The mystery of my rapidly dissolving femur neck bone has been solved. I had a follow-up bone
densitometry (DXA) done at the hospital where all original tests had been performed using the
same machine. That test showed a 4.5% improvement in L2-L4 spinal bone mineral density
(BMD) and 2.67% improvement in left femur neck BMD compared to the test performed about 1.5 years
earlier. Incidentally, this is about a 21% improvement in L2-L4 BMD since I have been taking Fosamax.
When I received these results, I was relieved, but felt the hospital where the faulty test was done
should be informed so an effort could be made to find the source of the problem. I wrote the chief of
nuclear medicine explaining what had happened. She replied, "On examination of our report, we found
the locum tenens physician in attendance erroneously reported the left femoral neck wards area value of
0.660 g/cm2 rather than the neck area value of 0.806 g/cm2." Additionally, they reprocessed the left
femoral data on newer software and found the neck value to be 0.903 g/cm2. I was not familiar with
software that could change the results of the tests, but mention it for your information.
The real source of the problem in this case was that neither I nor my physician got a copy of the
actual test results. Instead, only a copy of the attending physician`s summary was placed in my medical
record. It would have been a routine matter to see exactly where the source of the problem was had we
had a copy of the Lunar printout. In retrospect, I should have asked for one before asking for a repeat
DXA to be performed where my original testing was done. Hopefully, others will learn from the mistakes
in this case. Once again, it points to the importance of getting involved in your own health care. Without
my insistence on finding the source of the problem, I would still be living with the thought that I had lost
a huge percentage of my femur neck BMD and wondering when the next step would lead to a fractured
Fraser Lang, one of our members, spoke to me this quarter and mentioned that he has a theory about the possibility of childhood diseases being linked to adult osteoporosis. He`s aware of no
studies that suggest this, it is only a feeling that he has. He mentioned to me that he had spinal meningitis
when he was a youngster. Oddly, I also had spinal meningitis and I had pneumonia as a child that
required about the same amount of hospitalization and several medications to resolve it. If anyone else
had similar serious childhood diseases and you now have osteoporosis, would you mind
e-mailing me so I
can keep a tally of those that respond. Thanks in advance
for the responses.
I`m particularly concerned about the effects of corticosteroid use and its negative effect on BMD.
Some recent studies even implicate fairly short-term use and low doses with an increase in markers of
bone destruction. I wondered who, if anyone, sets standards for giving patients bone-forming or
antiresorptive medications in conjunction with corticosteroids. So, I e-mailed the Centers for Disease
Control to ask if they were involved with this. I did receive an answer and was informed that there are
recommendations from the American College of Rheumatology Task Force on Osteoporosis. If you are
interested, go to http://www.rheumatology.org/guidelin/osteo/osteo.html
to read the entire article.
Thanks to all the members who called, e-mailed, or sent in items of interest this quarter.
Recently, I even had a longtime friend mail a story from the Denver Post that concerned men with
osteoporosis. I didn`t realize he was that aware of osteoporosis, although I had sent him our Web site
information previously. Remember, this is your newsletter, so I appreciate hearing from you about its
Ask the experts
As mentioned in the last newsletter, Dr. Jeffrey Jackson, our men`s osteoporosis expert, has
consented to answer some questions from the men in the support group. If you have a
question for Dr. Jackson, please e-mail the editor`s address at the end of this newsletter and
questions will be forwarded to Dr. Jackson. This quarter Dr. Jackson answers a question e-mailed to me
from one of our members concerning the risk of prostate cancer.
Question: A recent study links excessive calcium intake with increased risk of prostate cancer.
Additionally, testosterone injections or patches have also been related to an increased prostate cancer
risk. Do those men with osteoporosis taking calcium supplements and/or on testosterone therapy require
extra diagnostic tests for prostate cancer, such as routine transrectal ultrasound?
Answer: There is only one study linking high calcium intake to prostate cancer, particularly
amounts greater than 1,000 mg per day. Additional confirmation from other studies will be needed to
completely assess the effect of calcium intake on prostate cancer risk. In the mean time, I normally do
recommend men limit their supplemental calcium intake to 1,000 mg per day. In some instances, based
upon specific needs of certain patients, I have them take 1,500 or 2,000 mg daily. An annual PSA
(prostate-specific antigen) and digital rectal exam, which I recommend for all men over age 50 who are in
normal risk categories, are adequate to detect prostate cancer. Men with osteoporosis under age 50 taking
calcium supplements and/or testosterone therapy may want to start the annual PSA and digital rectal
exam before age 50 as an added precaution after discussions with their physician. But, there is no need
for transrectal ultrasound or any other prostate cancer screening technique unless the PSA and/or digital
exam are abnormal. In summary, normal routine prostate cancer screening using the PSA test and digital
rectal exam are the only tests needed for men with osteoporosis taking calcium supplements and/or on
I was unable to summarize all the noteworthy topics from the Autumn 1998 issue of LunarNews in
the last issue of the newsletter. Here are a few other topics from it that were interesting.
Vitamin D update. LunarNews is very positive on the effect of vitamin D in treating
osteoporosis and not particularly positive about the effect of calcium supplementation on improving
BMD. On page 25, it is noted that: "Many studies over the past 20 years have shown that calcium
supplementation alone has no effect on spine, femur, or peripheral BMD. In contrast, vitamin D alone
increased axial BMD, including femur BMD, by 1 to 2% over a two-year period. As with
bisphosphonates, there is no effect on forearm BMD. In the immediate postmenopausal period, there is a
smaller effect on spine BMD, but still a substantial effect on femur neck BMD." They show a diagram
that displays the effect of 24 months of treatment with placebo, calcitriol (0.5 micrograms/day)
alendronate (10 mg/day), and calcitriol and alendronate (n=30 in each group). (See Frediani et al, 1998,
Clin Drug Invest 15;235-244). They compared the effect on the arms, spine, and total body. In every
case, there was a net loss of BMD when placebo was used. With all test medications there was a gain.
Calcitriol had the least effect, followed by alendronate, and then the combination of alendronate and
calcitriol. So, this study, along with several others they cite, shows that "Supplementation with vitamin
D decreases bone turnover, improves axial BMD in the elderly, and halves the rate of fracture."
Bisphosphonate update. This topic is
discussed on page 28 and 29. As you probably know,
"Bisphosphonates decrease bone turnover and increase axial BMD in osteoporotic patients even at low
doses. In a recent study of Japanese women, the effects of 2.5 mg/day of alendronate were identical
to 10 mg/day." (See Shiraki M, et al, (1998). Endocr J 45:191-201). They point out that, "Studies in US
and European women showed similar responses of the 5 and 10 mg/day doses, and also showed larger
increases in older women than those near the menopause." (Editor`s comment: This could be very
important for individuals having problems tolerating the 10-mg/day dose of alendronate, e.g., gastric or
esophageal discomfort. After stopping alendronate a few days or weeks to relieve any discomfort, it
could be restarted at either 5 or 2.5 mg/day doses. This very well might not cause any gastric
distress while adequately improving BMD. A previous edition of LunarNews also suggested a once
weekly dose of 40 mg of alendronate should be effective for osteoporosis. This single weekly dose might
not cause any gastric distress either while still improving BMD. These options should be discussed with
your physician if problems develop on 10 mg/day of alendronate. Also, note that Fosamax apparently is
only made in 10 and 40 mg tablets. Cutting 10 mg tablets in half to create the 5-mg dose would create a
rough pill that could more easily stick in the esophagus causing symptoms. So another way to get the 5-
or 2.5-mg dose should be investigatedand discussed with your physician if you decide to try this method).
They also point out that, "Bisphosphonates can be combined with other agents such as
estrogen or calcitriol to obtain additive effects. . ." (See the comment above on the Frediani study in
the Vitamin D update). Also, "A recent study showed alendronate could be given together with human
PTH to better stimulate bone formation." (Editor`s comment: Human parathyroid is available only in
clinical trials at this time).
There are newer third-generation bisphosphonates being developed and tested now.
"Ibandronate and zolendronate are even more potent than alendronate and pamidronate. The
former is being developed for injection every 3 months, while the latter has been developed as a
patch. Long-term administration of ibandronate increased bone mass in rats and maintained bone
Estrogen update. See page 31 and 32 for this discussion. Low estrogen is normally only thought
of as a problem for postmenopausal women, and as the cause of their osteoporosis. However, "New
studies are suggesting that estrogen also may play a role in the skeletal state of older men as well as
women." (See Khosla S et al (1998) J Clin Endocrinol Metab 83;2266-2274 and Riggs BL et al (1998) J
Bone Miner Res 13:763-773. (Editor`s comment: The finding of a link between male estrogen levels and
osteoporosis suggests that it may be necessary to test both serum estradiol and testosterone levels when
looking for a cause of male osteoporosis. This is new enough that men may have to ask their physicians
to perform these tests. Some physicians may not be aware of the possible link between low male estrogen
In the interest of brevity, I`ll list only the author`s names and the Medline UI number as the means
of finding the abstracts for the articles that are reviewed here. Here is how to use the UI number.
Go to Medline at http://www.ncbi.nlm.nih.gov/PubMed/ and enter only the numbers in the search
block, not the letters "UI." Then click on "Search" to find the referenced article.
Sex steroids and BMD in men. This topic was mentioned in the LunarNews section, but I
wanted to highlight some articles that you might want to review to get more information. The first is by
Slemenda CW et al, UI 97460000. This study tried to determine whether bone density in older men
(older than 65) was associated with serum sex steroids (estrogen [E2] and/or testosterone) or sex hormone
binding globulin (SHBG). They found that, "Bone density was significantly positively associated with
greater serum E2 concentrations. . ." Additionally, "There were weak negative correlations between
serum testosterone and bone density. . ." The authors concluded: "These data suggest that estrogens may
play an important role in the development or maintenance of the male skeleton, much as is the case in the
female skeleton. These data also indicate that, within the normal range, lower serum testosterone
concentrations are not associated with low bone density in men." Note that this study only looked at men
older than 65. You should not necessarily correlate these findings to men younger than 65-they may or
may not hold true.
In a study done at the Mayo Clinic, Khosla S et al, UI 98326239, the authors looked at sex steroid
levels in 346 men aged 23-90 years. They concluded: "These studies suggest that in contrast to
traditional belief, age-related bone loss may be the result of E (estrogen) deficiency not just in
postmenopausal women, but also in men."
The last study on this topic by Gillberg P et al, UI 99147953, compared 12 men with idiopathic
osteoporosis, aged 27-55 years with 12 age-matched men, with respect to serum levels of sex steroids,
and other factors. They found that there were decreased estradiol levels and decreased free androgen
index along with elevated sex hormone-binding globulin levels in the men with idiopathic osteoporosis.
Even the abstract of this article is difficult for the lay person to decipher. But, its finding may be
significant for any man with idiopathic osteoporosis. He should probably be tested for the various
significant factors found in this study, and then treated if they are found to be abnormal. It is one to print
and take to your physician if you are in doubt.
Hypercalciuria and osteoporosis. A recent study by Giannini S et al, UI 98391619 may have
significance for men with osteoporosis and hypercalciuria. Once again, this is a difficult study to
interpret and one I suggest you print and take to your physician if you think it may apply to you. My
interpretation may be completely wrong, so please don`t rely upon it without confirmation from your
physician. That being said, here is my understanding of the study. The authors looked at 49 patients,
aged 19-60 with calcium kidney stones and idiopathic hypercalciuria (excess urine calcium). They did
DXA measurements to determine BMD at the spine and femur. Patients were classified as either fasting
hypercalciuria (FH) or absorptive hypercalciuria (AH). The authors concluded: "A disordered bone
metabolism and bone loss are present only in patients with fasting hypercalciuria. An excessive acid
load, possibly of dietary origin, might be involved as a pathogenic factor." Osteoporosis patients are
often treated with diuretics if they are found to have hypercalciuria. From the findings of this study, it
would appear that only if hypercalciuria is noted after a fasting (as defined in this study) urine test, should
diuretic treatment be started. Otherwise, the hypercalciuria would apparently be unrelated to the loss of
BMD. This could be due to excess calcium, vitamin D, sodium, protein, or a potassium- or phosphate-deficient diet which would increase serum calcium levels, thus increasing urine calcium levels.
Hypercalciuria noted while fasting would indicate that the hypercalciuria is due to excessive bone
mineral breakdown. The non-fasting hypercalciuria should not need diuretic therapy, but the fasting type
should. So, a properly conducted 24-hour urinalysis for calcium is important before starting diuretic
therapy. If a fasting test was not done, I would be suspicious of the results. Another study that is a
review of the topic, and that describes the details of correct urinalysis testing, is by Bataille P et al, UI
Sunscreens and vitamin D level. I have been warned by my endocrinologist that wearing
sunscreen while outside could be blocking production of vitamin D, and I`ve read or heard similar
warnings elsewhere. A search of the literature turned up three articles that concluded that proper vitamin
D level can be maintained while using sunscreen and protective clothing. These include studies by
Farrerons J et al, IU 99069002, Sollitto RB et al, UI 98079984, and Marks R et al, UI 95243665 .
Although the protocols in all three studies were different, they all involved regular use of sunscreen (at
least SPF 15) and protective clothing. All subjects maintained serum vitamin D level within the reference
range throughout the studies which ranged from one summer to six years in duration. Patients were
getting adequate dietary vitamin D during the studies. So, regular use of sunscreen does not appear to
hinder serum vitamin D level if dietary intake is adequate. Protect your skin and take your vitamins.
Tetracycline and osteoporosis. I`m always interested in new therapies that might be on the
horizon to treat osteoporosis. In the past several years many research studies have shown that tetracycline
(TC) has multiple positive effects on bone and other body tissues. This involves a non-antimicrobial
property that allows inhibition of matrix matalloproteinases (MMPs) such has collagenase. TC can be
useful for treating periodontal disease, arthritis, osteoporosis, and cancer. Additionally, there are now
studies involving chemically-modified TC (CMT). The modification removes the antimicrobial effect,
which in the case of treatment of arthritis or osteoporosis, is an unwanted property. Two recent studies
are of interest on this topic. The first is by Sasaki T et al, UI 99138073. Using a modified TC (CMT-8)
on three-month-old female ovariectomized (OVX) rats, the authors found: "CMT-8 therapy produced a
significant (p<0.05) inhibition of trabecular bone loss and also induced bone formation in the OVX rats."
The authors conclude, ". . .CMT-8 therapy effectively inhibits bone loss after OVX, not only by inhibiting
bone resorption but also by inducing new bone formation in the trabecular areas of long bones. The other
paper is by Golub LM et al, UI 99138064. It is a review of the effectiveness of TC and particularly
describes the recent FDA approval of a low-dose TC (doxycycline) to treat periodontal disease ( the break
down of bone that supports the teeth). The exciting potential of the CMTs for treating osteoporosis
evolves around the notion that they both prevent bone break down and simulate bone formation. This
might make them a good adjunct to use with alendronate or calcitonin which only block resorption, or
they may be effective when used alone. Unfortunately, the wheels of science move slowly. The potential
of the CMTs has been known for many years and it still is not even in clinical trials. I wish I knew some
way to speed the process of clinical trials and FDA approval of these medications, but I have no idea. If
anyone has any ideas, I`d love to hear them. Another point to consider is that TC could be used now to
treat osteoporosis since it is an FDA-approved mediation. This would be an off-label use and your
physician could prescribe it as such. If you are not responding to currently accepted therapies, I
recommend a thorough search of the literature to educate yourself about TC to treat osteoporosis. Then
take your information to our physician to discuss the possibility of using it as an off-label prescription.
TC has been used for many years to treat acne and rheumatoid arthritis with minimal side effects from
that long-term use.
The effect of essential fatty acids on bone metabolism. There are three recent articles that
discuss a new and natural way to decrease bone turnover and perhaps to increase BMD. In 1994,
Sakaguchi K et al, UI 94224923 conducted an interesting study on rats supplementing their diets with
eicosapentaenoic acid (EPA). This is a polyunsaturated fatty acid that has a wide variety of beneficial
biological functions. The authors divided ovariectomized rats into four groups: (1) normal diet, (2) low
calcium diet, (3) EPA-enriched diet, (4) EPA-enriched and low calcium diet. They concluded: "These
results suggest that an EPA-enriched diet prevents the loss of bone weight and strength caused by
oestrogen deficiency or inadequate nutrition. There is a possibility that EPA could be developed to be a
novel anti-osteoporosis drug." In 1995, Claassen N et al, UI 95406249, supplemented male Sprague-Dawley rats with gamma-linolenic acid (GLA) and eicosapentaenoic acid (EPA) in ratios of 3:1, 1:1 and
1:3. They found that "Intestinal calcium absorption (mg/24 h) increased by 41.5% in the 3:1-supplemented group, compared with the control group." They also noted that, "The calcium balance
(mg/24 h) and bone calcium (mg/g bone ash) increased significantly in the 3:1 (41.5% and 24.7%) group,
compared with the control." The third study is by Kruger MC et al, UI 99130934, and involves a pilot
study using the EFAs GLA and EPA on sixty-five women (mean age 79.5). These women had a
background diet low in calcium, and were randomly assigned to GLA + EPA or coconut oil placebo
capsules while they all received 600 mg/day of calcium carbonate. Markers of bone
formation/degradation and bone mineral density (BMD) were measure at baseline, 6, 12, and 18 months.
The authors found, "Over the first 18 months, lumbar spine density remained the same in the treatment
group, but decreased 3.2% in the placebo group. Femoral bone density increased 1.3% in the treatment
group, but decreased 2.1% in the placebo group. During the second period of 18 months with all patients
now on active treatment, lumbar spine density increased 3.1% in patients who remained on active
treatment, and 2.3% in patients who switched from placebo to active treatment; femoral BMD in the
latter group showed an increase of 4.7%. The authors concluded: "This pilot controlled study suggests
that GLA and EPA have beneficial effects on bone in this group of elderly patients, and that they are safe
to administer for prolonged periods of time."
Certain other essential fatty acids have been shown to reduce the risk of coronary heart disease, so
it is possible for essential fatty acids to have positive health benefits. It would not be proper to generalize
based upon two studies on lab rats and a pilot study on humans. But, like the CMTs mentioned above,
EFAs may be a weapon that can be used to treat or prevent osteoporosis in the future after further studies
clarify the effectiveness of using them to modify bone mineral metabolism.
Correct diagnosis and treatment of osteoporosis. A common theme in this newsletter is that
patients should become knowledgeable about osteoporosis so they can become involved in the diagnosis
and treatment of their case. Your health is too important to assume that someone else will always know
everything about your disease and provide the best therapy. Here`s an article from France to reinforce
this theme. Laroche M and Mazieres B, UI 98303214 used questionnaires to patients and general
physicians to determine if the diagnosis and treatment of newly discovered osteoporosis were correct.
The disturbing results were that, "The initial biological investigation was correctly carried out by only 6%
of physicians. Treatment was correctly prescribed in only 34% of cases of osteoporosis with fractures,
50% of osteoporosis without fractures, and 50% of senile cortical osteoporosis." Also, "More than half
the general practitioners started treatment of osteoporosis without fractures on the basis of standard spinal
X-rays where the radiologist suggested bone mineral loss." Please note that is a French study and the
results certainly can`t be applied directly to this or any other country. But, they are disturbing enough to
make me want to know all I can about osteoporosis, or any other disease I have to see a physician about.
They substantiate the need to question anything that does not seem proper according to your
understanding of the diagnosis or treatment of osteoporosis. I hope this study makes you want to become
more knowledgeable and to not be afraid to ask appropriate questions, too.
Disclaimer. Diagnosis and treatment of osteoporosis are the responsibility of the patient and his or her physician. Nothing in this
newsletter is to be interpreted as a recommendation for treatment or to change treatment that your physician has prescribed. Although we
attempt to assure that information in this newsletter is factual, errors will occur. It is the responsibility of the reader to verify that
information they are acting on is factual. There is no relationship between this newsletter and any national osteoporosis group, including the
National Osteoporosis Foundation. All references to any such groups are for informational purposes only.