Showing posts with label calcium. Show all posts
Showing posts with label calcium. Show all posts

Calcium phosphate kidney stones

   ›      ›   Calcium phosphate kidney stones.
Calcium phosphate kidney stones are less common than those formed with calcium oxalate. Calculi containing both phosphate (PO43−) and oxalate of calcium are common. However a greater proportion of the constituting chemical is usually oxalate.
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Kidney stones (renal calculi) of calcium phosphate (CaP) and those calculi containing greater amounts of phosphate are to be thoroughly investigated for the underlying medical cause.

The most important calcium and PO43- involved renal stones are carbonate apatite, hydroxyapatite, and brushite. The struvite calculi are formed of magnesium, ammonium and phosphate. The basic cause is the supersaturation of calcium compounds in the urine. When the solubility threshold is exceeded under the given conditions in the kidney, nucleation begins. If the conditions are stable slow crystalline growth commences.

The existing supersaturation of calcium and phosphate in the urine is the driving force for the spontaneous precipitation and crystallization. One of the factors conducive to supersaturation of these salts is increase in urine pH. Carbonate apatite calculi may sometimes associate with urinary infection.

Causes of phosphate stone formation

Several medical conditions lead to calcium phosphate kidney stone formation. The primary hyperparathyroidism, secondary hyperparathyroidism, renal tubular acidosis, hyperphosphaturia, hypercalciuria and Fanconi syndrome are some of the causative factors. Certain medications, such as Topiramate (TPM), acetazolamide, zonisamide are associated with the development of metabolic acidosis, hypocitraturia, hypercalciuria and elevated urine pH.

Hyperparathyroidism

The parathyroid glands produce parathyroid hormone (PTH). The parathyroid hormone regulates and maintains calcium and phosphate levels in the body.
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Primary hyperparathyroidism and the over secretion of PTH results from a hyperfunction of the parathyroid glands. This hyperactivity can be due to parathyroid adenoma, parathyroid hyperplasia, parathyroid carcinoma or genetic disorders.

The primary hyperparathyroidism leads to hypercalcaemia (raised serum calcium levels). The serum PO43- levels tend to be low as a result of decreased renal tubular phosphate reabsorption and resultant loss in the urine. The hypercalcemia results in active removal of calcium into urine. The availability of Calcium and PO43- helps in seeding of renal calculi.

Hyperphosphaturia and Hypercalciuria

Phosphaturia is a condition wherein phosphate is excessively excreted by the kidney, making these ions easily available for calculi formation. There are two form of phosphaturia. The primary type is direct excess excretion of PO43− by the kidneys either due to generalized dysfunction of the proximal tubular cells in kidney (Fanconi syndrome) or due to the action of diuretics. The secondary phosphaturia is due to both primary and secondary types of hyperparathyroidism.

Hypercalciuria is a condition wherein Calcium is excessively excreted by the kidney. Hypercalciuria is caused due excessive release from the bones, excessive calcium supplementation, elevated serum levels of calcium, excessive sodium intake or due to certain genetic disorders.

The conditions of hypercalciuria and hyperphosphaturia, individually or as a combined action, initiate calcium phosphate stone formation in the event of saturated levels of these ions in the urine. The stone formation is further helped by high pH of urine.

Renal tubular acidosis (RTA)

RTA is a medical condition is which there is acid accumulation in the body. The condition is due to inefficiency of kidney in resorbing and recovering bicarbonate ions from the filtrate in the proximal tubular cells or inefficiency in eliminating hydrogen ions into lumen of nephron at distal tubule. The distal renal tubular acidosis characterized by hyperchloremic acidosis, hypocitraturia, and high urine pH. The net effect is insufficient acidification of urine to a pH of less than 5.3 and accumulation of acid in the body and acidemia.

Treatment and management

In the management of these renal calculi, reducing urine saturation and limiting of calcium excretion are important steps. With sufficient intake of water, urine can be diluted. Restricting sodium ingestion can reduce sodium excretion as well as calcium excretion. Citrate, though tends increase the urine pH, has the capacity to bind to ca2+ and eliminate it from the system. Thiazides also lower urine calcium excretion. The persisting calcium phosphate kidney stones are removed by extracorporeal shock wave lithotripsy (ESWL), Percutaneous stone removal or surgery.
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References:
1.Vega D, Maalouf NM, Sakhaee K. Increased propensity for calcium phosphate kidney stones with topiramate use. Expert Opin Drug Saf. 2007 Sep;6(5):547-57.
2.David S. Goldfarb. A woman with recurrent calcium phosphate kidney stones. Clin J Am Soc Nephrol. 2012 Jul;7(7):1172-8.
3.Gault MH, Chafe LL, Morgan JM, Parfrey PS, Harnett JD, Walsh EA, Prabhakaran VM, Dow D, Colpitts A. Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. Medicine (Baltimore). 1991 Nov;70(6):345-59.
4.Fredric L. Coe, Andrew Evan, Elaine Worcester. Kidney stone disease. J Clin Invest. Oct 1, 2005; 115(10): 2598–2608.
5.Hesse A, Heimbach D. Causes of phosphate stone formation and the importance of metaphylaxis by urinary acidification: a review. World J Urol. 1999 Oct;17(5):308-15.
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Calcium intake - Calcium absorption

› › › Calcium intake and absorption

Calcium intake

Calcium absorption by the intestines and its utilization by the body depends upon many factors.
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Vitamin D is needed for the assimilation of calcium. vitamin C, vitamin E, vitamin K, magnesium, and boron also assist in the assimilation of the mineral. Large doses of calcium ingested at a time will get wasted. In large quantities much of the mineral will get excreted by the body. For better calcium absorption, less than 500 mg must be consumed at a time and its consumption must be spread out throughout the day to get the daily requirement.

Calcium absorption

Calcium absorption occurs by both active transport as well as passive paracellular transport in the small intestines. When the nutritional status of the mineral is high, the mineral is taken up through passive paracellular transport in the jejunum and ileum parts of the intestine. Passive transport is independent of Vitamin D level in the body. When the mineral ingestion is low, active transport of the mineral into the body becomes the primary pathway and much of the incorporation takes place across the brush border membrane in the duodenum portion of the intestine.
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The entry of the mineral into the enterocytes from the apical side is regulated by calcium channel TRPV6. Expression of TRPV6 is vitamin D dependent in humans. Calbindin-D9k, a vitamin D-dependent calcium-binding S-100 protein, is present in the intestinal epithelial cells (enterocytes). It is coded by S100G (CALB3) gene. The active vitamin D metabolite, calcitriol stimulates the calbindin-D9k expression.
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Calbindin-D9k increases the absorption of Ca2+ by buffering the ions in the cytoplasm. It mediates in the transport of the mineral across the enterocyte to the basolateral side by stimulating the adenosine triphosphate (ATP) dependent taking in of Ca2+ ions into duodenal basolateral membrane vesicles. Calbindin-D9k stimulates the basolateral calcium-pumping ATPs. Calcium pumps such as PMCA1 utilize intracellular ATP to pump calcium into the intercellular fluids.

What impairs the absorption of calcium

Many factors like old age, excessive consumption of sodium, proteins, alcohol and caffeine, prolonged corticosteroid therapy, food containing phytic acid and oxalic acid can impair calcium absorption and/or increase its excretion from the body.
Age related malabsorption
Children and young adults can assimilate as much as 50% of the ingested calcium. However this capability decreases with aging. Hence in middle-age and old age more supplements has to be ingested to make up for the poor absorption. Further there is increased bone turnover loss of the mineral in old age.
Alcohol
Alcohol reduces assimilation of this mineral and increases its excretion. It can also interfere with the production of enzymes in the liver for vitamin D metabolism. The diuretic effect of alcohol causes loss of many minerals by urinary excretion from the body.
Caffeine
Caffeine reduces absorption of this mineral and increases its urinary excretion as well as fecal excretion. The excessive consumption of caffeine containing drinks like coffee, tea and cola drinks hampers the assimilation of the mineral.
Oxalate and phytates
Phytic acid and oxalic acid found in some plant sources of food binds to the calcium, inhibiting its assimilation. Spinach, chard, collard greens, chocolate and sweet potatoes are high in oxalic acid.
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Whole grain products, beans, seeds and soy isolates are rich in phytic acid. For better absorption of the mineral the above foods may not be taken along with supplements.
Sodium, protein and dietary fiber
Foods containing high levels of sodium or protein interfere with assimilation of the mineral. Further they cause more calcium to be lost in urine. Fiber from sources like wheat bran can bind the mineral to the intestinal tract. Excess soluble fiber can reduce the absorption of calcium.
Medications
  • Administering intravenous ceftriaxone (Rocephin) along with calcium supplements can be life threatening.
  • Quinolone antibiotics like ciprofloxacin, levofloxacin and ofloxacin can decrease the assimilation of the mineral.
  • Tetracycline antibiotics can bind to this mineral and decrease efficacy of both the antibiotic as well as the mineral.

How to optimize calcium absorption

  • Sufficient exposure to sunlight and vitamin D supplementation can help in increasing the assimilation by the body.
  • The quantity of Ca consumed at a time should not exceed 500 mg to reduce loss in fecal excretion.
  • Eating the supplements along with food help in stomach acid acting on the mineral to increase its absorption.
  • For better absorption of the mineral, calcium binding foods may not be taken along with the supplements or food rich in calcium.
  • Avoid excessive consumption of alcohol, caffeine and sodium.
  • According to a study from Purdue University, consuming honey along with supplements enhanced calcium assimilation.
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References:
1.http://www.health.gov/dietaryguidelines/dga2005/document/html/AppendixB.htm#appB4
2.http://www.health.gov/dietaryguidelines/dga2005/document/html/AppendixB.htm#appB5
3.http://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/

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Calcium food sources - List of calcium rich foods

› › › List of calcium rich food sources
Calcium is present in rich proportions in a variety of plant and animal food sources.
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We can certainly make a fairly long list of calcium rich food sources. Calcium, a very important mineral in bone metabolism, is also necessary for the neuromotor, cardiovascular, hematological, hepatic and nephrological functions of the human body. About 1,000 milligrams of the mineral is required daily for active men and women. In elderly people intestinal absorption of the nutrients decreases and the calcium requirement may increase to 1,200 milligrams per day.

As is interdependent on vitamin D status, for effective absorption and utilization of the mineral, sufficient vitamin D must be consumed. Depending upon the form of the mineral and also the presence of certain other nutrients, calcium absorption may get suppressed. If phytates and oxalates are present in the food, calcium may get bound to them and become unabsorbable. Boiling and fermentation can reduce the binding of the mineral to other nutrients. In many processed foods, calcium is added as part of the manufacturing process or added to increase the nutritive status.

List of 20 calcium rich foods

A list of very rich sources of the mineral is given below.
List of dairy sources
Yogurt
Cheese
Milk
List of animal sources
Sardines
Mackerel
List of plant sources
Tofu
Collard greens
Spinach
Turnip greens
Mustard greens
Beet greens
Bok choy
Swiss chard
Kale
Sesame seeds
Broccoli
Brussels sprouts
Green beans
Oranges
Almonds
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Rich dairy sources
Except for the fat concentrates like butter and ghee, all dairy products contain rich amounts of calcium.
Eight ounces plain yogurt has about 400 mg.
Five ounces of mozzarella cheese contains 330 mg of the element.
Three ounces of cheddar cheese contains 600 mg.
One cup of cottage cheese contains about 140 mg of the mineral.
Eight ounces of whole milk contains about 280 mg of the mineral.
Eight ounces nonfat or low fat milk has about 300 mg.
Eight ounces of lowfat buttermilk has about 280 mg of this nutrient.
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Animal food sources
Among the animal sources, only fish yield rich amounts of calcium. The fleshy part of the fish is low in the mineral. The fish has to be consumed along with the soft bones to get the calcium.
Three ounces of sardines canned in oil, when taken with bones give 325 mg of the element.
Three ounces of canned salmon with bones contains 180 mg.
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Rich plant food sources
When compared plant foods are not as rich as animal sources. However certain leafy green vegetables have fairly rich amounts of calcium.
One cup of fresh boiled turnip greens contain about 200gm.
One cup of raw kale contains 100 mg.
Eight ounces of collard greens contain up to 350 mg of the mineral.
Eight ounces of green boiled soybeans may contain 175 mg.
Eight ounces of cooked Chinese cabbage (bok choy) has 160 mg.
One cup of canned white beans has 190 mg of the mineral.
One ounce of dry roasted almonds contain 75 mg.
Fortified food sources
Fortified milk (soymilk etc) has about 300 mg of calcium in eight ounces.
Rich fortified fruit juice contains up to 300 mg of the mineral in six ounces.
One cup of firm rich tofu made with calcium sulfate has about 500 mg of the mineral.
One cup of soft tofu made with calcium sulfate has about 280 mg.
Depending upon the level of fortification, ready-to-eat cereals may contain up to 1,000 mg of calcium.
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References:
1.http://www.health.gov/dietaryguidelines/dga2005/document/html/AppendixB.htm#appB4
2.http://www.health.gov/dietaryguidelines/dga2005/document/html/AppendixB.htm#appB5
3.http://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/

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Calcium homeostasis - Calcium metabolism - Calcium levels

› › Calcium levels, homeostasis and metabolism.
What is calcium homeostasis or metabolism?
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Calcium homeostasis or metabolism refers to the controlled regulation of calcium level in the extracellular fluid within a narrow range. The extracellular fluid levels of the mineral must be maintained to achieve optimal functionality. Any increase in the levels above the regulated range may cause disorders like hypercalcemia; decrease in levels will cause hypocalcemia and osteoporosis.

Calcium is the most abundant mineral in the human body and contributes to many biochemical processes including functioning of the neuromotor systems and blood coagulation. The biological processes that contribute to its homeostasis are intestinal absorption pathways, bone remodeling processes, renal reabsorption and excretion processes and endocrine metabolism and regulation.

calcium metabolism
Calcium homeostasis
The predominant endocrine regulators of calcium homeostasis are parathyroid hormone (PTH) and active vitamin D, and, to a lesser extent, calcitonin. Fibroblast growth factor 23 (FGF23), transmembrane protein enzyme (klotho) and transient receptor potential cation channel subfamily V member 5 (TRPV5), also have roles in the mineral homeostasis in serum levels. The interplay between the biological and biochemical factors in the metabolism is described below.

For new bone formation and growth calcium has to be taken through food. Many factors inhibit or aid in the absorption of the mineral in the intestine. By stimulating production of active vitamin D (1,25-dihydroxyvitamin D3), parathyroid Hormone (PTH) enhances the intestinal absorption of the mineral. Calcium transport mechanism accounts for the major portion of the mineral absorbed from the intestine, whereas passive diffusion accounts for less than 20% of the absorption.

Total and free calcium homeostasis

Nearly 99% of the body's calcium is present in bones, mostly as hydroxyapatite crystals.
    • Nearly 1% is present in the extracellular fluid (ECF) for maintaining total serum levels (8.8 to 10.4 mg/dL) of the mineral. Of this more than 40% is albumin bound. Less than 60% of the calcium is ionized and free available for metabolism. However in clinical laboratory serum analysis, it technically difficult to analyze the free ionic form and only the total serum levels are determined. The ionized mineral maintained by homeostasis is assumed to be half of the total serum level.

    Bone remodeling process and homeostasis

    Bone metabolism is a continuous process. Old bones are resorbed and new bone is formed to keep pace with the growth and repairs. Further bone is the source for maintaining calcium homeostasis in case of lowered levels in the serum. When the serum concentration of the mineral increases, to maintain the homeostasis, the mineral is actively removed from the serum by deposition on to the bones and also by excretion.

    Parathyroid Hormone (PTH) in metabolism

    Parathyroid Hormone (PTH) is the main player in bringing about the homeostasis or metabolism in the serum levels of the mineral.
    • PTH by stimulating the osteoclasts causes the bone resorption and increase in serum levels of the mineral. The calcium-sensing receptors (CaSRs) on the surface of the parathyroid cells as well as in the bone and kidney are activated by the ionized serum levels of the mineral.

    The PTH secretion is controlled by negative feedback from the serum levels. PTH also stimulates production of hormonally active form of vitamin D in the kidney. PTH also decreases the excretion and increases reabsorption of this mineral by the kidneys for the mineral metabolism.

    Active vitamin D in metabolism

    Along with PTH, active vitamin D (1,25-dihydroxyvitamin D3), is also required in the metabolism of the bone remodelling, especially resorption. Active vitamin D increases the dietary absorption of the mineral. It also increases the renal reabsorption of calcium in the urine. The source vitamin D is food. In the skin vitamin D is formed after exposure to sunlight/ultraviolet light.

    Calcitonin and homeostasis

    The parafollicular cells (C-cells) of the thyroid gland secrete calcitonin, a 32-amino acid polypeptide hormone regulator of homeostasis.
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    The main function of calcitonin in the homeostasis is to lower the calcium levels in serum. The action of calcitonin is antagonistic to PTH on bone reabsorption. In metabolism of bones, calcitonin increases the deposition of the mineral on to the bones and soft tissues. The concentration levels of the calcium ions in the extracellular fluids is the stimulus for calcitonin secretion and metabolism.
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    References:
    1.Lumachi F, Motta R, Cecchin D, Ave S, Camozzi V, Basso SM, Luisetto G. Calcium metabolism & hypercalcemia in adults. Curr Med Chem. 2011;18(23):3529-36.
    2.Munro Peacock. Calcium Metabolism in Health and Disease. CJASN January 2010 vol. 5 no. Supplement 1 S23-S30.
    3.Gregory R. Mundya and Theresa A. Guise. Hormonal Control of Calcium Homeostasis. Clinical Chemistry August 1999 vol. 45 no. 8 1347-1352.
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    Functions of calcium - Health benefits of calcium

    May 2014   › › › › › Functions of calcium and its health benefits
    Calcium supports the structure and function of bones and teeth. Multiple health benefits of calcium include regulation of vasoconstriction and vasodilation, neuromotor transmission and several critical cell metabolic functions.
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    It is the most abundant mineral in the human body. The bones and teeth contain 99% of the calcium present in the human body. The remaining 1% is found in the blood serum, soft tissues and interstitial fluids of the tissues. One of the health benefits of the mineral is the alkalizing effect.

    Calcium presence in the blood serum is tightly regulated and the normal levels of its ionized form is 4.65 to 5.25 mg/dL (1.16 to 1.31 mmol/L). Irrespective of the quantity in diet, the levels are maintained by sourcing the mineral from the bones by demineralization. Mineral deficiency diseases like hypocalcemia occur when the concentration of free calcium ions in the blood serum falls below 4.0 mg/dL. Certain adverse health conditions may result in higher concentration of calcium ions in the blood serum and lead to diseases like hypercalcemia or milk-alkali syndrome.

    Functions of calcium

    Calcium has many functions in the human body. Apart from being the structural component of the bone tissue it has several physiological and biochemical functions. Some functions of calcium are listed below.
    functions as a primary structural component of bones and teeth.
    It functions as an universal intracellular messenger, activating or inhibiting several cellular processes.
    Its another function is in signalling cellular secretions and hormone releases.
    It is necessary for production and transmission of electrical signals within the nervous system.
    It has major function in neuronal signal reception, neuronal signal transmission and the regulation of neuronal excitability.
    It functions in bringing about cellular changes that underlie learning, cognisance, perception, creativity and memory.
    Critical for the function of endothelial cell junctions (adherens and tight junctions) of the blood–brain barrier (BBB).
    Calcium signaling pathways function as regulators of gene transcription and gene expression.
    It functions as the necessary ion in the formation of the mitotic spindle for cell division and cell proliferation.
    Required for coagulation factors to bind to phospholipid for coagulation cascade and blood clotting.
    It has mediatory function in excitation and contraction of muscle fibres.
    Regulating heartbeat is its major function.

    Health benefits of calcium

    Health benefits of calcium include protection from osteoporosis, hypocalcemia, amenorrhea, cardiovascular disease, hypertension, stress fractures, weight gain and certain cancers.

    Benefits of calcium in bone health and function

    Bone mass keeps increasing in childhood and adolescence.
    • The increase in bone size and mass reaches its peak by about 30 years of age. Greater bone mass delays serious bone loss in old age. If calcium intake is low or if there is poor absorption during childhood and teenage, sufficient bone mass is not attained. Such individuals are at high risk of developing osteoporosis. They become highly vulnerable to fractures of the hip, vertebrae, pelvis, ribs and other bones. Supplementation can benefits such persons and improve their health.

    Postmenopausal women health benefits

    With the onset of menopause, the estrogen production decreases causing many physiological changes in postmenopausal women. Decrease in estrogen production leads to increased bone resorption and decreased resulting in bone loss. Women affected by low estrogen levels are at the increased risk of hypocalcemia, osteoporosis and stress fractures. Taking calcium supplements and undergoing hormone replacement therapy (HRT) may benefit and improve their health by improving the bone function.

    Amenorrhea and health benefits of calcium

    Amenorrheic women and many female athletes tend to have decreased estrogen levels.
    • The condition primarily arises due low fat and high protein diet. The decrease in estrogen production, apart from causing amenorrhea can upset the calcium balance. There is increased excretion of the mineral in the urine and decreased rate of bone formation. Diet rich in calcium or intake of supplements may benefit such women and add to their bone health.

    Cancers

    Several observational and experimental studies have established the link between higher calcium intake and prevention of colon cancer. High levels of intake even reduced the risk of adenoma, a nonmalignant tumor, which sometimes become malignant. A.Galas et al in their study "Does dietary calcium interact with dietary fiber against colorectal cancer? A case-control study in Central Europe" published in Nutrition Journal, 2013 Oct 4;12:134, concluded that the study confirmed the effect of high doses of dietary calcium against the risk of colon cancer development.

    Cardiovascular health benefits

    The benefits of the mineral in cardiovascular health is still being debated. Chronic overdoses of the mineral had been found to cause cardiovascular disease. Some studies claim that moderate levels of supplementation can prevent cardiovascular disease.

    Hypertensive patients health

    It is well established that calcium supplementation, reduces the systolic blood pressure by 2–4 mmHg in hypertensive patients. However in normotensive individuals, supplementation does not appear to have any function and does not affect systolic or diastolic blood pressure.

    Calcium benefits for weight loss?

    The benefits of the mineral in weight loss is still being debated. A meta-analysis of randomized controlled trials had reported lack of significant effect on weight reduction. However the following studies show that supplementation with the mineral may help in weight loss.

    Genevieve C Major et al published their study "Supplementation with calcium + vitamin D enhances the beneficial effect of weight loss on plasma lipid and lipoprotein concentrations" in American Society for Clinical Nutrition (2007). They have concluded that regular intake of calcium and vitamin D during a weight-loss intervention in overweight women with low daily intake of the mineral, had beneficial effect on body weight loss.

    Zhu W et al of Department of Nutrition, Shanghai Institute of Health Sciences, have published their study "Calcium plus vitamin D3 supplementation facilitated fat loss in overweight and obese college students with very-low calcium consumption: a randomized controlled trial." in Nutrition Journal 2013, 12:8. They had reaffirmed the health benefits of the mineral by reporting that supplementation of the mineral plus vitamin D3 for 12 weeks facilitated body fat and visceral fat loss during energy restriction in overweight or obese very-low calcium consumers.
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    References:
    1.Dietary Supplement Fact Sheet. National Institutes of Health.
    http://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/
    2.Reinwald S, Weaver CM, Kester JJ. The health benefits of calcium citrate malate: a review of the supporting science. Adv Food Nutr Res. 2008;54:219-346. doi: 10.1016/S1043-4526(07)00006-X.
    3.Bootman MD, Rietdorf K, Hardy H, Dautova Y, Corps E, Pierro C, Stapleton E, Kang E, Proudfoot D. 2012. Calcium Signalling and Regulation of Cell Function. eLS.
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    Calcium overview - Calcium nutrition

    Apr 2014   › › › Calcium in human nutrition
    Calcium nutrition
    Calcium, a highly essential mineral, is required in human nutrition for several critical biochemical processes.
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    Calcium brings about several metabolic functions like intracellular signaling, hormonal secretion, enzyme secretion, muscle contraction and nerve transmission. Skeletal system and teeth account for 99% of the calcium present in the body. Rest of the mineral is dispersed among soft tissues and blood serum. Dairy products are the best dietary sources of the mineral.

    For the smooth functioning of the bone remodeling process, adequate dietary nutrition of the mineral is necessary. Postmenopausal women, due to decrease in estrogen production and intestinal absorption of the mineral, suffer loss of bone mass and develop osteoporosis. The presence of oxalic acid and phytic acid in the diet reduces the bioavailability of calcium present in the diet. Too much calcium supplementation can cause hypercalcemia, kidney stones and renal failure.

    Adequate calcium intake is vital for bone and dental health. Many of the biological processes require adequate calcium in the system for their efficient function.
  • Adequate dietary calcium nutrition is required for optimising bone mass, bone mineral accretion and bone homeostasis.
  • The growth, mineralisation and maintenance of the mineral composition of teeth depend on the mineral status.
  • Intracellular calcium is vital for triggering cellular events like intracellular signals, vesicular secretion, cell aggregation, cell transformation and cell division.
  • Several extracellular digestive enzymes require the intervention of the mineral for optimum activity.
  • The presence of adequate calcium in nutrition brings about the skeletal, heart and smooth muscle contraction and neurotransmitter release.
  • Adequate intake of the mineral lowers the high blood pressure and reduces the risk of hypertension.

    • Plasma ionic calcium is tightly regulated between 1.1 and 1.3 mmol/L irrespective of its nutrition and the bones function as storage buffers. If the concentrations decrease considerably, tetany may occur. If the levels increase considerably, hypercalcemia, kidney stones and kidney failure may occur. Parathyroid hormone, either directly, indirectly or along with calcitonin and calcitriol, controls the homeostasis of calcium in the kidneys, bone and gastrointestinal tract.

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    • In an healthy individual only about 20% to 30% of the dietary calcium is absorbed in the gastrointestinal tract; the rest being excreted in faeces. During growing phase, pregnancy and lactation the percentage of absorption may increase marginally. Further the form of the mineral salt, its solubility, relative presence of minerals like zinc, iron and magnesium in the diet, age of the individual and vitamin D status of the individual promotes or inhibits the absorption. The presence of oxalate in the diet reduces the nutritional bioavailability of the mineral.

    The richest food sources of the mineral are milk and dairy products with the exception of butter. Broccoli, cabbage, beans and kale are good plant sources. Fortified cereals and soy products also contain fairly good amounts of the mineral. Eggs, fish and animal products also have calcium. Canned small fish becomes a very good source if eaten with bones. The drinking water may also contain useful levels of dissolved salts of the mineral, especially if it is hard water.

    The basic cause of the deficiency is the inadequacy of the mineral in the nutrition. Certain disorders, physiological conditions and hormonal imbalances can also cause the deficiency of the mineral. The insufficiency of vitamin D and lack of exposure to sunlight can also cause insufficient absorption from the intestinal tract. Persons with lactose intolerance cannot take milk and may develop the deficiency. Short term deficiency may not have any apparent symptoms. Calcium deficiency can cause loss of bone mass, osteoporosis or hypocalcemia.

    The supplementation of the mineral below the tolerable upper intake levels is normally tolerated and rarely has any side effects. In some individuals, irritation of the gastrointestinal tract, flatulence, belching and constipation may be noticed. Individuals with decreased renal function may develop hypercalcemia, renal stones, metastatic calcification and related symptoms. Supplements of the mineral are known to react/interfere with absorption of certain dietary minerals, certain types of medicines and antibiotics.

    • The condition of overdose may occur in case of too much intake of the mineral in the form of supplements, antacids, intravenous administrations and fortified food. In normal conditions there is limited and controlled absorption of the mineral from the intestines. Intake of excess of vitamin D can also cause excessive absorption of the mineral from the gastrointestinal tract.

    Accidental or intentional ingestion of the mineral exceeding the upper tolerance levels of 2,500 milligrams can result in hypercalcemia with symptoms like nausea, constipation, arrhythmia, confusion, polyuria, kidney stones and kidney failure. Taking high doses of alkaline supplement of the mineral or taking absorbable alkali along with calcium supplement can lead to milk-alkali syndrome with symptoms of hypercalcemia, alkalosis and renal failure.
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    References:
    Dietary Supplement Fact Sheet. National Institutes of Health.
    http://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/

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    Milk alkali syndrome - Burnett's syndrome - Calcium alkali syndrome

    Apr 2014   › › Milk alkali ((Burnett's) syndrome - causes, symptoms and treatment
    Milk alkali syndrome (MAS) also known as Burnett's syndrome is actually calcium alkali disorder caused by repeated overdose of calcium along with absorbable alkali.
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    The syndrome was first described by Charles Hoyt Burnett (1913–1967), an American physician. Initial symptoms of milk alkali syndrome include nausea, vomiting, high urine output followed by volume depletion and alkalosis. The treatment regimen includes volume restoration with intravenous infusion of normal saline and discontinuance of calcium and vitamin D supplements. Left untreated, it can lead to soft tissue calcification and permanent kidney damage.

    What is milk-alkali syndrome?

    In 1915, Bertram Welton Sippy (1866-1924), an American physician, introduced "Sippy regimen" for the treatment and management of peptic ulcers. The patients were advised hourly ingestion of milk and cream. Gradually eggs and cereals were added to the diet of milk and cream. Alkali powders, which were absorbable, were also given for the relief of peptic ulcer symptoms.

    • Later on, many peptic ulcer patients undergoing the Sippy regimen were found to develop hypercalcemia, alkalosis and renal failure. The discontinuance of the regimen resulted in the reversal of these adverse symptoms. As milk alkali syndrome is associated with taking large quantities of milk and absorbable alkali, it had come to be known as milk alkali syndrome. As milk alkali syndrome was first described by Charles Hoyt Burnett, it was also called Burnett's syndrome in his honor.

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    • The advent of histamine-2 blockers and proton pump inhibitors and eradication of causative Helicobacter pylori bacteria with antibiotics, has lead to drastic change in the peptic ulcer treatment approach. The incidence of this classic Burnett's syndrome had decreased drastically.

    Now there is increasing awareness about osteoporosis. There is also increase in self medication of calcium carbonate formulations for treating osteoporosis, hyperacidity and gastroesophageal reflux disease (GERD). This trend has contributed to the increase in the current version of milk alkali syndrome. Several cases with symptoms of hypercalcemia, metabolic alkalosis and renal failure are being reported. Medical investigations reveal that the common cause is the excessive use of over the counter supplements and antacids containing calcium carbonate.

    How is Burnett's syndrome caused?

    The excessive ingestion of calcium, milk and absorbable alkaline compounds has been the main triggering factor for developing the Burnett's syndrome. Excess calcium causes hypercalcemia and alkali ingestion causes alkalosis. Due to alkalosis there is reduced glomerular filtration rate (GFR) and increase in tubular reabsorption of calcium. Hypercalcemia, by inducing renal vasoconstriction reduces glomerular filtration rate. This leads to reduction of extracellular volume, reduction in renal excretion of calcium and its retention in the body.

    Once the Burnett's syndrome develops, it contributes to its own maintenance because of volume depletion from increased sodium and water excretion and increase in tubular reabsorption of calcium.

    Milk alkali syndrome symptoms

    Considering the severity of symptoms, Burnett's syndrome is categorized into subacute, acute and chronic forms. The symptoms of Burnett's syndrome include:
    • lack of appetite,
    • nausea,
    • vomiting,
    • headache,
    • constipation,
    • abdominal pain,
    • back pain,
    • weakness,
    • fatigue,
    • drowsiness,
    • depression,
    • symptoms of altered mental status,
    • malaise,
    • symptom of confusion,
    • dry oral mucosa,
    • poor skin turgor,
    • symptoms of hypercalcemia,
    • symptoms of metabolic alkalosis and renal failure.
    The symptoms of chronic form of the Burnett's syndrome include myalgia, tremor, polyuria, polydipsia, soft tissue calcification, nephrocalcinosis and irreversible renal failure.

    Milk-alkali syndrome treatment

    The first line of treatment is volume restoration with intravenous normal saline to improve renal function and facilitate calcium and bicarbonate excretion. All the supplements containing calcium and vitamin D should be discontinued. Milk intake the patients may be reduced. The intravenous hydration and furosemide (a loop diuretic) medication usually reverses hypercalcemia and alkalosis. Early recognition of symptoms, diagnosis and treatment can help in the recovery and normalization of renal function.

    During the course of treatment, transitional hypocalcemia may result, which may be treated by judicial administration of calcium supplements.

    Susceptibility to Burnett's syndrome

    The elderly people have a lower glomerular filtration rate in the kidneys, decreased calcium clearance and reduced skeletal buffering of calcium. They are highly susceptible.
    Any form of dehydrating debility or chronic dehydration can predispose a person to calcium-alkali syndrome.
    Patients suffering from anorexia nervosa or bulimia nervosa are particularly susceptible due to their erratic food habits.
    Patients who have preexisting renal impairment or failure are highly susceptible.
    Women suffering from excessive vomiting during pregnancy (hyperemesis gravidarum) are vulnerable.
    In pregnant women calcium is absorbed at a higher rate from the GI tract. They are also advised to take more milk. Gastric reflux is a common problem with them and taking over-the-counter antacids containing an abosorbable base may predispose them to the Burnett's syndrome.
    Postmenopausal women and transplant patients taking high doses of calcium supplements and vitamin D to treat or prevent osteoporosis are also susceptible develop milk-alkali syndrome.
    The use of thiazide diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin receptor blockers or angiotensin-converting-enzyme inhibitor can predispose a person to milk alkali syndrome.
    Betal nut chewers in Asia usually blend the nuts with oyster shell lime paste. This habit increases the ingestion of alkaline calcium many folds.

    If such susceptible patients are to be given mineral supplements, care must be taken not to include any alkaline forms of trace minerals. They should not also be given excess milk. There is a great need to educate the patients on proper use and dosing of all non prescription medicines and supplements to prevent syndromes like Burnett's arising out of inappropriate medication.

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    References:
    1.Altun E, Kaya B, Paydas S, Balal M. Milk alkali syndrome induced by calcitriol and calcium bicarbonate in a patient with hypoparathyroidism. Indian J Endocr Metab 2013;17:191-3
    2.Almusawi A, Alhawaj S, Al-Mousawi M, Dashti T. No more milk in milk-alkali syndrome: a case report. Oman Med J. 2012 Sep;27(5):413-4.
    3.Michelle V Gordon, P Shane Hamblin and Lawrence P McMahon. Life-threatening milk-alkali syndrome resulting from antacid ingestion during pregnancy. Med J Aust 2005; 182 (7): 350-351.

    Current topic on nutritional deficiency diseases: Milk alkali syndrome (Burnett's syndrome or calcium alkali syndrome) symptoms.
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