Fosamax - Recent Studies
Dynamic Chiropractic – August 26, 2008, Vol. 26, Issue 18
Fosamax (Alendronate Sodium)
By Daniel Hough, DC
These days, we are bombarded with advertisements for prescription drugs.
Many of our patients are taking these drugs. In 2007, total revenue for
the pharmaceutical industry was more than half a trillion dollars and its
profits were more than $79 billion.1 As chiropractors, we need to be
informed about these prescription drugs so we can educate our patients
about their effects, side effects and dangers, as well as suggest safer
alternatives when appropriate. (Don't count on their medical doctor or
pharmacist to fully inform them.)
Candidates for osteoporosis commonly are advised to get a dual-energy
X-ray absorptiometry (DEXA) scan, an enhanced form of X-ray that detects
bone density. The test results are reported in the form of two scores. The
T score shows the amount of bone you have compared to a young adult of the
same gender with optimal bone mass. A T score above -1 is considered
normal. (A -1 T score represents a 10 percent loss of bone density.) A T
score between -1 and -2.5 is classified as osteopenia and a score below
-2.5 is defined as osteoporosis. The Z score reflects the density of your
bones compared to others of your gender, age and size.
Once bone density is determined, Fosamax (alendronate sodium) often is
prescribed to treat and prevent osteoporosis. Fosamax works by inhibiting
osteoclastic activity. Normally, old bone is removed by osteoclasts and
then replaced with new bone by osteoblasts. While Fosamax does, in fact,
increase bone density, it does not particularly increase bone strength.
It's similar to trying to repair an old house by nailing new boards to a
rotted structure; the walls are denser, but not a whole lot stronger.
Merck & Co., Inc., the manufacturer of Fosamax, claims the drug is proven
to prevent fractures. However, this is somewhat misleading. Although the
Fracture Intervention Trial (a randomized, double-masked,
placebo-controlled trial designed to test Fosamax's ability to reduce the
rate of fractures in postmenopausal women with low hip bone marrow
density) did show a reduction of fractures in patients with a T score
below -2.5, there was no reduction in fractures for those who had a T
score above -2.5.2
On the contrary, a recent study published in the Journal of Bone and Joint
Surgery suggests an increase in femur fractures with long-term use of
Fosamax.3 Numerous lawsuits have been filed claiming osteonecrosis of the
jawbone was caused by Fosamax. And according to the Physicians' Desk
Reference, possible side effects include abdominal pain, bone and joint
pain, constipation, diarrhea, indigestion, muscle pain, nausea, abdominal
distension, acid backup, difficulty swallowing, esophageal ulcers, gas,
headache, vomiting, changes in taste, inflammation of the stomach, rash
and skin redness.4
Nevertheless, Merck is not experiencing much setback. Merck's 2006 sales
of Fosamax were $30 billion. In 2007, Merck spent $7.6 billion on
marketing and administration and $4.9 billion on research and
development.5 The local CVS pharmacy in my town charges $94 for a month's
supply of Fosamax.
John R. Lee, MD, in his book What Your Doctor May Not Tell You About
Menopause, makes a good case that estrogen dominance contributes to
osteoporosis and estrogen dominance can be controlled with natural
progesterone.6 Adequate weight-bearing exercise and intake of calcium and
vitamin D have been shown to strengthen bones.
Hyperthyroidism has long been thought to cause bone loss. A recent study
published in Molecular Endocrinology confirms this idea and indicates high
levels of thyroid hormones do cause bone loss, but contrary to popular
belief, low thyroid stimulating hormone (TSH) is not contributory to
osteoporosis.7 Most medical doctors base the dosage of thyroid medication
on TSH levels and consider a low TSH level to be indicative of
hyperthyroidism, which is not necessarily true. A free T3 test, along with
clinical correlation of the patient's signs and symptoms, is a much better
indicator of thyroid status than a TSH test.8
Likewise, another study presented in Molecular Endocrinology indicates
it's a lack of thyroid hormones (hypothyroidism) rather than elevated TSH
levels that cause abnormal skeletal development.9 Consequently,
undermedicated hypothyroid patients might be at increased risk for bone
Fortune Magazine, July 23, 2007.
Cummings SR, et al. Effect of alendronate on risk of fracture in women
with low bone density but without vertebral fractures: results from the
Fracture Intervention Trial. JAMA, 1998 Dec 23-30;280(24):2077-82.
Goh SK, et al. Subtrochanteric insufficiency fractures in patients on
alendronate therapy. Bone Joint Surg Br, 2007 Mar;89(3):349-53.
Sifton DW, et al. The PDR Pocket Guide to Prescription Drugs, 5th
Edition. New York: Simon and Schuster, pp.540-2.
Merck & Co., Inc. www. merck.com.
Lee JR, Hopkins V. What Your Doctor May Not Tell You About Menopause.
New York: Warner Books, Inc., pp. 150-87.
Duncan Bassett JH, et al. Thyroid hormone excess rather than TSH
deficiency induces osteoporosis in hyperthyroidism. Molecular
Endocrinology, 2007 May;21(5):1095-107.
Hough D. "What Every Chiropractor (and MD) Should Know About the
Thyroid." Dynamic Chiropractic, April 7, 2003.
Duncan Bassett JH, et al. A lack of thyroid hormones rather than excess
thyrotropin causes abnormal skeletal development in hypothyroidism.
Molecular Endocrinology, 2008 Feb;22(2):501-12.
Dr. Daniel W. Hough is a 1991 graduate of Western States Chiropractic
College. A former member of the Montana Chiropractic Association Ethics
Committee, he practices in Bozeman, Mont.