1 and 6 years have been the main victims of lead poisoning, chiefly from the ingestion of flaking paint (pica) from old houses and apartments (Mahaffey, 1981; Lin-fu, 1970). whereas exposure in adults is often associated with the consumption of moonshine whiskey made in lead-contaminated stills (Conrad and Barton. 1978)."

    "Nutritional factors are thought to play an important role in lead poisoning (Mahaffey, 1981). Studies in animals have shown that certain substances bind lead and increase its solubility, thus enhancing its absorption. These dietary components consist of sodium citrate, ascorbate, amino acids (Kehoe, 1961), vitamin D (Smith et al., 1978; Barton et al., 1980), protein and fat (Barltrop and Khoo, 1976) and lactose [no one is ingesting isolated lactose, milk is inhibitory for the most part] (Bushnell and DeLuca, 198 1, 1982; Nutr. Rev., 1982; Stephens and Waldron, 1975). Nutritional iron deficiency and during rapid periods of growth (infancy) in laboratory animals also enhances lead absorption and promotes lead toxicity, thereby giving concern that pregnant women and young children may be more susceptible to dietary lead (Mahaffey, 1981). Iron (Barton et al., 1978a; Flanagan et al., 1979; Flanagan et al., 1982), zinc (Cerklewski and Forbes, 1976), calcium (Barton et al., 1978b), phosphorus, ethanol and magnesium decrease the absorption of lead without affecting its solubility, probably by competing for shared absorptive receptors in the intestinal mucosa (Conrad and Barton, 1978)."

    "The total bodily amount of lead does not affect lead absorption. Thus, lead does not have a feedback mechanism which limits absorption."

    "Kehoe (1976) performed a long-term balance study with chemical lead determinations. Their data suggest that under ordinary circumstances in eating food and beverages containing customary amounts of lead (0.1-0.4 mg/day), only 5% (food lead) to 10% (water-soluble lead) of the lead is absorbed. Rabinowitz et al. (1976) showed that the average absorption of stable lead tracers from food over a period of 124 days varied from 6.5 to 13.7% in five adult males."

    "Barltrop and Khoo (1976) observed that the level of dietary fat had an influence on lead absorption. They showed that lead absorption is dependent upon both the quantity and type of dietary fat. Their work pointed out that by increasing the corn oil content from 5 to 40% of a diet, this resulted in a 7-14-fold increase in the lead content of several tissues. It has also been observed that lecithin when mixed with bile salts and choline (type of dietary fat) increased lead uptake (Mahaffey. 1981)."

    "Shields and Mitchell (1941) showed that lowering the calcium and/or phosphorus intake could increase the lead content of bone or soft tissue at low levels of lead intake (32 ppm). These workers also observed that the influence of calcium intake on lead metabolism was seen primarily at low levels of calcium intake; increasing dietary calcium to high levels, 1.1% of the diet, did not decrease tissue stores of lead below those found on a normal calcium diet (Mahaffey and Rader, 1980)."
    "A reduction of dietary calcium to approximately 40-50% of the dietary recommendation was necessary before increases in tissue lead content occurred (Mahaffey et al., 1973; Hsu et al., 1975)."
    "Vitamin D appears to play a role in this as well. In animals low in vitamin D, less lead is absorbed; this implies a competitive interaction between the two divalent cations. Both lead absorption and calcium absorption are stimulated by 1.25-dihydroxycholecalciferol, but this occurs primarily in the distal small intestine for lead and in the duodenum for calcium (Smith et al., 1978; Barton et al., 1978b: Mahaffey et al., 1979: Frolik and DeLuca, 1971)."

    "Rats were found more sensitive to lead intoxication if they were iron deficient (Mahaffey-Six and Goyer, 1972). Iron-deficient (not severe) rats also had increased concentrations of lead in kidney and bone compared with rats ingesting equivalent amounts of water containing 200ppm lead and an iron-adequate diet (Mahaffey, 1981; Mahaffey-Six and Goyer, 1972)."

    "Recent work (Levander et al., 1980) suggests that lipid peroxidation plays a vital role for increased sphericity of erythrocytes from vitamin E-deficient rats and that a couple of different mechanisms are considered for the increase in toxicity of lead poisoning. Lead could react with certain membrane components, such as the phosphate groups of phospholipids, to disrupt the structure of the lipid bilayer, thus rendering the polyunsaturated fatty acids more susceptible to peroxidative attack (Levander et al., 1980). Lead is also known to be a weak catalyst of lipid peroxidation and could therefore promote loss of structural integrity."​
  6. OP

    Amazoniac Member

    Sep 10, 2014
    ..and probably the contaminants in magnesium supplements as well.
  7. Dave Clark

    Dave Clark Member

    Jun 2, 2017
    Did you make it using the milk of magnesia formula, re-acting it with carbonated water, etc.?
  8. haidut

    haidut Member

    Mar 18, 2013
    USA / Europe
    Yes, I bought the Milk of Magnesia from the local CVS and mixed with club soda.
  9. OP

    Amazoniac Member

    Sep 10, 2014
    It would be impractical to fix these, but I'm saving just in case.


    that large amounts of calcium are

    required for strong bones, to calm

    nerves and for other characteristics

    of good health. Some nutritionists

    recommend up to three grams of

    calcium a day to prevent calcium

    deficiency. The purpose of this

    editorial is to review some aspects

    of Human Evolution, Physiology,

    Biochemistry and Dietary Habits in

    order to clarify calcium requirements

    and its close relationship to intake of

    other nutrients, mainly magnesium.


    Over the past 6000 years or more man evolved in a magnesium and

    potassium-rich, but calcium and sodium-poor, environment. For survival, the

    human body had to develop efficient conserving mechanisms for sodium and

    calcium. To conserve sodium, the Zona Glomerulosa of the Adrenal Cortex secretes

    a very potent mineralocorticoid, Aldosterone, which increases sodium retention

    via the kidney27. To conserve calcium, the skin developed a synthetic process

    that manufactures Vitamin D3 from a cholesterol derivative, under the influence

    of solar ultraviolet radiation. Vitamin D3 is then hydroxylated by the liver to

    25-OH-D3. The kidney is the site of the most important step: 1-hydroxylation

    of 25-OH-D3 to generate 1, 25 (OH)2 D3, the most potent calcium-conserving

    substance16. It increases calcium and phosphate absorption in the small intestine

    and decreases calcium excretion in the urine:


    The 1-hydroxylase is located in the kidney as a mitochondrial enzyme. It is sensitive

    to intramitochondrial calcium and phosphate. Intromitochondrial accumulation

    of both calcium and phosphate depress the activity of 1-hydroxylase, thereby

    decreasing formation of 1, 25 (OH)2 D322. A low phosphate diet increases and a

    high phosphate diet depresses 1, 25 (OH)2 D3 production20.

    Besides 1, 25 (OH)2 D3, there are two hormones that play an important role in

    calcium metabolism: Calcitonin (CT) and Parathyroid Hormone (PTH)3. Both

    hormones are sensitive to serum ionized calcium levels. An increase in serum

    ionized calcium results in stimulation of CT secretion and suppression of PTH

    secretion. CT and PTH regulate skeletal turnover of calcium and availability

    of cytoplasmic calcium3. The major skeletal effect of PTH is to increase bone

    resorption by stimulating osteoclasts, thereby increasing mobilization of calcium

    from bone. PTH also favors cellular uptake of calcium by soft tissues and

    phosphate excretion by the kidney. CT has the opposite effect, that is, it increases

    deposition of calcium in the bone matrix and blocks cellular uptake of calcium by

    soft tissues. Magnesium suppresses PTH and stimulates CT secretion28, therefore

    favoring deposition of calcium in the bone and removal of calcium from soft

    tissues. Furthermore magnesium enhances calcium absorption and retention5, 12,

    whereas increasing calcium intake suppresses magnesium absorption2, 25.


    Calcium and magnesium are often antagonistic in their effect of biological

    reactions7. For example, the biosynthesis of both phospholipids and proteins

    involve enzymatic steps which have an obligatory requirement for magnesium

    and are calcium-inhibited. The glycolytic pathway contains five enzymatic

    reactions that have an absolute requirement for magnesium and require optimal

    magnesium/calcium ratio for peak performance.

    In order for the cell to maintain the proper magnesium/calcium ratio, several

    levels of regulation are available, acting on the removal of calcium from the

    cytoplasm. One such mechanism is the ATP-dependant calcium pump in the cell

    membrane9, 10. The other important mechanism is the transport of calcium inside

    the mitochondria. The mitochondria uptake of calcium is reversible if calcium

    concentrations in the microenvironment are kept below certain limits. Above

    these limits, calcification of mitochondria occurs with subsequent cellular death.

    In the presence of magnesium, the uptake of calcium by mitochondria can be

    slowed down. Since ATP utilization is magnesium-dependent, it becomes obvious

    that the calcium pump at the cell membrane is also magnesium-dependent. The

    generation of ATP itself through the glycolytic pathway is in part magnesium-

    dependent and inhibited by calcium.


    Stable civilizations have arisen only when primitive hunting communities have

    learned to cultivate cereals, such as wheat, rice maize, millets, barley, oats and

    rye. In many rural areas, cereals provide more than 70% of the energy consumed9.

    Table I shows the magnesium and calcium concentrations in these staple foods.

    They contain two to eight times more magnesium than calcium, and as much

    as one thousand milligrams of magnesium could be consumed if two thousand

    calories were obtained from these sources. One may argue that dairy products

    contributed to most of the ingested calcium. This is unlikely since 50% of individuals

    tested so far show allergic reactions to dairy products and lactose intolerance is

    common in most ethnic groups, occurring in 70% of Black Americans and over

    70% of Orientals, Jews, Arabs, Greeks, Japanese, Eskimos, Indians, Africans and

    Asians23, 17, 13, 14, 15, 1, 24, 18, 8, 19 ,30, 31.

    Considering that 99% of the total body calcium is located in the bones, it is not

    surprising that academic proponents of high calcium intake have used as an

    argument the possible role of calcium deficiency in osteoporosis11, 4, 29. There is

    no evidence, however, to support this view. Osteoporosis is not more common

    in those parts of Asia and Africa where diets are relatively low in calcium

    (300-500 mg/day) than in Europe and North America where consumption of

    dairy products contributes to more than 1000 mg of calcium/day When patients

    with severe osteoporosis were given massive doses of calcium they went into

    positive calcium balance, but radiographic studies revealed no changes in the

    osteoporotic process. Where did that calcium go? Obviously into the soft tissues

    where it does not belong.

    Calcium balance studies have indicated that man can adapt to relatively

    low calcium intake by increasing calcium absorption and decreasing

    urinary excretion10. There is not such a mechanism for magnesium26. The

    adaptation to low calcium intake is most likely via synthesis of 1, 25 (OH)2

    D3 by the kidney. It was previously discussed that high intramitochondrial

    concentrations of phosphate and calcium in the kidney suppress the formation of

    1, 25 (OH)2 D320, 22. Therefore, mechanisms that increase intracellular and

    intramitochondrial calcium would prevent adaptation to low calcium intake.

    Failure of the calcium-pump at the cell membrane and increased uptake of

    calcium by mitochondria are two such mechanisms which are both magnesium-

    dependent as previously discussed. Since a low phosphate diet increases

    formation of 1, 25 (OH)2 D320 and a high magnesium diet would keep calcium

    out of the mitochondria, it seems therefore that one approach to improving the

    adaptation to low calcium intake is to ingest a diet low in phosphate and high

    in magnesium. Such an approach to the management of osteoporosis would

    seem more appropriate than the ingestion of massive doses of calcium. The latter

    approach blocks magnesium absorption and creates a magnesium deficiency,

    conducive to a failure of the calcium- pump and intracellular accumulation of

    calcium in soft tissues that eventually leads to irreversible cell damage. Also,

    magnesium deficiency results in elevated PTH which prevents the utilization of

    the absorbed calcium for bone formation and favors soft tissue calcification.

    Recent studies suggest that calcium requirements are increased by acid-ash,

    high- protein and high sulfur diet21. In order to increase the efficiency of the

    adaptation mechanism to low calcium intake, every attempt should be made to

    ingest foods containing a magnesium/calcium ratio of two or more, with neutral

    or alkaline ash, not excessive in phosphate, sulfur, proteins, refined sugar, fats and

    other substances that drain the body of both calcium and magnesium. Magnesium

    deficiency causes a reduced intestinal absorption of calcium and decreased

    serum ionized calcium. Magnesium has a calcium-sparing effect and decreases

    the need for calcium.

    Since magnesium suppresses PTH and increases CT, adequate magnesium intake

    would improve the phosphorous balance from a low phosphate diet by increasing

    phosphate absorption via the 1, 25 (OH)2 D3 mechanisms and by preventing the

    PTH induced phosphaturia. Furthermore, a high magnesium intake would enhance

    calcium absorption by the 1, 25 (OH)2 D3 mechanisms, increase serum ionized

    calcium, promote deposition of calcium in the bone matrix where it belongs and

    minimize cellular uptake and mitochondrial accumulation of calcium. With such an

    approach there would be no need for pharmaceutical companies to develop new

    and improved calcium blockers in the management of cardiovascular diseases,

    since magnesium works naturally to produce the same end result. ■


    Guy E. Abraham, MD, is a former professor of Obstetrics and, Gynecology, at the UCLA

    School of Medicine. Some 45 years ago, he pioneered the development of assays to measure

    minute quantities of steroid hormones in biological fluids. His contributions have been

    acknowledged with several awards: General Diagnostic Award from Canadian Association of

    Clinical Chemist, 1974; the Medaille d’Honneur from the University of Liegc, Belgium, 1976;

    the Senior Investigator Award of Pharmacia Sweden, 1980.

    Some 30 years ago Dr. Abraham developed a magnesium emphasized nutritional program

    for women with premenstrual tension syndrome and post-menopausal osteoporosis. This

    magnesium emphasized program is currently part of the nutritional management of PMS and

    osteoporosis of many gynecologists. In 2000 he initiated the Iodine Project, a reevaluation

    of the role of the essential element iodine in medical practice. In order to better understand

    iodine metabolism, he developed a simple technique to measure iodide and other halides in

    biological fluids. Ten years ago, he introduced the concept of Orthoiodosupplementation,

    that is, iodine supplementation for whole body sufficiency, based on an iodine/iodide test

    that he developed. He is currently involved in research on the effects of negatively charged

    electrolyzed water on aging and degenerative disease.


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