Calcium is important for many bodily functions.
The normal concentration of total serum calcium (bound calcium plus free calcium) is in the range of 8.8-10.4 mg/dL.
About 40% of the total calcium in the plasma is loosely bound to proteins; this calcium is referred to as bound calcium. The normal range of free calcium is 4.8-5.2 mg/dL.
Hypocalcemia (low calcium)
Hypocalcemia occurs when serum free calcium ions fall below 4.4 mg/dL, or when total serum calcium falls below 8.8 mg/dL. Hypocalcemia can result from (among other things) hypoparathyroidism (low parathyroid hormone), from failure to produce 1,25-dihydroxyvitamin D, from low levels of plasma magnesium, and from phosphate poisoning.
Most sarcoidosis patients have normal blood levels of calcium, although some do develop hypercalcemia and/or hypercalciuria. However, it has been known for more than 25 years that sarcoidosis patients can have elevated levels of Hormone D (1,25) even when they have normal calcium levels, and high levels of this hormone make people feel very ill.
Hypercalcemia (high calcium)
High levels of calcium ions (hypercalcemia) occur at free calcium ion concentrations over 5.2 mg/dL or total serum calcium above 10.4 mg/dL. Hypercalcemia usually occurs when the body dissolves bone at an abnormally fast rate, increasing both serum calcium and serum phosphate. Sudden hypercalcemia can cause vomiting and coma, while prolonged and moderate hypercalcemia results in the deposit of calcium phosphate crystals in the kidneys and eye.
Hypercalcemia is not just the result of excess vitamin D; it’s far more complex than that. Many normocalcemic sarcoidosis patients have suffered from kidney stones and calcium deposition into the soft tissue as a result of excess levels of 1,25D in their tissue.
When the calcium level is elevated, the parathyroid hormone (PTH) level should be checked to rule out parathyroid tumor.
The normal concentration of calcium and phosphate in blood and extracellular fluid is near the saturation point; elevations can lead to diffuse precipitation of calcium phosphate in tissues, leading to widespread organ dysfunction and damage.
Calcium requirements vary by age, gender and diagnosis.
It’s important to maintain adequate calcium intake (not too high or too low) to promote normal endocrine metabolism and bone health.
Patients are advised to maintain an adequate calcium intake but no more than their Recommended Daily Allowance (RDA) with a combination of both food intake and supplements (if necessary).
Recommended intakes are at this link.
Patients who have a history of hypercalcemia or hypercalciuria (high calcium levels) should consult their doctor regarding calcium intake.
Articles of interest:
Food Sources of Calcium
It's best to obtain adequate calcium from your diet.
An extensive list of the calcium content of foods is available online from the U.S. Department of Agriculture:
Keep in mind that some foods that are high in calcium contain high levels of vitamin D also. These are to be avoided.
Here are the calcium levels of a few foods:
Be sure to check packaged food labels to ensure no vitamin D has been added.
Calcium supplementation isn't necessary unless serum calcium levels are low and the diet is deficient in calcium-rich foods. Ideally, all daily calcium should come from food but sometimes supplementation is necessary. Patients should supplement with a calcium tablet that does not contain vitamin D. For each 500mg of calcium taken, a dose of 200-250mg of magnesium should be taken for better absorption. Calcium without vitamin D can be found at most stores that sell vitamins, or online.
Calcium supplements are available over the counter; labels commonly include both the total milligrams of calcium salt and the milligrams of elemental calcium in each tablet. Determination of the dose required to meet daily calcium requirements is based on the amount of elemental calcium. Calcium carbonate provides relatively high elemental calcium content (40%) and is inexpensive and widely available.
Be sure to take only the amount needed to equal the RDA of 1000-1500mg/day of calcium with both food and supplement combined. If too much calcium is ingested at one time, it may not all be absorbed. It's best not to consume more than 500 mg of calcium at any one time.
Calcium supplements may interact in various ways with many other medications, including fluoroquinolones, beta blockers, calcium channel blockers, digoxin and furosemide.
If too much calcium is ingested at one time, it may not all be absorbed. It’s best not to consume more than 500 mg of calcium at any one time.
Calcium supplementation is more likely to cause vascular events than to prevent fractures.Calcium supplements may interact in various ways with many other medications, including fluoroquinolones, beta blockers, calcium channel blockers, digoxin and furosemide.
Calcium can interfere with the body's ability to absorb tetracycline medications and, therefore, diminish their effectiveness. Calcium-containing supplements and antacids should be taken at least two hours before or after taking antibiotics.
Studies prove excess calcium does not strengthen bones
BMJ and The Lancet recently published studies showing that calcium supplements (and vitamin D) do not strengthen bones:
The role of caffeine as a risk factor for osteoporosis is controversial, though several studies have shown that caffeine consumption is associated with decreased bone mineral density (BMD).
This study concluded, "In summary, our data provides evidence of a direct effect of caffeine on VDR protein expression and osteoblast activity, which could be one of the probable responsible molecular mechanisms for the role of caffeine in osteoporosis."
Osteoporosis and osteopenia
Osteoporosis literally means "porous bones." It is characterized by gradual loss of bone mass, causing the bones to become thinner, fragile and more likely to break. The risk of fracture is the major concern. Vertebral fractures due to osteoporosis can result in decreased height and cause the spine to curve. The most common sites of osteoporotic fractures are the hip, vertebrae and wrist.
Osteopenia describes a lack of calcification in bones. It’s the term used to describe bones that are losing mineralization, but not as significantly as in osteoporosis.
Many inflammatory diseases are associated with a higher risk of osteoporosis, including rheumatoid arthritis, celiac disease, anorexia nervosa, inflammatory bowel disease and lupus.
Bones are constantly in the process of remodeling and renewing through the work of specialized cells known as osteoclasts and osteoblasts. Osteoclasts dissolve bone, usually old bone cells. As osteoclasts work, calcium is released from dissolved bone cells into the blood supply. Normally, osteoblasts, the bone-building cells, work in near-balance with osteoclasts to lay down new bone as soon as old bone is dissolved. Factors that can upset the normal balance between bone resorption and bone formation include hormonal imbalances and lack of nutrients/minerals necessary for forming bone.
Inflammatory cytokines and elevated hormone 1,25-dihydroxyvitamin D can disrupt the balance between osteoclasts (bone dissolvers) and osteoblasts (bone builders). As osteoclasts dissolve increasing amounts of bone, calcium and other minerals are released from bone. Calcium may be deposited in soft tissue, and circulating serum calcium levels may reach clinical hypercalcemia, which if untreated will cause kidney damage.
Causes of bone loss
Th1/Th17 inflammation may cause calcium depletion from bones and excess circulating calcium. Thus, it is the disease process that causes a calcium deficit which results in osteopenia and osteoporosis. The Vitamin D Receptor (VDR) transcribes the genes which are the key to shuttling calcium through the epithelium. Thus, it is not vitamin D which causes absorption of calcium from the gut, it is a competent VDR.
At levels above about 42 pg/ml, the 1,25-D generated by Th1/Th17 inflammation begins to stimulate bone osteoclasts causing bone to be resorbed back into the bloodstream. This leads to osteoporosis (including dental fractures) and to calcium deposition into the soft tissues, including lungs, breasts, muscle bundles (fibromyalgia) and kidneys (kidney stones).
The Danish epidemiologist Brot studied 500 healthy women (i.e., they were not drawn from a population with particular health issues) aged 42 to 58 and concluded that in this group bone density was strongly inversely proportional to 1,25-D levels (i.e., low bone density was strongly associated with high 1,25-D levels) and only rather weakly directly proportional to 25-D levels. The sample was chosen randomly - and was not done to test the impact of any particular treatment program.
Relationship between bone mineral density, serum vitamin D metabolites and calcium: phosphorus intake in healthy perimenopausal women.
High levels of 1,25D in persons with uncontrolled Th1/Th17 inflammation stimulate osteoclasts that break down bones. IT patients don't experience 'deprivation in vitamin D' because inflamed tissues produce enough hormonal vitamin D. A reduction from excessive levels of 1,25-D will help bones because there will be a better rate balance between bone formation and bone breaking down.
A healthy person will 'turn over' their total skeleton in about 10 years, with structurally weak bone being broken down and replaced with stronger new bone. Bone density can be complicated because the very structure is as important as density; in some cultures people have decreased bone density but a near absence of fractures. Everyone loses bone density over time; it's normal and doesn't have a good predictive relationship with possible fracture. Bone structure is what is most important and IT is the best thing chronically ill patients can do to help their bone structure. A lack of dietary D does not cause osteoporosis; whereas a high level of 1,25-D does.Activity
Lack of activity is another factor in loss of bone density in Th1/Th17 disease, because weight-bearing exercise, or any activity that causes muscles to pull against bones, provokes the formation of stronger, denser bones. This is especially problematic when chronic illness results in inactivity or prolonged bed rest.
Simple, carefully selected exercises can slow Bone Mineral Density (BMD) loss and help build stronger bones. Patients who are not able to exercise now, can look forward to recovering stamina and then working up to exercises that will focus on building strong bones. Studies have shown that even postmenopausal women can improve bone density by adding weight bearing and muscle strengthening exercises to their routine.
Other factors that can interfere with strong bone development:
Use of drugs such as corticosteroids and other immunosuppressants, high-dose thyroid replacement therapy, some anti-seizure medications, and contraceptives (injected DepoProvera) can lead to loss of bone mineral density.
Elevated parathyroid hormone (hyperparathyroidism) and elevated thyroid hormone (hyperthyroidism) can result in osteoporosis.
Loss of bone density is usually painless - which is why many people do not know they have the problem until they suffer a fall or fracture (which can be painful). If you have back pain or bone pain, your doctor may evaluate you to see if you have suffered fracture. Th1/Th17 disease can cause bone pain and patients have reported bone pain as a Herx symptom.
Assessing bone density
The most widely used test to screen for osteoporosis is a bone density test (densitometry) that uses an enhanced X-ray technology called Dual-energy X-ray Absorptiometry (DXA or DEXA). This test is not the same as a bone scan which relies on a radioactive injection to help detect areas of increased bone metabolism due to fracture, infection or tumors.
During a bone density test, a low energy source is passed over the body. Information evaluated by a computer allows an estimate of bone mass. This helps the doctor assess bone strength, osteoporosis and risk of fracture.
The results of a DEXA bone density test are interpreted by a radiologist and a report is sent to the doctor who ordered the test. The results will have two scores or numbers.
The T-score compares patients to a young adult of the same gender with peak bone mass. Any T-score larger than -1 is considered normal.
The Z-score reflects the amount of bone compared to other people your own size, age and gender. This number is related to percentiles. Originally, only Z-scores were calculated, but when bone density machines became commercially available beginning in the 1980s, T-scores were devised because different manufacturers could not agree on a standard measurement.
Be careful in interpreting bone tests results because bone density, while an excellent measurement of compressive strength, does not reveal tensile strength, i.e. whether or not your bone will resist breaking from being pulled or stretched, as commonly occurs in a fall or similar trauma.
Also, "osteoporosis," as presently defined by bone scans (DXA scan) using the T-score, inappropriately defines "normal bone density" according to the standard of a 25-year old, young adult. In other words, if you are 40, 50, or even 100, the T-score-based system says your bones are not normal, or even diseased if they are not as dense as they were when you were a young adult. If they used the age-appropriate Z-score, some cases of "osteopenia" and "osteoporosis," would disappear because they were inappropriately classified.
For detailed explanations of DEXA scores, see these links:
The reproducibility of DEXA scores is frequently reported at 1-2 percent. That 1-2 percent is the average, but the range of reproducibility can vary as much as seven percent. Variations come from changes in machine reading (using the same machine), technologists who are doing the test, and slight changes of body positioning, all of which can affect the end results. The most frequent source of error in repeat tests is patient positioning. The technology is limited because BMD is a two-dimensional image of a three-dimensional object.
It’s important for patients to get repeat BMD measurements done on the same machine each time, or at least a machine from the same manufacturer. Error between machines or trying to convert measurements from one manufacturer's standard to another can introduce errors large enough to wipe out the sensitivity of the measurements.
This Medscape article (registration required, but it is free) Uses and Limitations of Bone Mineral Density Measurements in the Management of Osteoporosis concludes:
“BMD measurement remains the most useful diagnostic tool for identifying patients with osteoporosis. Although they are helpful in guiding decisions to initiate osteoporosis treatment, subsequent changes in BMD provide an imperfect indicator of treatment efficacy. Analyses of clinical trials show an inconsistent relationship between increased spinal BMD and a decreased risk of vertebral fracture. Increased BMD accounts for less than 25% of the overall reduction in fracture risk in most instances. Consequently, fracture risk reduction itself remains the most clinically relevant therapeutic outcome of osteoporosis therapy.”
Other tests that are used to evaluate bone health include bone ultrasound (usually of the heel) and quantitative computed tomography (QCT) of the spine.
Here is a link to an interesting interview with Gillian Sanson, the author of The Myth of Osteoporosis: What Every Women Should Know About Creating Bone Health. Although she doesn’t have our new information on ‘vitamin’ D and does not understand that a low 25-D is most frequently associated with a high 1,25-D, she is generally on the right track. You can see that BMD test scores are not a good predictor of fracture.
See also Dexa Scan Overuse.
Osteoporotic fractures can occur without any trauma (spontaneous), but falls are the greatest cause of fractures in people with or without bone loss.
People who are at risk should take measures to prevent falling:
Medications touted to prevent osteoporosis
The Biphosphonates (Fosamax, Actonel, etc.), commonly prescribed for osteoporosis, are on our list of medications to avoid because they can cause calcium deposition into the soft tissues and reduced organ function.
Evista (raloxifene) is a new medication sometimes ordered to treat osteoporosis. It is neither an estrogen nor a hormone. It is a Selective Estrogen Receptor Modulator, or SERM, which mimics estrogen's effects in some tissue while blocking its effects in other tissues. It helps build bone without negatively affecting the breast or uterus.
Doctors prescribing Evista are cautioned that it may interfere with thyroid hormones such as levothyroxine. They are also warned to use it with caution in women who have a high level of blood triglycerides, liver disease or vitamin D deficiency which are all common among patients with Th1/Th17 inflammation.
This indicates that it will introduce an unknown and potentially detrimental variable into the restorative treatment equation and, thus, should be avoided.
Inflammation Therapy resolves the inflammatory process that is the cause of calcium metabolism abnormalities, but remodeling bone mass takes time (the skeleton regenerates every ten years).
During the early phases of therapy, skeletal remodeling may not change very much because the immune system response is still influencing homeostasis.
Until the pathogen load is reduced to healthy levels there may not be much improvement in skeletal parameters. So a stable bone scan is a positive sign.
Vitamin D and Osteoporosis
Updated December 2, 2015