Here is the wrap-up of the three part series on osteoporosis by Dr. R. Keith McCormick whose Chiropractic practice can be found at 145 Old Amherst Rd. Belchertown, MA 01007 – Telephone # (413) 253-9777. Enjoy the final installment of what I think is an important issue and should be shared with all of your friends and relatives, especially females who might be taking bisphosphonate drugs.
WHY USE NUTRITIONAL THERAPY BEFORE RESORTING TO DRUGS? Strategic nutritional therapy can reduce a patient’s fracture risk without the risks for adverse effects posed by drug therapy. It therefore makes clinical sense to first use nutritional therapy before resorting to pharmaceuticals. There are, of course, situations where a patient may have already sustained one or more fragility fractures or has been determined to be in imminent fracture risk and may require a combination of drug (such as teriparatide, the 1-34 amino acid segment of parathyroid hormone) and nutritional therapy. But in the clinical setting, there is often a window of time where the use of nutritional therapy can be used as a first choice.
Specific biomarkers shown to be related to bone health can be used to identify metabolic dysfunction that can be improved through nutrition. In addition, because osteoporosis is a catabolic disease with high correlation to diabetes, Alzheimer’s, and cardiovascular disease, improving these indicators may reduce etiopathologic mechanisms of other disease processes. Drug therapy as a first choice does nothing to improve a person’s overall health. It can only reduce fracture risk and that only possibly for a limited time period.
WHAT FACTORS MUST BE CONSIDERED PRIOR TO PRESCRIBING A BISPHOSPHONATE? All too often, physicians look at improving bone density with a bisphosphonate as being the means to an end, when in fact the bone loss is just one symptom within a system struggling against a catabolic tide of inflammation-induced destructive forces. Before a person is placed on bisphosphonates as a panacea for bone loss, many factors should and must be ruled out. These include vitamins D and K deficiency, hypercalcemia, mineral deficiencies, high oxidative stress, chronic systemic inflammation, chronic low-level metabolic acidosis, malabsorption syndromes such as celiac disease, food allergens leading to chronic systemic inflammation, and heavy-metal toxicity. Artificially increasing bone density with a bisphosphonate while leaving the catabolic fires of destruction to burn on is both shortsighted and irresponsible.
Because there are currently no adequate guidelines available, it is difficult to assess an individual’s true fracture risk. The best we can do is to assess the patient’s lifestyle and superimpose upon this their level of bone mineral density to make a judgment call as to their risk for fracture. But laboratory tests can also be used to improve our assessment of risk and guide the application of a nutritional treatment program. These lab values include the resorption markers N-telopeptide and deoxypyridinoline, but other indirect markers such as morning urine pH, urine organic acids, chemistry screen, CBC, 24-hour urine calcium, TSH, anti-tissue transglutaminase, antigliadin antibodies, glucose, 25-hydroxyvitamin D, homocysteine, hsCRP, and others can also be used to assess fracture risk and overall health. When biomarkers are abnormal, they may reflect a rise in the patient’s risk for fracture. Prescribing a bisphosphonate before laboratory tests are obtained is not an optimal approach to improving a patient’s bone health.
In summary, when bisphosphonates are used before adequate laboratory evaluation and before appropriate strategic nutrition is used to reduce fracture risk, we have lost not only an important opportunity to normalize bone remodeling but a chance to reduce the catabolic forces of chronic inflammation and further disease.