Calcium can help you sleep

Calcium, especially when contained in food, has a sedative effect on the body. A calcium deficiency in the body causes restlessness and wakefulness. For adults, doses of approximately 600 milligrams of liquid calcium have been shown to have a relaxing effect.

Dosage: 1,500-2,000 mg daily, in divided doses, after meals and at bedtime.

Magnesium, in doses of approximately 250 milligrams, can help induce sleep. Magnesium deficiency is responsible for nervousness that prevents sleep. Magnesium-rich foods include kelp, wheat bran, almonds, cashews, blackstrap molasses, and brewer's yeast.

Dosage: 1,000 mg daily.

Note: The lack of calcium and magnesium can cause leg cramps during the night. Calcium and magnesium produce calming effects on the brain. They are essential for normal sleep. Calcium and magnesium taken 45 minutes before bedtime have a tranquilizing effect. Use a 2:1 ratio, such as 500 mg of calcium and 250 mg of magnesium in tablet or capsule form.

Calcium Prevent Menstrual Cramps

Dysmenorrhea, or painful menstruation, is classified as either primary or secondary. Primary dysmenorrhea generally occurs within a couple of years of the first menstrual period. The pain tends to decrease with age and very often resolves after childbirth. Secondary dysmenorrhea is commonly a result of endometriosis, starts later in life, and tends to increase in intensity over time.
As many as half of menstruating women are affected by dysmenorrhea, and of these about 10% have severe dysmenorrhea, which greatly limits activities for one to three days each month.

Calcium may help prevent menstrual cramps by maintaining normal muscle tone. Muscles that are calcium-deficient tend to be hyperactive and therefore more likely to cramp. Calcium has been reported to reduce pain during the menstrual phase of the cycle and reduce water retention during the premenstrual phase.5 Calcium supplementation of 1,000 mg per day can be taken throughout the month. During acute menstrual cramps, calcium can be taken in the amount of 250–500 mg every four hours for pain relief, up to a total of 2,000 mg per day.

References:
Galeao R. La dysmenorrhee, syndrome multiforme. Gynecologie 1974;25:125

Penland J, Johnson P. Dietary calcium and manganese effects on menstrual cycle symptoms. Am J Obstet Gynecol 1993;168:1417–23.

Muscle Fatigue May Be Caused by Calcium Loss

New research from Columbia University in New York shows that muscle fatigue during and after exercise may be caused by loss of calcium from muscle cells and that drugs that block the release of calcium from muscle cells may prolong endurance (Proceedings of the National Academy of Sciences, February 11, 2008).

When you exercise, your cells use food to generate electricity that causes nerves to send messages and muscles to contract. The energy from food generates electricity by driving minerals inside and outside of the cells, creating an imbalance of the minerals between the outside and inside of cells that causes electrons (electricity) to flow. A major source of this flow of electrons is from muscle cells pushing calcium outside their cell walls. This paper shows that muscles lose calcium continuously during exercise, and eventually do not have enough calcium to continue pumping calcium outside of cells, and therefore cannot generate as much electricity. This causes the muscles to weaken, hurt, lose coordination and feel tired.

The authors timed mice exercising to the point of exhaustion. Then they gave the mice an experimental drug that blocks the loss of calcium from muscle cells, and they were able to exercise longer. The researchers demonstrated the same process of calcium loss in the muscles of trained cyclists. However, they have not taken the next step of testing the drug to see if it improved endurance, because the drug has not been approved for use in humans.

Calcium and Kidney Stone

Kidney stones occur frequently. As many as 10 percent of men and 3 percent of women have a stone during their adult lives. About 80 percent of all stones are composed of calcium oxalate, alone or with a nucleus of calcium phosphate (apatite). The first step in the formation of calcium stones is the formation of microscopic crystals in the lumen of renal tubules as a result of supersaturation of the luminal fluid with calcium oxalate or calcium phosphate. Crystal growth, and therefore stone formation, is enhanced by the attachment of crystals to the surface of cells in the papillae and is reduced by the inhibitors of crystal growth and aggregation that are normally present in renal tubular fluid. Currently, however, attempts to prevent calcium stones remain focused on efforts to reduce urinary concentrations of calcium and oxalate by reducing the rate of urinary excretion of these substances and by increasing urine volume. In addition, efforts may be directed toward increasing urinary citrate excretion in order to increase the formation of calcium citrate, a highly soluble calcium salt whose formation decreases urinary concentrations of free calcium.

Among healthy subjects, an increase in dietary calcium intake results in an increase in urinary calcium excretion equal to about 8 percent of the amount by which the dietary calcium intake is increased. Among the approximately 30 to 50 percent of people with calcium stones who have hypercalciuria (urinary calcium excretion greater than 300 mg [7.5 mmol] per day in men and 250 mg [6.2 mmol] per day in women), urinary calcium excretion increases by about 20 percent of increased dietary calcium intake, because of the increased efficiency of intestinal calcium absorption that may be either dependent on calcitriol (1,25-dihydroxyvitamin D₃) or independent of it. It is standard practice to recommend dietary calcium restriction to prevent stone recurrence in patients with hypercalciuria, even though prospective trials have not established the efficacy of such restriction. In addition, advice to restrict dietary calcium intake is often extended, without a clear rationale, to patients with calcium stones who do not have hypercalciuria.

Lemann, J., Composition of the Diet and Calcium Kidney Stones, The New England Journal of Medicine, Volume 328:880-882

Calcium and Hypertension

Regulation of intracellular calcium plays a key role in hypertension and obesity. Dysregulation of calcium homeostasis appears to be a fundamental factor linking these conditions. Regulation of intracellular calcium in key disease-related target tissues by calcitrophic hormones provides the opportunity to modulate disease risk with dietary calcium.

Overall, sub-optimal calcium intakes contribute to the etiology of salt-sensitivity and hypertension. High salt diets exert a calciuretic effect, serving to exacerbate the physiological consequences of sub-optimal calcium diets. Among these are increases in 1,25-dihydroxyvitamin D, which increases vascular smooth muscle intracellular calcium, thereby increasing peripheral vascular resistance and blood pressure. Dietary calcium reduces blood pressure in large part via suppression of 1,25-dihydroxyvitamin D, thereby normalizing intracellular calcium.

The practical relevance of this approach has been confirmed in the DASH (Dietary Approaches to Stop Hypertension) trial, which demonstrated that increasing low-fat dairy product and fruit and vegetable consumption exerted profound blood pressure-lowering effects. The magnitude of this effect among hypertensives was comparable to that typically found in pharmacological trials of mild hypertension. 1,25-dihydroxyvitamin D also stimulates calcium influx in human adipocytes, resulting in stimulation of lipogenesis, inhibition of lipolysis and expansion of triglyceride stores.

Accordingly, suppression of 1,25-dihydroxyvitamin D by dietary calcium has been identified as a target, which may contribute to the prevention and management of obesity. Indeed, laboratory, clinical and population data all indicate a significant anti-obesity effect of dietary calcium, although large-scale prospective clinical trials have not yet been conducted to definitively demonstrate the scope of this effect. Thus, available evidence indicates that increasing dietary calcium intakes may result in reductions in fat mass as well as in blood pressure.

By. Zemel, M. B., Calcium Modulation of Hypertension and Obesity: Mechanisms and Implications Journal of the American College of Nutrition, Vol. 20, No. 90005, 428S-435S (2001)

Calcium and Infertility in Man

Sperm are a lively bunch to begin with, but they become even more excited when they zero in on an egg. They swim faster and their tail movements become more forceful and erratic.

Now scientists have linked this behavior, called "hyperactivity," to selective protein channels in the sperm's tail.

Sperm hyperactivity is necessary for breaking through two physical barriers that protect the egg from fertilization.

The current study links two key findings made in recent years about sperm hyperactivity. The first was that a sperm's whip-like tail is studded with selective channels made from a protein called CatSper1 that allows only calcium ions through. Scientists also knew that hyperactivity was associated with sudden influxes of calcium into the tails.

A sperm's tail is called a flagellum, and it spins like a boat propeller to move the sperm forward.

Using a cellular recording technique called patch-clamping, the researchers established
definitively that the opening of CatSper1 is responsible for the influx of calcium into the sperm.

The calcium surge causes the sperm's tail to spin faster and more unevenly and the sperm is propelled through its viscous environment more forcefully.

In experiments involving mice, the researchers showed that sperm lacking CatSper1 can't achieve the hyperactive state they need for egg fertilization (Than,2006).

Hyperactivity has its place. In the last seconds before fertilization, a sperm, somehow spurred by a spike of intracellular calcium, launches into high gear. Without this final, frenzied burst of energy, the sperm cannot penetrate the egg’s outer layers and will never merge its DNA with that cloistered within the egg’s protective membrane (Garbers, 2003).

Garbers, D. et al. Hyperactivated Sperm Motility Driven by CatSper2 Is Required for Fertilization. Proc Natl Acad Sci USA 100, 14869-14874 (December 9, 2003).

Than, K. 2006. How Sperm Get Hyperactive, LiveScience Staff Writer

The Role of Calcium to Prevent Osteoporosis

Calcium makes bones strong. In fact, bones and teeth contain 99% of the body's total calcium, with the remaining 1% in intracellular and extracellular fluids. Bones act as a storehouse for calcium, which is used by the body and replaced by the diet throughout a person's life. If enough calcium is not consumed, the body takes it from the bones. If more calcium is removed from the bones than is consumed in the diet, the bones become fragile and weak as a person gets older, leading to osteoporosis and fractures.

Osteoporosis prevention begins during childhood and adolescence by getting enough exercise and the proper nutrients, including calcium and vitamin D. However, adults can help prevent osteoporosis in the same ways.

The importance of calcium in developing and maintaining bone mass varies throughout a person’s life. At times of rapid and significant bone growth (during the teenage years) or rapid bone loss (after age 50 years), calcium is more important. Therefore, to reduce the risk of osteoporosis, calcium intake should be the highest during adolescence and after age 50 years.