Calcium Supplements Can Make Things Worse

Resolving the Calcium Conundrum

by Bill Sardi

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The dietary supplement industry is such a mixed bag these days. It has such promise, but often fails to deliver. For example, garlic pills were once the number one herbal supplement. But studies showed most garlic pills failed to deliver the active ingredient produced by fresh-crushed garlic cloves. Subsequently garlic pills fell from their top-seller spot. Turns out that stomach acid destroys the enzyme (alliinase) that produces the active ingredient allicin. Only if a garlic clove is crushed outside the acidic stomach is allicin produced. Only enteric-coated or buffered garlic tablets produce what a fresh-crushed clove of garlic delivers.

This is not to say that there haven’t been a plethora of negative studies that were designed to unfairly smudge the reputation of dietary supplements. Namely, the infamous beta carotene/smokers study, released just prior to the 1994 vote in Congress on the Dietary Supplement Health & Education Act which falsely claimed beta carotene increased the risk for lung cancer. Beta carotene was just ineffective (no benefit, no harm), that’s all.

Then there were those contentious vitamin E studies which manipulated statistics in an attempt to show miniscule differences in health risks would kill millions of Americans if they took too much vitamin E. However, subsequent re-analysis and inclusion of data from additional studies reveals statistical variation between studies (a higher proportion of male subjects in these trials) which explains the slightly increased mortality rate among vitamin E supplement users. Researchers now conclude that "high dose vitamin E supplementation can not be regarded proved to increase mortality."

But now the dietary supplement industry is once again, crying foul, and circling its wagons around calcium supplements, its number-two seller next to vitamin C and used by 43% of the American public (2003—2006), claiming a recent analysis of pooled studies shows calcium pills increase the risk of a heart attack by about 30% represents "cherry picking" of studies. But the dietary supplement industry reacted more out of protection of their vested interests than in delivering solid public health information.

The change of life is a change in calcium metabolism

Regardless of any argument over whether calcium pills are problematic or not, the change of life among females signals a redirection of calcium metabolism.

I often ask groups of women to fill in the blank to this question: "As menopause sets in, women experience a shortage of _______?" Women often appear puzzled at this question. They don’t know the obvious answer. Some will answer by saying calcium. But the onset of menopause doesn’t cause women to suddenly reduce their intake of calcium en masse.

Menopause is a shortage of estrogen, not calcium. Pouring more calcium into a menopausal woman is like pouring calcium into a barrel with a hole in the bottom. This seems too obvious.

Estrogen sends a signal for calcium to be held in bones. Without that signal, calcium slowly exits bone and is deposited in arteries. The risk for heart disease rises by 360% with the onset of menopause. Calcium released from bone is deposited in arteries, which causes loss of elasticity, inability to control blood pressure, and eventual blood clots or calcium plaque that can block a coronary artery that feeds the heart oxygen. This arterial blockage is called a heart attack.

Strangely, modern medicine acts as if it is baffled and dumbfounded when it is commonly reported that arteries calcify at a rate that correlates with loss of calcium from bone. This is called the "calcification paradox." There is no paradox, except in the minds of ill-informed physicians.

When women are young and fertile, and producing babies, they are donating calcium to their offspring and their estrogen holds calcium in their bones. Calcium from any source, dietary or supplements, does not generally produce calcifications in this era of life.

However, as calcium is lost from bone in menopause, it is deposited in the arteries (leading to arterial stiffness and high blood pressure), kidneys (leading to kidney stones), and breast (doctors believe this is often the first sign of breast cancer), as well as soft tissues (producing symptoms commonly experienced among patients with fibromyalgia). Postmenopausal women who have the highest levels of estrogen have the least amount of arterial stiffness. Similarly, women with the greatest amount of bone loss experience the most severe progression of calcification of their abdominal aorta.

Calcium supplementation in menopause is futile. Studies do show calcium supplementation helps to slow down the loss of calcium from bone, but there is no gain in bone density. On a net sum basis, calcium is still being lost from bone.

A recent review of 32 studies reveals that the use of calcium supplements (averaging around 1000 mg per day) for a period of two years reduced the rate of bone loss from —1.07% to —0.27%. Calcium loss from bone was slowed, but women were still losing bone! This is why virtually every woman taking calcium supplements fails their bone density test. Furthermore, the effect of calcium supplementation appeared to be lost after 4 years of treatment. Advocates of calcium supplementation often fail to mention these facts.

Repeated bone density tests for menopausal women have become a mindless ritual without understanding how to retain calcium in bone. The biological signal to hold calcium in bone must be restored. That signal is supplied by osteocalcin, a hormone secreted by osteoblast cells within bone. It has been said that elderly women have "sleepy osteoblasts" that need to be reawakened to produce new bone.

A major point of confusion is that women are mistakenly informed cholesterol plaque rather than calcium plaque is the primary cause of arterial disease. While the explanation for the age-related increase of plaque within arteries is largely centered on the accumulation of fatty material (cholesterol), more than 90% of these fatty plaques undergo calcification. Cholesterol is soft and waxy and does not stiffen arteries. Calcium deposits are like plaster, they stiffen like a statue. It is calcium, not cholesterol, which induces arterial stiffness.

As if all this wasn’t enough evidence to re-think the idea of calcium supplementation for menopausal women, there is also no evidence that the primary objective of calcium supplementation, to prevent hip fracture risk, is actually achieved. How could modern medicine be so misdirected?


Don’t think alternative medicine is the only party that got this wrong. Conventional medicine embraced calcium pills as well. But the science got lost in translation and commercial interests massaged the science to sell calcium-rich dairy products and calcium pills.

The International Osteoporosis Foundation recommends 1000 milligrams of calcium per day for young females and 1300 milligrams per day after menopause.

But that recommendation represents both dietary and supplemental sources. Since the American diet provides 800—1200 milligrams of calcium per day, supplements are not needed in most instances. Furthermore, in other countries throughout Asia where calcium intake levels are far lower (400—600 mg per day) than in Western countries, there are lower hip fracture rates among older females.

Why don’t women simply replace estrogen?

The answer to the above question is that women have literally been frightened away from estrogen replacement without adequate scientific evidence. This is despite the fact that estrogen replacement decreases the incidence of osteoporotic bone fractures by 25% to 50%. Instead, doctors now prescribe alternate medications to inhibit bone loss (Fosamax, Boniva, Actonel) which produce abhorrent side effects such as esophageal erosion, stomach irritation and even jaw-bone damage.

Hormone replacement therapy reduces bone turnover, increases bone mineral density (BMD), and decreases vertebral fracture rates by approximately 40%, even in women over 70 years of age.

It will come as a surprise to learn that abandonment of hormone replacement therapy in 2002 was a false alarm. Investigators were recently surprised by the "enormous discrepancy they found between the belief that hormones are dangerous and the lack of supporting data."

But wait, the Women’s Health Initiative study, costing nearly $1 billion, couldn’t be wrong, could it? Data from that study, initially released in 2002, horrified menopausal women as they learned their hormone pills might meaningfully increase their risk for breast cancer, Alzheimer’s disease and stroke. Over a million women abandoned hormone replacement therapy. But upon careful examination, researchers recently found that the recommendation to back away from estrogen replacement was based upon "findings reported in press releases and interviews of the principal investigators that were often distorted, oversimplified, or wrong."

The unfounded fear over hormone replacement is explained by how modern medicine assesses risks statistically. On a relative risk basis, critics of the "hormone horror" report say: "If women are going to stop taking hormone replacement solely to avoid breast cancer, then, on the basis of the studies to date, they should also stop eating fish, consuming grapefruit, taking antibiotics, using electric blankets, or serving as flight attendants on Scandinavian airlines — all of which have been reported to have stronger (though non-meaningful) associations with breast cancer than does hormone therapy."

What the National Institutes of Health reported in 2002 was that the risk for breast cancer increased by 26% among women prescribed hormone therapy compared to women taking an inactive placebo tablet. However, this was a relative risk assessment. The public reads this and think 26 out of 100 women will face an increased risk for breast cancer when in take the alleged risk rose from 5 in 100 to 6 in 100. The news media also failed to report that any imagined risk vanished in the same group of women in a follow-up study published in 2006.

Critical reviewers warned of alarmist news reporters. They write: "in one worst-case analysis, researchers calculated that a 50-year-old woman taking estrogen and progestin for 10 years has only a 4% risk of breast cancer. Without hormone replacement, her risk would be 2%. An alarmist headline writer might report this finding by stating that a woman’s risk is “doubled” if she takes estrogen/progestin for 10 years, whereas a reassuring statistician would say that she has a 96% chance of remaining free of breast cancer versus 98% if she does not.”

Another contradiction is that hormone therapy allegedly increases the risk for breast cancer, but other research suggests women taking estrogen pills live longer than women who don’t. The investigators asked: "How can the very hormones that allegedly increase the risk of breast cancer also be responsible for a better survival rate from that cancer?"

But haven’t the breast cancer rates declined dramatically since menopausal women abandoned estrogen replacement? Well, yes, but that trend began in 1990, long before women backed away from estrogen replacement.

These justifiably critical investigators say hormone replacement therapy is of great benefit to women as they approach menopause and face an array of unpleasant symptoms. Hormone replacement therapy may have beneficial effects on the heart for women who start taking hormones early in menopause (around age 50), but probably has little or no protective effect on women who begin use of hormone therapy in their mid-60s.

A lone news report, issued in Britain, assails the needless abandonment of hormone therapy by over a million women. The U.S. news press won’t dare address this topic, which is suggestive of a commercially manipulated news media. Hormone replacement therapy was itself replaced by a myriad of drugs — bone hardeners, antidepressants and blood pressure pills — to the glee of pharmaceutical companies. A most recent analysis suggests women should be happy, not fearful, about hormone replacement therapy. But will American women ever hear this, and will they be able to overcome their fear of estrogen?

Yes, but what about those calcium pills?

So far, this report has only addressed the loss of calcium from bones, its deposition into arteries with subsequent increased risk for arterial stiffening and possible heart attacks. But apart from calcium obtained from the diet, and calcium lost from bones, does calcium from supplements further increase the risk for arterial disease?

Some analysts say no. But the initial report which sparked this whole controversy, published in the British Medical Journal, which showed a 45% increased risk for a heart attack among menopausal women taking calcium pills, has faced its critics. But as the authors of that 2008 paper state in a follow-up rebuttal published in the Medical Journal of Australia:

    • The alleged risk, an increase of one heart attack among 29 calcium supplement users over a 5-year period, needs to be compared to its proposed benefit, which is prevention of 1 fracture among every 50 calcium supplement users over a 5-year period. The decreased risk of a bone fracture appears to be outweighed by the potential for a mortal event.
    • Furthermore, claims that calcium supplements don’t increase risk for heart disease cannot utilize data from studies where vitamin D was employed with supplemental calcium since vitamin D is an anti-calcifying agent.

While there are published studies which conclude that there is "compelling evidence that calcium supplementation of 1,200 mg daily does not significantly increase the risk of atherosclerotic vascular disease in elderly women," what’s the point? Women are not preventing life-threatening hip fractures by taking these pills.

Failure to heed an early warning

It was Stephen Seely in 1992, a British researcher, who proposed that arterial disease is primarily caused by the consumption of calcium-rich dairy products. Seely noted that countries of the world where dairy-calcium intake was high (New Zealand, North America, Ireland and Scandinavia) have the highest rates of heart disease.

Seely took an opposite view from today’s health officials in saying that the human body needs less calcium in old age than the growth years. He noted that age-related high-blood pressure is explained by calcification and stiffening of the aorta, the first blood vessel outside the heart. There is no increase in blood pressure with advancing age in undeveloped countries where calcium intake is low.

Dr. Seely was the first to prescribe IP6 phytate from bran as an anti-calcifying agent. Despite Dr. Seely’s warnings, public health authorities mindlessly continue to recommend American adults consume more calcium.

What to do about calcified arteries now?

What to do about calcified arteries for all those menopausal women who have been taking calcium pills? Running back to the doctor’s office for advice, in light of the information provided in this report, may not produce answers osteoporotic patients are searching for. Many patients prescribed calcium pills are likely to be taking blood pressure drugs and mother medications that would be unnecessary were they on hormone replacement or nutritional therapy sans calcium.

Calcium from diet or supplements?

One of the perplexing issues involving calcium and health is why some studies indicate calcium from the diet poses little or no risk for arterial calcification while calcium from supplements does. The answer to this question may be answered by the fact the diet provides nature’s master anti-calcifying agent in IP6 phytate.

Dietary IP6 phytate has been shown to have a favorable effect upon bone mineral density. Low amounts of IP6 phytate in the diet predispose menopausal women to osteoporosis. Higher intake levels of phytate, confirmed by urine sampling, indicates IP6 works in a similar manner to some bisphosphanate drugs at improving bone mineral density. IP6 is suggested as an alternative to bone-hardening drugs.

Get this. IP6 phytate not only builds bone, but it is a major antidote to calcifications throughout the human body.

Animals fed IP6 have strikingly reduced calcification of their aortas (first blood vessel outside the heart). In a rodent study, rats fed IP6 phytate were found to have 0.9 mg of calcium per gram of dry aorta tissue, compared to 21.0 mg per gram of calcium in non-treated rats. IP6 phytate is a remarkable anti-calcification agent.

IP6 also plays a strong role at inhibition of calcification in soft tissues like muscle and connective tissue.

IP6 is provided in bran, seeds, nuts and whole grains. A typical vegetarian diet provides around 1500 mg of IP6 per day, a carnivorous diet about 750 mg per day, a western processed food diet only about 250 mg per day. IP6 is also available as a dietary supplement. Tsuno Foods & Rice Company of Wakayama, Japan, provides the IP6 as an extract of rice bran in most brands of IP6 dietary supplements throughout the world today.

Vitamin D and bone health

Vitamin D is another bone-building nutrient that also acts as a decalcifying agent.

Vitamin D is a co-factor, enhancing the utilization and absorption of calcium and magnesium. Studies involving vitamin D alone have not shown a reduction in bone fractures.

Vitamin D facilitates proper utilization of calcium and inhibits coronary artery calcification. In a recent study, the provision of 2000 international units of vitamin D3 reversed stiffness (calcification) in the aorta of a black youth.

Vitamin D is often mischaracterized as an agent that induces calcification, but this has only been demonstrated in animals given mega-dose D (1 million international units). In more practical doses, ranging from 1000—10,000 IU, it is an anti-calcifying agent.

Fortunately, many dietary supplements designed to improve bone health provide calcium with vitamin D, which blunts some of the calcification induced by supplemental calcium.

Inexplicably, the amount of vitamin D required for children (200 IU) is not sufficient to prevent rickets in African American babies, and the amount of vitamin D in fortified milk and multivitamins (400 IU) is simply not enough to achieve optimal bone health for adults.

While the loss of estrogen explains bone loss in early postmenopausal period, a shortage of vitamin D accompanied by hyperparathyroidism explains bone loss later in life. Supplementation with at least 2000—3000 international units of vitamin D3 per day is needed to normalize parathyroid hormone levels.

A confounder is that being overweight appears to interfere with vitamin D supplementation. The provision of vitamin D among overweight women did not increase bone density in a recent study. Fat-soluble vitamins like D may be stored in fatty tissue rather than reach bone.

A special tip is that vitamins A and D are fat-soluble nutrients that compete for absorption and storage in the liver. A dominance of vitamin A and a shortage of vitamin D may worsen osteoporosis.

Magnesium and bone health

Magnesium alone suppresses hyper-parathyroid hormone production and increases levels of osteocalcin, the hormone that stimulates new bone production. Therefore, magnesium inhibits loss of bone in postmenopausal females.

Magnesium, an essential mineral in bone that interrupts calcium crystals to produce flexible rather than brittle bone, is an overlooked nutrient in osteoporosis. In a rodent study, animals were deprived of magnesium at 10%, 25% and 50% of their recommended mineral requirement, a deficiency state that is commonly found in humans, and bone loss and a decrease in bone-forming osteoblast cells resulted.

Vitamin K and bone health

Vitamin K has been called an omnipotent nutrient in the preservation of bone. It is an essential vitamin that is overlooked in various public health recommendations to avert age-related osteoporosis.

Among bone nutrients (calcium, magnesium, vitamin D and vitamin K), one study found vitamin K exhibited the strongest independent effect at inhibiting arterial calcification. Surprisingly, vitamin K2 has also been found to act as a free-radical scavenger (antioxidant) in arteries in a similar manner to vitamin E.

In rabbits, vitamin K2, at a 1 mg per kilogram of body weight dose (equivalent to 70 mg in a 160-lb human), was found to prevent the formation of progressive arterial plaque in artery walls and unexpectedly inhibited blood clots via its ability to reduce total cholesterol even though it is a necessary blood-clotting factor.

As previously indicated in this report, osteocalcin is a key hormone that stimulates osteoblast cells to produce new bone. Osteocalcin is dependent upon vitamin K to stimulate its production in bone-forming cells called osteoblasts.

Blood serum levels of vitamin K can be used as a marker for osteocalcin status. Among postmenopausal women with atherosclerosis, the lower the blood serum vitamin K levels the greater the arterial plaque (atherosclerosis), whereas there is no association between vitamin K and women who do not have blood vessel calcification. Vitamin K appears to control mineralization in atherosclerotic plaque. Unlike calcium, vitamin K prevents bone and arterial disease and protects against the side effects posed by vitamin K-blocking/ anti-blood-clotting drugs.

While Warfarin, a well-known blood-thinning drug, is a vitamin-K blocker which rapidly induces arterial calcification, the provision of vitamin K2 was shown to reduce arterial calcium content by 50% in an animal study, which also restored normal arterial elasticity.

In a state of vitamin K deficiency, osteocalcin lacks carboxylic acid, what is called undercarboxylation, which increases calcification of tissues. To put it more simply, without vitamin K, bones lose strength and blood vessels stiffen.

However, the focus of modern medicine is to measure bone density rather than bone strength. Vitamin K only modestly increases bone density, and the consensus is that vitamin K prevents fractures by increasing bone strength. Even with only modest improvement in bond density, vitamin K has been shown to reduce fracture risk.

Quite remarkably, vitamin K2 has been shown to increase bone strength in animals given a low calcium diet.

The combined used of vitamin D3 and vitamin K2 appears to both strengthen bone and improve bone density.

Vitamin K2 is compatible for use with bone-hardening drugs like Fosamax, Actonel and Boniva.

Even low-dose vitamin K2 (1.5 mg per day) has been reported to markedly increase carboxylated osteocalcin, a blood serum marker of bone strength, in middle-aged Japanese women.

Anti-blood clotting drugs (aka blood thinners, anticoagulants) interfere with vitamin K metabolism and have the side effect of inducing bone loss and arterial calcification. The very thing that blood-thinning drugs are prescribed for, to prevent blood clots in atherosclerotic arteries and veins, is promoted by the drug itself. The advice to avoid vitamin K-rich foods among patients with blood clotting problems appears to be counterproductive. Vitamin K supplementation stabilizes the blood-thinning properties of anticoagulant drugs. There is no reasonable substantiation for intentionally inducing a deficiency of an essential nutrient like vitamin K by avoidance of certain foods among patients with blood clotting issues. The provision of supplemental vitamin K with blood thinners averts drug-induced hemorrhage and mortality. Unfortunately, many patients on blood-thinning drugs have become fearful of vitamin K-rich foods.

Sadly, vitamin K is generally not found in dietary supplements designed to improve bone health.

Supplemental vitamin K, in doses typically provided by the diet, does not confer any additional benefit for bone health at the spine or hip when taken with recommended amounts of calcium and vitamin D.

Vitamin K1 is the form of this vitamin found in plants. Vitamin K2 is the form of this vitamin as produced by fermentation in the human digestive tract. Vitamin K2 is the preferred form in dietary supplements. The only company that has been able to synthetically produce K2 via fermentation processes so that it can be provided in a concentrated form (10-times the concentration, or 1000% greater concentration, than naturally-produced vitamin K2 from soy natto) is Blue California, a Santa Margarita, California company. The Blue California vitamin K2 makes it possible, for the first time, for this vitamin to be economically used in multivitamins, foods and beverages.


If women now have an aversion to hormone replacement therapy, nature provides estrogen-like molecules (phytoestrogens) that may have similar biological action to estrogen. While physicians often steer patients away from phytoestrogens, they don’t understand that these natural molecules dull the effects of natural estrogen (reduce estrogen dominance) while they act like estrogen in states of deficiency.

In an animal study, the provision of plant estrogens (phytoestrogens) both helped to maintain calcium in bone and helped to maintain adequate vitamin D levels, vitamin D being essential for proper utilization of calcium.

In one human clinical study, phytoestrogens from soy (isoflavones) reduced whole-body bone loss but did not slow bone loss at common fracture sites in healthy postmenopausal women.

In an animal study, flaxseed lignans (phytoestrogen) + low-dose estrogen therapy provided the greatest protection against bone loss at the lumbar spine in non-menstruating female rats.

A natural phytoestrogen, resveratrol, known as a red wine molecule, has been demonstrated to stimulate osteocalcin, the hormone that triggers new bone formation. Resveratrol may be an ideal candidate for estrogen replacement as it mildly mimics estrogen (1/7000th is biological activity) without tumor-promoting activity.

Final notes and recommendations

Oddly, most bone-mineral dietary supplements offered on store shelves today only provide calcium, magnesium and a smidgen of vitamin D. Two key nutrients identified in this report — vitamin K and IP6 phytate — are not found in any dietary supplements designed to promote bone health.

The pharmacologically-oriented medical profession took it upon themselves to define osteoporosis in practical terms as a drug deficiency rather than a nutrient deficiency. The bone-hardening drugs currently offered by pharmaceutical companies are fraught with side effects. The dietary supplement industry holds the keys to solving the explosion of osteoporosis in the growing population of senior Americans. But it too is misdirected. Dietary supplements formulated to promote bone health have not significantly changed in years, despite the changing science.

Public health officials are largely influenced by commercial interests such as the dairy industry that spends millions of dollars to over-promote calcium-rich dairy products (that, by the way, so many millions of Americans, among them African Americans, Italians and Asians, cannot tolerate due to lactose intolerance).

When it comes to age-related bone loss, it is the blind leading the blind. Dietary supplement companies misread recommendations concerning calcium intake levels, and massively overdose American women on calcium. A typical milk-drinking female might consume as much as 3000 milligram a day of calcium from her diet plus supplements. She is overdosing.

Osteoporosis is an estrogen deficiency, and later in life it is particularly a vitamin D shortage as an overactive parathyroid gland gets involved. The proven nutrient that reduces hip fractures, vitamin K, is overlooked in most bone-mineral formulas. In evidence of vitamin K2’s effectiveness, it has been an approved heart drug in Japan for decades.

It’s a sad day because so many Americans dutifully follow their doctor’s and dietician’s misdirected advice to take calcium pills as the change of life approaches. Such advice produces dire problems over time.

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