I am currently on vitamin D and calcium with a hope of preventing fractures from osteoporosis. Recently I read in the newspaper that vitamin D and calcium weren't useful in preventing fractures! Have I been wasting my time?
Probably the best way to answer this question is to give a summary of osteoporosis, the disease process, and what is useful in prevention and treatment. The short answer to the question, however, is that the study used too little vitamin D too late (they only treated patients older than 75), and in fact far more studies have shown great benefit with vitamin D, if the dosage is optimized.
Osteoporosis is a term that often strikes a cord of fear in patients. This disease forces many patients to come to the realization that they are getting older, and that they are not in fact immune to these chronic degenerative diseases. Osteoporosis, or the loss of bone density and structure, is also unique in that most patients usually think that it is inevitable; a certain degree of helplessness also manifests because patients are not aware that there are pro-active steps they can take to stop and even reverse the disease. New advances in both diagnostic and therapeutic tools have recently come into the prime-time of active treatment.
By definition, osteoporosis is a clinical entity of impaired bone strength with low bone mineral density, poor bone quality, and increased fracture risk. Bone is an active metabolic tissue, with two main types of cells involved in remodeling of the bone. One type is called the osteoblast, which is responsible for adding new bone the other is called the osteoclast, which is responsible for removing set bone. The balance or rate of these activities is roughly equal through life until menopause, where the rate of bone loss is greater than the rate of bone formation. This is important: the bone mineral density decreases because there is an overall loss of bone. It is this eating away of the bone structure by osteoclasts, without sufficient repair by osteoblasts, which lowers the density of bone and more importantly destroys the architecture and structure of the bone that leads to fragile, fracture-prone bone tissue. The analogy is how bone can be compared to a good walking stick, which is relatively thin but can support great weight. When notches and small holes are made in the walking stick, it may look normal from afar but sooner or later the stick is going to collapse and break. In the first 20 years of life, we lay on the most bone mass and thus osteoporosis can often happen from inadequate bone formation during these years. Females are at about twice the risk compared to males. The main difference between the sexes is that about 10% of total bone density is lost in the first 5 years following menopause.
There are several factors important in the natural process of building bone density. Peak bone mass occurs in early adulthood. Heredity definitely plays a role, as body size as certain genes define our risk for osteoporosis. Interestingly, many of these genes can be detected and then controlled by changes in our environment. This is in direct contrast to the commonly held belief that we can't do anything about our genes. This test is called Genovations and involves sequences areas of a patient's genome for abnormalities in proteins; this information is then used to customize therapeutics and increase bone mineral density. Poor nutrition during the growing years has been implicated in increased risk of osteoporosis. It is also very interesting to note that calcium deficiency in growing years is usually only important when it is extremely severe, a condition not often seen in the developed world. Lack of physical activity in children, late or delayed puberty, and excessive corticosteroid (immune suppressants) also decrease bone mineral density. On the other extreme, excessive exercise in athletes (in females it is exercise so extreme as to cause suppression of menstruation) also decreases bone mineral density.
In terms of having excessive bone loss, factors that are important include the following: prolonged estrogen or androgen insufficiency (as seen in cases of early menopause, either surgical or natural), long life (at the age of 85, 50% of all women would have osteoporosis), and specific medical problems (such as interference of calcium and vitamin D absorption, and kidney diseases leading to improper handling of calcium). Net bone loss tends to start in the 30's with women, and in the 40's with men.
At actually menopause, 10-12% of bone loss is from the spine, with significantly less loss from the hip. This disparity is important because it implies that some parts of the skeleton are more receptive and responsive to estrogen, and thus loss of estrogen at menopause imparts a selective loss of skeletal bone. It is also interesting that much of old age bone loss comes from vitamin D deficiency, and this is a very simple state to detect and correct adequately.
The standard assessment of osteoporosis has always been the DEXA scan. DEXA stands for dual energy x-ray absortiometry. Other tests (for example finger or heel scans), may be useful but they cannot diagnose osteoporosis. From this type of imaging, we get two "Scores" which have confused many patients. The "T" score defines how far you deviate in bone mineral density from average young people. A positive T score shows you have bone mineral density about an average young person, and a negative score means you have below average. Thus, a negative value is below average but not necessary abnormal nor indicative of significant disease. The Z score compares the patient's bone mineral density to that of average levels for matched age and gender. Importantly, for every negative whole number decrease in the T score, fracture risk increases by 1.5 fold. Thus a person with a T score of 2.5 has 1.5X increased fracture risk compared to 1.5.
There are certain limitations to DEXA testing alone, as it does not determine the actual structure and architecture of the bone. For example, if a patient who never put on much bone when she was young had a T score of 2, was compared to a patient who had regular bone density as a youth but now after menopause has a T score of 2, the second patient would have a much greater risk of fracture. This is because for the second patient to achieve a score of 2, she would have had to lose significant bone density and thus, the architecture of the bone would have been severely compromised. In the first patient, although she also has the same bone density according to DEXA scan, her architecture and structure of the bone is likely still intact imparting greater protection from fracture.
It should be noted that calcium intake over the life span is not a strong risk factor for osteoporosis. Vertebral fractures are highly associated with decreased quality of life. These fractures occur earlier than hip fractures. Single fractures lead to transient and short periods of pain, whereas multiple fractures are associated with persistent pain. Hip fractures are associated with later age, and rise in frequency rapidly after the age of 75. With a hip fracture, there is a short term increased risk of mortality. Research has often focused on hip fractures because the cost of management is high, whereas as clinicians vertebral fractures may be more important to the patients quality of life. Hip fractures almost always occur after a fall, whereas falls are a minor determinant in spinal fracture.
Strong risk factors for fracture include:
-
age
-years of estrogen deficiency
-low body weight
-personal history of fracture
-family history of fracture
Other risk factors for fracture:
-increased biochemical markers of bone turnover
-genetic markers
-vitamin D deficiency
-vitamin A toxicity (note severe deficiency is also associated with fracture)
-elevated homocysteine levels
-low protein levels
Undoubtedly, calcium is often the first nutrient thought of when considering bone health. While it has been shown that only severe deficiency in growing years is important, a nutritional amount of calcium is important especially during the growing years. Twin studies have indicated that mega-dosing on calcium does not increase bone density in the supplemented patient indefinitely. Therefore, a nutritional dose of 1200-1500 mg of calcium (total intake of food and supplements) is a good goal. If taken during the years of growth, especially adolescence, stature and peak bone mass is optimized. In premenopausal women calcium preserves bone mass, but it is extremely difficult to make them calcium deficient. In menopausal women, no study has shown that giving calcium decreases bone loss as the condition is an estrogen deficiency, not a calcium deficiency!
Calcium is important in conjunction with vitamin D to prevent bone loss and fractures. Tissues become less sensitive to vitamin D as age increases. Fall frequency, bone loss, and fracture frequency decreases with supplementation. Note that recently in the news there was attention paid to a study that seemed to show that vitamin D, with or without calcium, did not decrease fractures. This study should be taken with a grain of salt for three reasons. Firstly, the dosage of vitamin D was likely far too low at 800 IU. At my clinic we test vitamin D using the DiaSorin assay (more expensive but much more accurate) and then supplement to an optimal amount. Some patients need 2000-4000 IU a day, not 800 IU (note that such high levels should only be done after testing and with blood monitoring). Secondly, they studied older patients, all above the age of 75; starting vitamin D at such a late age and at such a low level is likely to underestimate the effectiveness of treatment. Thirdly, similar studies have been done previously which have shown great benefit.
Magnesium is not useful in calcium absorption. This urban legend came into play from an extrapolation from the opposite observation: namely that magnesium deficiency causes low calcium levels. In reality, magnesium is necessary for the secretion and activity of a hormone that regulates blood calcium levels; and interestingly, calcium absorption goes down as you add magnesium. The effects of protein, caffeine, fiber, and phosphates on the need for calcium are minimal in patients who have a regular intake.
Perhaps the most exciting new treatment in the field of osteoporosis reversal is the use of a hormone called PTH or parathyroid hormone. Drug companies are coming out with synthetic analogues to this natural hormone and administering it to stop and reverse the disease process of osteoporosis itself. When the blood receives a "pulse" of PTH, the net effect is a change in the activity of bone formation and bone destruction. The overall effect is that the osteoblasts increase their activity of bone formation and the osteoclasts decrease their activity of bone breakdown. Overall then, bone density tends to improve with such treatment! Currently the PTH analogues can cost up to 3000 USD a month to administer. Naturopathically, we can almost triple the amount of PTH in the blood by taking advantage of another therapy that is mainly used in cardiovascular disease and in heavy metal toxicity. This is chelation with disodium EDTA. When we administer this agent intravenously, the blood level of calcium drops because the EDTA binds up free calcium. The response of the body is to have PTH secreted in order to restore blood calcium levels. This secretion of PTH is what changes bone metabolism and what can cause the bone mineral density to increase! In fact, the use of this therapy in osteoporosis was hinted at in the early years when doctors asked the question whether or not the cardiovascular patients being treated with chelation were at increased risk of fracture because the blood levels of calcium dropped during treatment. A study was then done comparing before and after chelation of bone mineral density; instead of the expected loss in bone mineral density, it was found that the bone mineral density improved!
Conclusions:
Vitamin D is much more important than calcium supplementation. The RDA of 400-600 IU is usually grossly inadequate. The source of vitamin D includes the sun, and thus patients who live in the northern latitudes usually have deficiencies. In fact, in Portland, the prevalence of vitamin D deficiency in women is close to 50%! The absolute lower limit of serum concentration of vitamin D is 20 ng/ml, but optimal levels are around 45 ng/ml. Vitamin D levels should be monitored in the blood to ensure optimal but not toxic levels; the best assay for this is available in labs in the US (my clinic sends samples to a lab in Seattle).
Treatment at my clinic involves testing of the vitamin D levels to get an approximate daily dose for supplementation, retesting in one month, and then at 3 months to ensure adequate dosing. Calcium is given in conjunction to supplement daily intake. Exercise is prescribed as this is especially important with aging (note that exercise is minimally important in terms of bone mineral density between the ages of 20 and 60). Finally, chelation once a week is given to triple the amount of parathyroid hormone (PTH) in the blood, so that bone formation is stimulated and bone breakdown is slowed. With this comprehensive approach, the risk of fracture can truly be minimized effectively.
