Never Calcium Without Magnesium

January 17, 2008

Calcium tablets as monotherapy increase the risk of blood clots in the heart and brain.

Last year, the British Medical Journal in their web version published a scientific article with the above-mentioned gloomy message.

1,471 healthy women over 55 years were randomly divided into two groups, one with 732, who took a supplement of calcium citrate for 5 years and a group of 739 who took placebo.

During these five years, they were examined every six months, and for each year, the distance between the two groups increased with statistic significance.

It was found that in the group who took calcium tablets, there was a significant increase in the risk of blood clots in both the brain and the heart.

The authors are surprised by the result and have reservations until the matter has been investigated further with more studies.

But do we have to wait five years for a new study of this result?

Is not it predictable?

Most people who have experience with the use of minerals for disease prevention are well aware that you should never take calcium without taking magnesium at the same time.

Magnesium is the key
(If you think it becomes too biochemical, then just read the conclusion at the end).
Magnesium sits like a bolt in the calcium channel of the cell membrane.

The moment calcium wants to enter a cell, magnesium closes the door and when calcium wants leave the cell, magnesium will open up. It’s the opposite in bone cells.

Therefore, the cells in the soft tissues are almost empty of calcium. The calcium concentration outside of a cell is about 10,000 times as high as within a cell. Thanks to magnesium.

If we lack magnesium, the calcium channels will open.

This means that through the open calcium channels, calcium flows into the cells, causing the cell to cramp and, in the long term, (hours) destroy its mitochondria.

The cramp causes immediate contraction of the blood vessels due to the smooth muscle cells around the small arteries, resulting in increasing blood pressure and risk of brain hemorrhage and destruction of calcification plaque and thus risking a blood clot in the heart. At the same time, the energy production of the cell is minimized due to the destruction of the energy-producing mitochondria with their vital content of coenzyme Q10.

This not only results in less energy production in the cells, but also a smaller consumption of oxygen absorbed in the cell, which in turn means that a greater proportion of this oxygen are then used to produce harmful free radicals, IF there is iron present as a catalyst for this process, and this is precisely the case in this group of women who no longer menstruate.

Then the roulette runs with destruction of the cell membrane and the surrounding cells from within, because now the cell has suddenly had its own little “Chernobyl meltdown”.

If we lack magnesium, we have no control over the distribution of calcium, and it is distributed more or less evenly throughout the cell phase, ie. both in bone cells and in soft tissue cells, muscle cells, skin cells, connective tissues, etc.

But are we lacking magnesium?
Yes we are. More than 70% of the population do not even get the recommended daily allowance of 300 mg of magnesium.

Why not?

The food has gradually become more and more low in magnesium. In part, the industrialization of the diet has resulted in a large loss of magnesium in the finished product, and we eat less vegetables where we find this magnesium and when we cook the vegetables, we pour the magnesium out with the boiling water.

Furthermore, many elderly people loses magnesium because they take diuretic medicine or because they drink too much coffee.

70% of research participants with low intracellular magnesium are more than sufficient to explain the significant increased risk associated with calcium intake as monotherapy.

There is therefore no surprise in the achieved result, and it should not be necessary to wait a lot of years to take extra magnesium along with ones calcium supplement. This will not only benefit muscles, heart, brain and bones, but also a variety of processes in the body that rely on the more than 300 enzymes for which magnesium is required.

So: Never take calcium without magnesium!

By: Claus Hancke, M.D.

 

References

Horne, Ruth Ames, Gregory D Gamble, Andrew Grey and Ian R Reid
Mark J Bolland, P Alan Barber, Robert N Doughty, Barbara Mason, Anne
Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial
BMJ published online 15 Jan 2008;doi:10.1136/bmj.39440.525752.BE

Calcium supplements with vitamin D against colon cancer?

February 18, 2006

A large study attempted to show whether or not calcium and vitamin D prevent colon cancer. It was a strange study, using low doses over a short period.

There are probably those who believe that the latest study on calcium and vitamin D shows that neither is good for anything. But we should hesitate before going to that extreme. One can also believe that the study was not suited to draw this conclusion. Or, as it is stated in a leading editorial in “The New England Journal of Medicine:” the conclusion should be interpreted in light of the study was complicated and in light of the probability that the doses of calcium and vitamin D were too low.

The debate regards the insidious and widespread cancers of the colon and rectum. Half of a group of 36,282 American women between the ages of 50 and 79 took part in a seven year study where they received daily supplements of 1,000 mg calcium and 400 units vitamin D to see if reduced their risk of these diseases. The supplements given are the same as two normal calcium and vitamin D vitamin tablets, which many take to strengthen their bones. After the seven years the researchers assessed the number of women who developed colon and rectum cancer. The result was disheartening: Whether the women received supplements or placebo had not effect on the risk.

There was a single positive find buried in the data. The women who had the least vitamin D in their blood during the study had with statistical certainty the greatest probability of developing colon cancer. This could indicate that vitamin D has a positive effect. There was also a tendency, but only a tendency, that these women had the greatest benefit from the supplements.

Quite a lot of things contribute to that this conclusion be taken with a grain of salt. This is partially due to that the study was very complex.

Possibly the most important objection is that it “only” lasted seven years. It is believed that colon cancer takes 10-20 years to develop before it is diagnosed. It the supplements prevent a new cancer from forming it is clear that for this reason no effects will be found as early as after seven years. This has been considered: Participants in the study will be monitored further for the next five years.

Strong objections
If the goal was to show a difference within the seven year period, those responsible should have at least ended the study by examining the intestines of all of the participants in order to find early cancer stages, or polyps. This did not occur. There was neither the money nor the resources necessary to do over 35,000 intestinal examinations. It was only possible to establish that the number of independently undertaken intestinal exams and the number of discovered cancers in the two groups were about the same. But maybe nothing more can be expected.

One confusing detail is that the study participants were allowed to continue taking the supplements that they had taken before the study along with the supplements that they received as a part of the study. On average they received 1,100 mg calcium and 350 units vitamin D, both close to the recommended dosages, before the study began. Many of them therefore must have received very large doses of calcium, over 2,000 mg, per day. Is it reasonable to guess that this is the reason for the slightly increased frequency of self-reported kidney stones? 2.4% of those who received supplements and 2.1% of those who received placebo, got kidney stones during the seven years.

Also, the average age was relatively low (62), which reduced the risk of cancer, and therefore weakened the study. It was further weakened by the fact that more than one out of four participants did not finish the study. Whether this dropout rate is because calcium pills can cause constipation is not considered in the article.

Just as important, the dose of vitamin D, as referred to in the editorial, may have been too low. Recently it has been estimated that about 1,000 units daily is necessary for most people in order to achieve any supposed cancer preventing effect. This amount of vitamin D (or more accurately 25-(OH)-vitamin D) is necessary to achieve a serum concentration of over 30 nano-grams per litre (75 nanomols per millilitre). Nevertheless, only a minority of the study participants received this amount.

What can be concluded from this? The editorial gives some suggestions for new studies. Much indicates that vitamin D, and maybe calcium, prevents cancer. But we still lack sufficient knowledge.

By: Vitality Council

References:
1. Wactawski-Wende J et al. Calcium plus vitamin D supplementation and the risk of colorectal cancer. N Engl J Med 2006;354:684-96.
2. Forman M C et al. Calcium plus vitamin D3 supplementation and colorectal cancer in women. N Engl J Med 2006;354:752-4.
3. Garland C F et al. The role of vitamin D in cancer prevention. Am J Publ Health 2006;96:9-18.

Calcium, Research references

January 1999

1. Adams P, Davies GT, Sweetnam P. Osteoporosis and the effects of aging on bone mass in elderly men and women. J Med New Series 39: 601-615, 1970.
2. Angus RM, Sambrook PN, Pocock NA, Eisman JA. Dietary intake and bone mineral density. Bone Miner 4: 265-277, 1988.
3. Arnaud, DC, Sanchez, SD. Calcium and phosphorous. Present knowledge in nutrition. 6th edn. Washington DC: Nutrition Foundation. p 212-221, 371-373, 1990.
4. Arnaud CD, Sanchez SD. The role of calcium in osteoporosis. Ann Rev Nutr 10: 397-414, 1990.
5. Bhat KS. Plasma calcium and trace minerals in human subjects with mature cataract. Nutr Rep Int 37:157-63, 1988.
6. Calcium pantothenate in arthritic conditions. A report from the General Practitioner Research Group. Practitioner 224: 208-11, 1980.
7. Chu lY, Margen S, Costa FM. Studies in calcium metabolism. Am J Clin Nutr 28: 1028-1035, 1975.
8. Cook J, Dassenko S, Whittaker P. Calcium supplementation. Effect on iron absorption. Am J Clin Nutr 53: 106-111, 1991.
9. Dawson-Hughes B, Jacques P, Shipp C. Dietary calcium intake and bone loss from the spine in healthy postmenopausal women. Am J Clin Nutr 46: 685-687, 1987.
10. Desai S, Baran D, Grimes J et al. Relationship of diet, axial, and appendicular bone mass in normal premenopausal women. Am J Med Sci 293: 218-220, 1987.
11. Elders PJ, Netelenbos JC, Lips P et al. Perimenopausal bone mass and risk factors. Bone Miner 7: 289-299, 1989.
12. Ettinger, B. Role of Calcium in Preserving the Skeletal Health of Aging Women; Southern Medical Journal,  85; (8); 2S22-30, Aug. 1992.
13. Fletcher MP et al. Nutrition and immunology. New York: Alan R. Liss. p 215-239, 1988.
14. Freudenheim JL, Johnson NE, Smith EL. Relationships between usual nutrient intake and bone-mineral content of women 35-65 years of age. Longitudinal and cross-sectional analysis. Am J Clin Nutr 44: 863-876, 1986.
15. Garn SM, Rohmann CG, Wagner B. Continuing bone growth through life. A general phenomenon. Fed Proc 26: 1729-1736, 1967.
16. Goldman L. Treatment of subacute and chronic discoid lupus erythematosus with intensive calcium pantothenate therapy. J Invest Dermatol 11: 95, 1948.
17. Hallberg L, Brune M, Erlandsson M et al. Calcium. Effect of different amounts on nonheme- and heme-iron absorption in humans. Am J Clin Nutr 53: 112-119, 1991.
18. Heaney RP, Recker RR, Saville PD. Calcium balance and calcium requirements in middle-aged women. J Lab Clin Med 92: 964-70, 953-963, 1978.
19. Jowsey J. Osteoporosis. dealing with a crippling bone disease of the elderly. Geriatrics 32: 41-50, 1977.
20. Kanis JA, Passmore R. Calcium supplementation of the diet – I. Br Med J 298: 137-140, 1989.
21. Kanis JA, Passmore R. Calcium supplementation of the diet II. Br Med J 298: 205-208, 1989.
22. Kanders B, Dempster DW, Lindsay R. Interaction of calcium nutrition and physical activity on bone mass in young women. J Bone Miner Res 1988; 3: 145-149.
23. Laval-Jeanet AM, Paul G, Bergot C et al. Correlation between vertebral bone density measurement and nutritional status. In: Proceedings – osteoporosis. Glostrup: Glostrup Hospital. p 953-963, 1984.
24. Linkswiler HM, Joyce CL, Anand CR. Calcium retention of young adult males as affected by level of protein & of calcium intake. Trans NY Acad Sci 36: 333-340, 1974.
25. Mazess RB, Barden HS. Bone density in premenopausal women: Effects of age, dietary intake, physical activity, smoking, and birth-control pills. Am J Clin Nutr 53: 132-142, 1991.
26. New england – Heany, R.P.: Thinking straight about Calcium; New England Journal of Medicine; 328, ss. 503, 1993.
27. Nilas L, Christiansen C, Rodbro P. Calcium supplementation and postmenopausal bone loss. Br Med J 1984; 289: 1103-1106, 1984.
28. Nordin BE, Polley KJ. Metabolic consequences of the menopause. A cross-sectional, longitudinal, and intervention study on 557 normal postmenopausal women. Calcif Tissue Int 41: 1-59, 1987.
29. Penland JG and Johnson PE, Dietary Calcium and Manganese Effects on Menstrual  Cycle Symptoms, Am J Obstet Gynecol 168; 1417-23, 1993.
30. Riggs BL, Wahner HW, Melton LJ 3rd et al. Dietary calcium intake and rates of bone loss in  women. J Clin Invest 80: 979-982, 1987.
31. Riis B, Thomsen K, Christiansen C. Does calcium supplementation prevent post menopausal bone loss? A double-blind, controlled clinical study. New Eng J Med 316: 173-177, 1987.
32. Sowers MR, Wallace RB, Lemke JH. Correlates of forearm bone mass among women during maximal bone mineralization. Prev Med 14: 585-596, 1985.
33. Sowers MR, Wallace RB, Lemke JH. Correlates of mid-radius bone density among postmenopausal women. A community study. Am J Clin Nutr 41: 1045-1053, 1985.
34. Spencer H, Karmer L et al. Effect of a high protein (meat) intake on calcium metabolism in man. Am J Clin Nutr 31: 2167-2180, 1978.
35. Stevenson JC, Whitehead MI, Padwick M et al. Dietary intake of calcium and postmenopausal bone loss. Br Med J 297: 15-17, 1988.
36. Tylavsky FA, Anderson JJ. Dietary factors in bone health of elderly lactoovovegetarian and omnivorous women. B. Am J Clin Nutr 1988; 48: 842-849, 1988.
37. Van Beresteijn EC, van’t Hof MA, de Waard H. Relation of axial bone mass to habitual calcium intake and to cortical bone loss in healthy early postmenopausal women. Bone 11: 7-13, 1990.
38. Webb RC, Bohr DF. Mechanism of membrane stabilization by calcium in vascular smooth muscle. Am J Physiol 235: C227, 1978.
39. Calcium, vitamin D, milk consumption, and hip fractures: a prospective study among postmenopausal women. Diane Feskanich, Walter C Willett, and Graham A Colditz. Am J Clin Nutr 2003;77 504-511 http://www.ajcn.org/cgi/content/abstract/77/2/504

 

Sources
Joseph E. Pizzorno Jr., Michael T. Murrey & Melvyn R. Werbach.