Ca – Calcium is found in igneous rocks at 4 1,500 ppm; shales at 22, 100 ppm; sandstone at 39,000 ppm; limestone at 302,000 ppm; fresh water at 15 ppm; sea water at 400 ppm; soils at 7,000 to 500,000 ppm (lowest in acid soils and highest in limestone or alkaline soils); marine plants 10,000 to at 300,000 ppm (highest in calcareous tissues – red, blue-green and green algae and diatoms); land plants 18,000 ppm; marine animals 1,500 to 20,000 ppm; 350,000 ppm in calcareous tissue (sponges, coral, mollusks, echinoderms); land animals at 200 to 85,000 ppm; 260,000 ppm in mammalian bone, 200 to 500 ppm in soft tissue and < 5 ppm in RBC. Functions include essentiality for all organisms; cell walls of plants; all calcareous tissues and mammalian bones; electrochemical functions in cells and activates several enzymes.
Calcium is the fifth most abundant mineral element in the crust of the Earth and the biosphere and is essential to all earth life forms. There is evidence that clearly shows humans are designed to consume and use HIGH calcium diets. The late Paleolithic Period of 35,000 to 10,000 years ago was the most recent time that our human forebearers lived in the bios for which they had been biochemically designed. The agricultural revolution occurred 10,000 years ago and it reduced the wide variety of wild foods in the human food chain and increased food energy. These changes universally and forever decreased man’s dietary intake of minerals, trace minerals and Rare Earths.
The uncultivated food plants and wild game commonly available to Stone Age humans would supply 1600 mg at basal energy intakes and between 2,000 and 3,000 mg of calcium at the energy levels required to support hunting and work.
During the 20th century, American adults have a calcium intake of only one-fifth to one-third as much as did Stone Age humans. The National Health & Nutrition Examination Survey 11 reported a median calcium intake for American women of between 300 and 508 mg per day and only 680 mg for men.
Other nutrients that are rich in the American diet aggravate the national calcium deficiency. Diets rich in salt and protein (phosphates) result in an increased calcium “cost”, that in effect increases the requirements for calcium. As protein (phosphate) intake is doubled the output in urinary calcium increases 50 %.
There are no less than 147 deficiency diseases that can be attributed to calcium deficiency or imbalances. The most recent clinical research clearly points out that the entire scope of American diets are critically deficient in calcium and that the only practical way to get enough calcium is through supplementation (the allopaths doing the study failed again by recommending five cups of broccoli a day as a valuable source of calcium – try to get a kid or president to eat that!).
The more common calcium deficiency diseases are easy to recognize and run from poor clotting time of the blood when you nick yourself shaving (calcium is a co-factor in the clotting mechanism), arthritis (which the allopaths treat with pain killers), to the well known osteoporosis.
Calcium is the most abundant mineral in the human body, the average male has 1,200 grams and the average female has 1,000 grams ‘ makes up one to two percent of the body weight (water makes up 65 to 75 %) and up to 39 percent of the total mineral reserves of the body (ash); 99% is found in the bones and teeth, the other one percent is found in the blood, extracellular fluids, and within cells where it is a co-factor and activator for numerous enzymes.
Calcium in bones is in the form of hydroxyapatite salts composed of calcium phosphate and calcium carbonate in a classic crystal structure bound to a protein framework (put a chicken “drumstick” bone in vinegar for 10 days and the calcium will be leached leaving a protein matrix). Similar types of hydroxyapatite are found in the enamel and dentin of teeth, however, little is available from teeth to contribute to rapidly available Ca to maintain blood levels.
In addition to being a major structural mineral, Ca is also required for the release of energy from ATP for muscular contraction, blood clotting (ionized Ca stimulates the release of thromboplastin from the platelets, converts prothrombin to thrombin bin -thrombin helps to convert fibrinogen to fibrin – fibrin is the protein web that traps RBC’s to make blood clots); Ca mediates the transport function of cell and organelle membranes; Ca effects the release of neurotransmitters at synaptic junctions; Ca mediates the synthesis, secretion and metabolic effects of hormones and enzymes; Ca helps to regulate the heart beat, muscle tone and muscle receptiveness to nerve stimulation.
Calcium is mainly absorbed in the duodenum, where the environment is still acid. Once the food in the intestine becomes alkaline, absorption drops. Calcium is absorbed from the small intestine by active cellular transport and by simple diffusion Metallic calcium absorption may be limited to 10 percent or less and is affected by many substances in the gut. Calcium may be absorbed in the organically bound plant derived colloidals and in the water-soluble forms.
Lack of vitamin D results in calcium deficiency, as well as deficiency of stomach acid (hypochlorhydria results from a restricted NaCI intake); lactose intolerance, celiac disease, high fat diet and low protein intake and high phytate consumption (phytic acid is a phosphorus containing acid compound found in the bran of grains and seeds as well as in the stems of many plants, especially oatmeal and whole wheat which combine to form calcium phytate which is insoluble and unavailable to humans) all result in calcium deficiency; oxalic acid in rhubarb, spinach, chard and greens combines with Ca to form an insoluble calcium oxalate which is not absorbed; fiber itself, besides the phytate content, prevents calcium absorption; alkaline intestine, gut mobility (too rapid-too much fiber, too much fruit, etc.), pharmaceuticals (anti-seizure drugs, diuretics,etc.) result in decreased absorption and retention; excess of caffeine from coffee, tea, colas, etc. will leach calcium from the bones.
Parathormone secreted by the parathyroid gland and calcitonin secreted by the thyroid gland maintain a serum calcium of 8.5 to 10.5 by drawing on calcium reserves from the bones. The parathormone can also affect the kidney so that it retains more calcium and the gut to be more efficient in absorption; when the blood calcium begins to rise from too much parathyroid activity, calcitonin reduces availability of calcium from the bones.
In 1980, McCarron, et al, theorized that chronic calcium deficiency probably led to hypertension. More than 30 subsequent studies supported the original theory of calcium deficiency as the cause of hypertension, additionally recent studies have shown that serum ionized calcium is consistently lower in humans with untreated hypertension. In a recent review article, Sowers, et al, noted that the association of calcium intake and blood pressure is most clear in people with daily calcium intakes of less than 500 mg a day.
The phenomenon of salt sensitivity consists of a rise in blood pressure and sustained increased in urinary loss of calcium in response to salt consumption. Among black and elderly whites with “essential hypertension”, restricted intakes of calcium and potassium, rather than elevated salt consumption is responsible for salt sensitivity. In a four-year study of 58,218 nurses, hypertension was more likely to develop in females who took in less than 800 mg of calcium per day.
In a 19-year observational study of 1,954 men, 49 cases of colorectal cancer were identified. Analysis of the results showed very clearly that the incidence of colorectal cancer increased 300 % as the calcium intake decreased from 160 mg/ kcal to 24,9 mg/100 kcal of diet.
Up to 75% of consumed Ca is lost in the feces, two percent is lost in the urine and sweat (15 mg per day is lost in normal sweating – this can double or triple in active athletes); in cases of excess urine loss of calcium (osteoporosis, NSH, excess P, etc.) kidney stones, bone spurs and calcium deposits will develop.
Bone spurs and heel spurs and calcium deposits always develop at the sites of insertions of tendons and ligaments during a raging osteoporosis. Bone spurs, heel spurs and calcium deposits can be reversed and eliminated by supplementing with significant amounts of water soluble calcium sources.
Not only are our soils and food deficient in calcium, additionally the American diet is rich in P, which is found in just about everything we eat (NPK fertilizers and food additives).
Calcium is an essential mineral nutrient and the most abundant mineral in the body. Calcium represents approximately 2% of the total body weight; about 98% of this occur in the bones and teeth. The small amount of calcium in body fluids and cells plays an important role in nerve transmission, muscle contraction, heart rhythm, hormone production, wound healing, immunity, blood coagulation maintaining normal blood pressure, and stomach acid production. Calcium promotes blood clotting through the activation of the fibrous protein FIBRIN, the building block of clots. It lowers blood pressure in patients with spontaneous hypertension (not caused by kidney disease) because it relaxes blood vessels, and it may also diminish the symptoms of PMS (premenstrual syndrome).
High intake of saturated fat tends to raise LDL-cholesterol (the less desirable form) and to increase the risk of colorectal cancer. On the other hand, calcium binds saturated fats, preventing their uptake by the intestine; consequently, calcium-rich diets may reduce LDL-cholesterol. A high calcium intake also seems to reduce the risk of colon cancer.
If blood levels of calcium decrease in response to low calcium consumption, the body pulls calcium out of bones to use elsewhere. Thus bones are dynamic tissues, constantly releasing calcium and reabsorbing it to maintain their strength. The level of calcium in the blood is carefully regulated by hormones. Parathyroid hormone from the parathyroid gland stimulates bone-degrading cells to break down bone tissue to release calcium and phosphate into the bloodstream (a process called bone resorption). Parathyroid hormone also stimulates calcium absorption from the intestines by activating vitamin D, and stimulates calcium reabsorption from the kidney filtrate back into blood. This effect is counterbalanced by calcitonin, released from the thyroid gland when blood calcium levels are high. Calcitonin triggers bone-building cells (osteoblasts) to take up calcium from blood to lay down new bone.
During growth spurts more calcium is absorbed than lost. “Growing pains” is another manifestation of a calcium deficiency, since these growth spurts occur in adolescence. Therefore, adequate calcium intake in childhood and adolescence is critical for bone building. In addition, zinc, manganese, fluoride, copper, boron, magnesium, calcium and vitamin D, together with exercise, minimize bone loss after the age of 35. Calcium absorption requires the hormone calcitriol, formed from vitamin D.
An estimated 100 million Americans risk calcium deficiency. They include women who are pregnant or lactating, or who are post-menopausal. The average adult male obtains 75% of the calcium RDA; the average female, 50%. An estimated 87% of adolescent women and 84% of women between the ages of 35 and 50 are calcium deficient. Older people absorb less calcium and the calcium RDA should probably be increased for elderly persons.
Symptoms of prolonged calcium deficiency include insomnia, heart palpitations and muscle spasms, as well as arm and leg numbness. Chronic low calcium intake can lead to easily fractured bones due to bone thinning (osteoporosis), and possibly hypertension. Severe deficiency symptoms are not common: convulsions, dementia, and osteomalacia, rickets (bent bones and stunted growth in children) and periodontal disease.
In addition to age and heredity, many life-style and dietary factors increase the risk of developing calcium related problems: age; heredity; chronic emotional stress; lack of exercise; dieting; excessive caffeine, sodium, phosphorus (as found in processed foods and soft drinks) or dietary fiber; high-fat foods; possibly high protein diets; low vitamin D intake; long-term use of corticosteroids; and cigarette smoking. Conditions like inflammatory bowel syndrome, low stomach acidity, lactose enzyme (lactase) deficiency, kidney failure and diabetes increase the need for calcium, while mineral oil (laxative), lithium carbonate (the water-insoluble form of lithium) and some diuretics (water pills) block calcium uptake. NOTE: The following abstracts are examples of a water-soluble mineral and how it is used effectively by the body and excreted if the body doesn’t need it.
Journal of Clinical Endocrinology and Metabolism
Calcium Bioavailability from Calcium Carbonate and Calcium Citrate
Michael J. Nicar, Charles Y.C. Pak
Section on Mineral Metabolism, Southwestern Medical School, University of Texas Health Science Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75235
ABSTRACT. Fourteen normal subjects took 1000 mg calcium orally as calcium citrate or calcium carbonate. The amount of calcium absorbed was estimated from the rise in urinary calcium. The urinary calcium following Calcium citrate load significantly higher (by 20-66%), whether expressed as the total amount or as the increment above basal (fasting) excretion. Thus, calcium citrate provides a more optimum calcium bioavailability than calcium carbonate.
Food Technology – June 1996
Calcium Citrate: A Revised Look at Calcium Fortification
Rivka Labin-Goldscher and Samuel Edelstein
Calcium, the most abundant mineral in our body, is a major constituent of bone and teeth. This mineral also plays an important role in several physiological systems. Inadequate calcium intake is associated with osteoporosis. Furthermore, recent research implies effects on oral bone loss, colon cancer, and hypertension (Cimming, 1990; Barger-Lux and Heany, 1994).
Since the body does not produce minerals, it is totally dependent on an external supply of calcium, nutritional or supplementary. The importance of adequate calcium intake is recognized during the whole life cycle of the human being: Baby’s growth, quick skeleton development of children and teenagers, achievement of peak bone mass in adults, women at the childbirth age and lactation, and elderly people, especially women at postmenopausal age in danger of osteoporosis. This recognition has led the NIH to revise the recommendations for calcium intake (NIH Consensus Development Panel, 1994).
The new recommended daily allowances for each age group are shown in Table 1. In particular, the daily allowance for adolescents/young adults and elderly people has increased from the previous recommendation of 8001,200 mg/day to 1,500 mg/day.
The basic source for calcium is the diet. Yet, based on normal diet and especially with the increasing trends of using processed food, ready prepared meals, “fast food,” and “TV meals,” only a part of the physiological need for calcium is actually supplied through food consumption (Fleming and Heimbach, 1994). This has led consumers to an awareness of the need for balancing their calcium intake with enriched food or supplements.
Choosing a Calcium Fortifier
Several commercial calcium salts are available to the food manufacturers for calcium fortification, including carbonate, phosphate, citrate, lactate, and gluconate. A responsible manufacturer, producing a successful brand, would consider a calcium additive with high nutritional value and low interference with the absorption of other nutrients in addition to cost effectiveness, kosher certification, and minimal effects on consistency, mouthfeel, and taste of the product.
Two common measures for comparison of the nutritional value of calcium additives are bioavailability and solubility. In this respect, several factors identified lately in research works are to be taken into consideration:
- In general, organic acid salts of calcium are more bioavailable than the inorganic salts.
- The interaction between calcium and phosphate metabolism suggests that excessive phosphate intake would result in low calcium absorption. 21 CFR section No. 101.72 regulates health claims of calcium-enriched food. A prerequisite is that calcium-to-phosphorous ratio will exceed 1:1 on weight basis. Since there are additional phosphates in food, it is recommended to apply other calcium sources to improve calcium-to-phosphate ratio and obtain sufficient calcium absorption.
- Carbonate, although widely used. neutralizes gastric acid and then much of it is excreted undissolved. The relative absorption of calcium from the different calcium sources is dose dependent in the normal dose range. Comparing calcium citrate to calcium carbonate, for instance, suggests a higher absorption of calcium from 0.5 g calcium dose in calcium citrate than from a 2 g calcium dose in calcium carbonate (Harvey et al., 1988).
- Calcium citrate was found to be absorbed regardless of the levels of gastric acid. Therefore, it is highly bioavailable, and does not cause gastrointestinal effect in individuals with low gastric acid secretion (Avioli, 1988; NIH Consensus Development Panel, 1994).
- The solubility model for prediction of bioavailability was found to be a paradigm (Heany et al., 1990). This is in accordance with the finding that there is an absorption mechanism of a calcium citrate complex in addition to the previous postulation of a single absorption mechanism of calcium ions only (Avioli, 1988; NIH Consensus Development Panel, 1994).
- Calcium citrate, as opposed to calcium in general, has only a marginal effect interfering with the absorption of other minerals, especially iron (Hallberg et al., 1992).
- A concern has been raised as to the effect of long-term calcium supplementation on the formation of kidney and urinary duct stones. Calcium citrate has been shown to attenuate this risk since it enhances renal excretion of citrate, an inhibitor for crystallization of stone-forming calcium salts, (Pak, 1994).
Citrate and renal calculi: an update.
Center on Mineral Metabolism and Clinical Research, University of Texas; Southwestern Medical Center at Dallas 75235-8885, USA.
Citrate is an inhibitor of the crystallization of stone-forming calcium salts. Hypocitraturia, frequently encountered in patients with nephrolithiasis, is therefore an important risk factor for stone formation. Potassium citrate provides physiological and physicochemical correction and inhibits new stone formation, not only in hypocitraturic calcium nephrolithiasis but also in uric acid nephrolithiasis. Inhibition of stone recurrence has now been validated by a randomized trial. Ongoing research has disclosed additional causes of hypocitraturia (sodium excess, low intestinal alkali absorption, but not primary citrate malabsorption). Moreover, new insights on potassium citrate action have been shown, notably that some of absorbed citrate escapes oxidation and contributes to the citraturic response, that ingestion with a meal does not sacrifice physiological or physicochemical action, that orange juice mimics but does not completely duplicate its actions, that potassium citrate may have a beneficial bone-sparing effect, that it may reduce stone fragments following ESWL, and that danger of aluminum toxicity is not great in subjects with functioning kidneys. Finally, the research on potassium citrate has led to two promising products, calcium citrate as an optimum calcium supplement and potassium-magnesium citrate which may be superior to potassium citrate in the management of stone disease.
Journal of Bone and Mineral Research 1988 Jun;3(3):253-8
Dose dependency of calcium absorption: a comparison of calcium carbonate and calcium citrate.
Harvey JA, Zobitz MM, Pak CY
Center in Mineral Metabolism and Clinical Research SWMS UTHSCD, Dallas.
Calcium supplementation is recommended as a prophylaxis against bone loss. This study was performed to determine the dose dependency of calcium absorption in an attempt to derive an optimum dose schedule. Using the well-described oral calcium load technique, we measured the calcium absorption from three different calcium doses (0.5, 1.0, and 2.0 g) of both calcium carbonate and calcium citrate administered to 21 normal subjects (4 men and 17 women, 22-60 years). Nine subjects underwent two additional loads with 0.2 g of elemental calcium as calcium carbonate and as calcium citrate. The intestinal calcium absorption from calcium carbonate and calcium citrate was estimated from the rise in urinary calcium following oral ingestion of the respective calcium salt. The increment in urinary calcium post-load, reflective of intestinal calcium absorption, rose rapidly from 0 to 0.5 g calcium loads with only slight subsequent increases from the 0.5 g to 2.0 g calcium doses. Thus, results indicate that 0.5 g of calcium is the optimum dose of either calcium salt. Moreover, the increment in urinary calcium post-load was higher from calcium citrate than from calcium carbonate at all four dosage levels. The increment in urinary calcium (during the second 2 hr) following calcium citrate load (0.5 g calcium) was 0.104 +/- 0.096 mg/dl glomerular filtrate (GF), which was higher than that of 0.091 +/- 0.068 mg/dl GF obtained from 2.0 g calcium as calcium carbonate. These results confirm the superior calcium bioavailability from calcium citrate as compared with calcium carbonate.
TITLE: Acute oral calcium-sodium citrate load in healthy males. Effects on acid-base and mineral metabolism, oxalate and other risk factors of stone formation in urine.
AUTHOR: Schwille PO; Schmiedl A; Herrmann U; Schwille R;
Fink E; Manoharan M
AUTHOR AFFILIATION: Department of Surgery, University of Erlangen, Germany.
SOURCE: Methods Find Exp Clin Pharmacol 1997
NLM CIT. ID: 98046701
ABSTRACT: The currently preferred calcium preparations for supplementation of food vary widely with respect to calcium availability, effects on systemic mineral metabolism, acid-base status, and the calciuria-induced risk of urinary tract stone formation. In eight healthy males we studied the response to an acute load with alkali(sodium)-containing soluble calcium citrate (CSC) (molar ratio calcium/sodium/citrate approx. = 1/1/1), when taken in three different doses (10, 20, 30 mmol calcium) together with a continental breakfast. Intestinal calcium absorption, serum calcium, calcitonin, parathyroid hormone (PTH) other markers of bone metabolism, net acid excretion and calcium oxalate crystallization in urine were evaluated. CSC evoked a dose-dependent increase in calcium absorption, calcium in serum and urine, but no overt hypercalcemia, and calciuria was low relative to the excess calcium ingested; PTH fell and calcitonin rose (p < 0.05 vs. breakfast alone), but the diet-independent markers of bone resorption declined only insignificantly, while the markers of bone formation and turnover remained unchanged. There was a significant “once-daily” effect (= cumulative 24 h postload response) of CSC: a decrease in urinary cyclic AMP, phosphorus, and ammonium, and an increase in urinary bicarbonate. Soon after CSC intake, urinary calcium oxalate and hydroxyapatite supersaturation increased dose-dependently, the calcium oxalate crystal diameter was increased, but crystal aggregation time, which is crucial for stone formation, remained statistically unchanged. Thus, CSC (Calcium Citrate) provides calcium in a bioavailable form, creates mild systemic alkalinization and inhibition of bone resorption, but leaves the risk of developing urinary stones unchanged.
Am J Clin Nutr 1994 Oct;60(4):592-6
Effect of calcium citrate supplementation on urinary calcium oxalate saturation in female stone formers: implications for prevention of osteoporosis.
Levine BS, Rodman JS, Wienerman S, Bockman RS, Lane JM, Chapman DS
Department of Medicine, Cornell University Medical College, New York, NY.
In 14 women aged 37-68 y with a history of renal calcium calculi, bone densities were 12.0% below those of age-matched control subjects at the L2-4 lumbar spine (P = 0.007) and 6.4% less at the femoral neck (P = 0.095). A low-oxalate diet was supplemented with 1 g Ca/d as citrate. In 6 mo., plasma 1,25(OH)2D concentrations fell from 53.2 +/- 18.8 to 41.9 +/- 15.2 ng/L (P = 0.02) and parathyroid hormone from 39.1 +/- 17.0 to 30.8 +/- 12.5 ng/L (P = 0.02). Calcium oxalate saturation was 2.15 +/- 1.38 at baseline, 2.27 +/- 1.00 at 1 mo., and 2.06 +/- 1.57 at 6 mo. The increase in urinary calcium at 1 mo. from 4.411 +/- 1.87 to 6.514 +/- 2.82 mmol/24 h (P = 0.01) was offset by a parallel increase in citrate excretion from 2.909 +/- 1.45 to 3.455 +/- 1.34 mmol/24 h (P = 0.03). Calcium citrate supplementation did not increase the lithogenicity (kidney stone formation) of the women in this protocol.
TITLE: [Behavior of selected bio-elements in women with osteoporosis]
AUTHOR: Kotkowiak L
AUTHOR AFFILIATION:Z Zakladu Medycyny Rodzinnej Pomorskiej Akademii
Medycznej w Szczecinie, Szczecin.
SOURCE: Ann Acad Med Stetin 1997;43:225-38
NLM CIT. ID: 98077870
ABSTRACT: The purpose of this study was to evaluate the concentration of calcium, magnesium, zinc and copper in serum, urine and hair in women with osteoporosis, and to find out whether deficiency of these bioelements correlates with BMD. The concentration of calcium, magnesium, zinc and copper was assessed in 80 women aged 40-68 years. The women had been menopausal for 9.3 years and had never undergone hormone replacement, drugs therapy or mineral supplementation. The bone mass density (BMD) in lumbar spine L2-L4 was measured in 80 postmenopausal women using dual energy X-ray absorptiometry. According to BMD values all women were divided into two groups. The first group (50 persons) comprised women with osteoporosis. The second group included 30 women without osteoporosis. After an overnight fasting the levels of calcium, magnesium, zinc and copper in serum, in urine and in hair were measured by AAS. Concentration of osteocalcin and ionized calcium as well as magnesium was also measured in serum. Calcium, magnesium, zinc and copper excretions were expressed as a ratio of urinary creatine. Data were compared with Wilcoxon-Mann-Whitney’s test and significance was assessed at p < 0.05. The regression and correlation analysis was performed between BMD and level of bioelements. It was determined that the mean serum osteocalcin in the examined group (2.067 ng/ml) was higher than in the control group (1.602 ng/ml). It was also disclosed that there was a lower level of total (Tab. 1) and ionized magnesium in serum (Tab. 2) and reduced excretion of this element in urine (Tab. 4) of fasting women with osteoporosis. The concentrations of calcium, zinc and copper in serum (Tab. 1) and in urine (Tab. 4) in both groups were similar to laboratory normal range. Hair calcium and magnesium levels in examined group were lower in comparison with the control group (Tab. 3). Concentrations of zinc and copper in hair were similar in both groups (Tab. 3). The study found out that women with osteoporosis displayed magnesium deficiency. The results showed that highly significant correlation existed between magnesium and calcium.
Calcium for “Syndrome X”?
Twenty non-diabetic patients with essential hypertension consumed a low-calcium diet (500 mg/day) for four weeks and were then randomly assigned to receive (in double-blind fashion) either placebo or oral calcium (1,500 mg/day from Calcium (Sandoz) for eight weeks. Patients receiving supplemental calcium showed a significant reduction in mean fasting plasma insulin levels and a significant increase in the insulin-sensitivity index (i.e., reduced insulin resistance. There were no significant changes in these parameters in the patients maintained on the low-calcium diet.
COMMENT: “Syndrome X is a condition characterized by insulin resistance, hypertension, hyperlipidemia, and hyperuricemia. It is a relatively common metabolic disorder that is associated with an increased risk of developing cardiovascular disease. There is evidence that ameliorating insulin resistance will reduce cardiovascular risk in individuals with Syndrome X. This may be accomplished by eliminating refined carbohydrates from the diet, doing regular exercise, and taking extra magnesium, chromium and other nutrients. The results of the present study indicate that calcium supplements are also useful. The bottom line is that one reliable way to remain healthy is to consume a good diet, do regular exercise, and take a broad-spectrum nutritional supplement.
Sanchez M, et al. Oral calcium supplementation reduces intraplatelet free calcium concentration and insulin resistance in essential hypertensive patients. Hypertension 1997; 29(part 2):531-536J Am Coll Nutr 1985;4(2):195-206
Magnesium and calcium dietary intakes of the U.S. population.
Morgan KJ, Stampley GL, Zabik ME, Fischer DR
Dietary intake levels of calcium and magnesium, as well as calcium/magnesium ratios, were assessed for 12 age/sex groups of the U.S. population through use of USDA’s 1977-78 Nationwide Food Consumption Survey. Results indicated that a majority of the U.S. population consumed less than recommended amounts (NRC-RDA) of both calcium and magnesium. Approximately 60% of 0 to 5 year olds and 40% of 6 to 11 year olds had average daily calcium intakes of less than 800 mg, while 60 and 85% of the male and female adolescents, respectively, had intakes below the recommended level of 1,200 mg/day. Approximately 80 to 85% of the adult female groups and 50 to 65% of the adult male groups had average intakes below recommended levels. With the exception of children ages 0 to 5 years, the average daily magnesium intakes of all age/sex classes were below the NRC-RDA. Magnesium consumption was particularly low among adolescent females, adult females, and elderly men, with 85, 80-85 and 75%, respectively, of the population groups having average magnesium intakes below their respective NRC-RDA. Furthermore, the majority of the population groups did not consume appropriate proportions of these two minerals to obtain optimal calcium/magnesium ratios. While adolescent females and adult females had more appropriate ratio values than other segments of the population, these ratios principally resulted from their very low intakes of calcium. The most inappropriate calcium/magnesium ratios, observed for children, male adolescents, and young adult males, were, in general, due to their more appropriate calcium intakes and their low magnesium intakes.
Preventing colon cancer with calcium
Some 175 patients with adenomatous colon polyps received 2 g/day of calcium carbonate. Fifty patients with colorectal cancer received long-term calcium supplementation after surgery, while 93 similar patients did not receive calcium. In the group with adenomatous polyps, the recurrence rate of polyps after a mean follow-up period of 3.1 years was 6.9% in patients receiving calcium, compared to 55% in patients not given calcium (statistical analysis not reported). Among the cancer patients, the cumulative survival rate was significantly higher in the calcium-treated group than in the untreated group.
COMMENT: This study suggests that calcium supplementation can prevent the recurrence of adenomatous polyps and can prolong survival in patients with colorectal cancer. A placebo-controlled trial is needed before the effect of calcium can be considered proven. However, the possible anticancer effect of calcium is consistent with epidemiological studies and experimental research in animals.
Duris I, et al. Calcium chemoprevention in colorectal cancer. Hepato-Gastroenterology 1996;43:152-15
TITLE: Calcium requirements of breast-feeding mothers.
AUTHOR: Prentice A
AUTHOR AFFILIATION: MRC Dunn Nutrition Unit, Cambridge, UK.
SOURCE: Nutr Rev 1998 Apr;56(4 Pt 1):124-7
NLM CIT. ID: 98245476
ABSTRACT: A randomized, placebo-controlled calcium supplementation study has investigated the benefits of increased calcium intake during 6 months of full breast-feeding and during the weaning period for lactating women with a dietary calcium intake below 800 mg/day, compared with nonlactating women who had recently given birth. The calcium supplement of 1000 mg/day had no impact on breast milk calcium concentration or on lactation-associated bone mineral changes in the lumbar spine, radius, or total body. Calcium supplementation produced a modest increase in spine bone mineral density in both lactating and nonlactating women, but the potential significance of this effect is unclear. The results of this study support and extend the findings from three previous supplementation studies and suggest that women do not need to consume extra calcium during breast-feeding.
NOTE:This abstract is rather interesting given the fact that every physician and literature I know has suggested increased calcium intake is critical at the time of lactation.