Friday, September 28, 2012

Oxytocin (and Nipple Stimulation) Improves Bone Density

Oxytocin is produced by the posterior pituatary gland in the brain. This hormone is best known for its role in promoting uterine contractions during childbirth but it is also involved in sexual arousal and orgasm, thus the label, "love hormone." Oxytocin is also important for social behaviors such as trust, contentment, empathy, bonding, and love. Without it we would have a pretty dull and detached life. Recently, researchers found yet another extremely important biological activity of oxytocin--it helps estrogen keep our bones strong and healthy.

Development of the fetus during pregnancy places substantial nutrient demands on a woman. Normally, estrogen levels increase during the 9 months of pregnancy. This helps to preserve bone by promoting an increase in calcium uptake from the gut and by stimulating osteoblastic bone-building activity in the skeleton. After delivery, estrogen levels return to normal and the heightened calcium loss through mother's milk during breastfeeding can severely stress skeletal calcium reserves. However, if the mother is consuming adequate calcium, bone density will typically recover within several months. A study from the Mount Sinai Bone Program at the Mount Sinai School of Medicine in New York shows us how.

Colaianni et al. (2012) found, through studies with mice, that the bone-building action of estrogen occurs, in part, through oxytocin produced by osteoblasts in bone marrow. This, they concluded, is the mechanism that facilitates "rapid skeletal recovery during the latter phases of lactation."

During childbirth there is a huge surge of oxytocin released into the mother's blood stream by the pituatary. This stimulates uterine contractions to facilitate the birth. Once the baby is delivered and begins to breast feed, this stimulation promotes oxytocin release, an important mechanism for aiding uterine postpartum recovery.

Nipple stimulation and oxytocin release throughout breastfeeding not only supports bonding behavior * between mother and baby but also helps the mother regain bone density. In a study by Karen L Pearce at the University of Massachusetts (2006), 35 women were assessed for the effect breastfeeding has on bone density. What Pearce found was that "greater intensity of breastfeeding in the amenorrheic months significantly attenuated bone density loss " and that "women who breastfed with less intensity showed greater decline in their bone mineral density."

Oxytocin is clearly extremely important for bone health and it does not stop when child bearing years are over. This love hormone can help maintain bone density throughout your life...all it takes is a little bit of love, and nipple stimulation. 

* Note: For more information on the health benefits of breastfeeding check out La Leche League International. This is a great organization. Their mission is to promote a better understanding of breastfeeding as an important element in the healthy development of the baby and mother.

Colaianni et al. 2012. Bone marrow oxytocin mediates the anabolic action of estrogen on the skeleton. Journal of Biological Chemistry 287(34):29159-67.

Pearce, L. Karen. 2006. Breastfeeding and bone density change. Electronic Doctoral Dissertations for UMass Amherst. Paper AAI3215777.



Friday, September 21, 2012

Low TSH (Thyroid-Stimulating Hormone) Increases Bone Loss

The thyroid gland is the body's major regulator of metabolism. By releasing T4 (thyroxine) into the blood stream (which is then converted to T3) the thyroid gland activates a multitude of chemical reactions throughout the body. From protein synthesis, to cell growth and tissue formation, to thermal control, the thyroid gland plays an integral role in all aspects of body metabolism including the regulation of bone remodeling activity. Thyroxine release into the blood is governed by thyroid-stimulating hormone (TSH) from the anterior pituitary gland in the brain. When thyroid hormone levels are insufficient, the anterior pituitary senses this and releases TSH which in turn stimulates the thyroid to release more T4. When T4 and T3 blood levels rise, the pituitary lowers it's production of TSH. This is called a negative feedback loop. The end result, when the body is running smoothly, is normal metabolism.

There are many hormones that affect bone health: estrogen, parathyroid hormone, cortisol, etc. Thyroid hormones are also involved through their influence on bone cells. In hyperthyroidism, the over-production of thyroid hormones causes bone loss. High levels of T4 and T3 stimulate the bone-destroying osteoclasts and, over time, can lead to osteoporosis. Investigators have known for over 10 years that the level of TSH in the blood also has a negative correlation to bone mineral density (BMD). When TSH levels go below 0.5 mIU/L (as seen in individuals with hyperthyroidsim) bone mineral density is often low. What researchers didn't know was if this connection was simply a reflection of the T4 and T3 stimulation upon the osteoclasts, or if the excessively low TSH was actually having a direct negative effect on bone density.

A recent report by Baliram et al. (2012) in The Journal of Clinical Investigation indicates that TSH does indeed have a direct effect on bone. In this study using mice, the researchers demonstrated that TSH has a direct stimulatory action on the bone building osteoblasts. This finding is extremely important especially in light of the fact that reference ranges for TSH are currently under review. Most doctors consider the normal reference range of TSH to be 0.5 to 5.0 mIU/L. This range may soon be narrowed to .03 to 3.0 mIU/L. By reducing the lower range of normal from 0.5 to 0.3, overly aggressive prescription of thyroid medications will have an adverse affect on patient's bone health.

Least you see high levels of TSH as your ticket to improved bone health, remember that all things need to be in moderation. Elevated TSH above 5.0 mIU/L in patients with hypothyroid also appears to be detrimental to bone health. Too much TSH may over-suppress bone resorption and lead to brittleness of bones and heightened fracture risk. My recommendation, if you are on prescription medication for thyroid control, is to keep TSH levels between 1.0 and 4.5 mIU/L. Use this reference range, along with symptomotology, to help you and your doctor fine-tune your prescription.

What I found most fascinating about this study was that it also yielded evidence that there may be local production of a form of TSH within the bone marrow itself. This finding highlights the incredible dynamic and complex nature of bone. Our skeleton, we are learning, is not only important for structural support and as a reservoir for minerals, but it is a vital active endocrine organ involved in helping to sustain our whole-body health. We need to take special care of our bone health!

[Note: In a condition called subclinical hyperthyroidism, thyroid hormone levels can be within the normal range but TSH abnormally low. This "hidden" condition can severely exacerbate bone loss in postmenopausal women. It's always wise to have your doctor check your TSH.]

Baliram et al. 2012. Hyperthyroid-associated osteoporosis is exacerbated by the loss of TSH signaling. The Journal of Clinical Investigation. doi:10.1172/JCI63948.




Monday, September 17, 2012

Exercises and Bracing for Fracture Prevention and Pain Relief

I have had the great pleasure of meeting two excellent therapists who specialize in exercise and postural therapy for patients with osteoporosis, Denise Pontbriand, the owner of Core Fitness, Wellness & Exercise, in Sturbridge, MA, and Renee King, PT of OsteoporosisPT in Auburn, MA.

Physical activity of all types will lower your risk of fracture. Many studies have shown that weight bearing exercise can help improve bone strength by increasing bone mineral density. Exercise also helps to improve muscle strength, balance, and coordination, all of which are important for reducing falls (the number one cause of fractures).

Engaging in some form of exercise program is extremely important for bone health. Unfortunately, it can also be risky especially if a person's bone density and bone quality are extremely low or if they have already sustained a fracture. If this is the case, it is wise to work with an expert. Denise and Renee are experts, full of energy and ready to help.

Denise has her Associate of Science degree in Physical Therapy. She is a Certified Senior Strength Trainer and a Certified Exercise Specialist using the "Meeks Method" for osteoporosis management. I will be giving a talk on osteoporosis at her Core Fitness, Wellness & Exercise center on September 27 at 7 pm. You can call her office at 508-344-2567 for more info and to sign up to attend.

Renee King is a physical therapist, osteoporosis exercise specialist (also using the Meeks Method), and Certified Spinomed Orthosis fitter. If you have sustained a compression fracture, the Spinomed brace can help you increase back strength and reduce pain. When used in conjunction with postural and exercise therapy, these braces actually help activate and strengthen specific spinal musculature. For this reason, using these braces, even if you haven't sustained a vertebral compression fracture but are at high risk, can be extremely useful. When a person sustains a compression fracture, the muscles in the back often tighten and eventually weaken. This sets the stage for more fractures especially in contiguous vertebrae. By using a Spinomed orthosis and engaging in a specific spine strengthening routine, chronic pain can be alleviated and the risk of further fractures reduced.

Friday, September 14, 2012

Exercise Helps Prevent Fractures In the Elderly

In a study out of Germany, Kemmler et al. followed 85 postmenopausal women for 12 years to determine if supervised long-term exercise training had an effect on bone mineral density and the incidence of fractures. The women participating in the study all had low bone density (osteopenia) but were not using medication. The exercise program consisted of two group sessions/week and two home training sessions/week. Bone mineral density was assessed through DXA scans. The authors concluded that engaging in a consistent exercise regimen plus supplementing with calcium and vitamin D improves bone strength (increased bone mineral density) and prevents fractures.

Kemmier et al. 2012. Exercise and fractures in postmenopausal women: 12-year results of the Eriangen Fitness and Osteoporosis Prevention Study (EFOPS). Osteoporosis International 23(4):1267-1276.

Wednesday, September 12, 2012

Gut Microbes Regulate Bone Mass

There are more than 500 species of microorganisms living in your gut. In fact, more individual microbes live there than there are cells in your body. These bacteria help you to digest your food, eliminate toxins, and manufacture nutrients such as vitamin K2. If your digestive tract is healthy, the "good" bacteria such as Lactobacillus and Bifidobacterium are so robust and plentiful that they will help prevent "bad" bacteria from colonizing and causing trouble. Your gut, and the bacteria that live there, are also key to maintaining a healthy immune system and if your immune system is struggling, chances are, so too is the health of your bones. (For an in depth explanation on how the immune and skeletal systems interact, check out chapter 5 of my book, The Whole-Body Approach to Osteoporosis.)

Most people are surprised when I become more interested in the bugs in their gut than I am with the amount of calcium they consume. They have no idea that bugs could have anything to do with bones...but they do. In the Journal of Bone and Mineral Research Sjogren et al. (2012) report how gut microbes are major regulators of bone mass in mice.

Let me explain. Eighty percent of the body's immune system is located within the walls of the gut. This makes sense since we are constantly consuming food that may harbor harmful bacteria. By locating the immune system within the walls of the gut we are able to destroy these bacteria before they have a chance to harm us. This is good. But when a person's gut is unhealthy, the immune system can produce a lot of inflammation and with it copious amounts of inflammatory signaling molecules. One of the connections between the immune and skeletal systems is that they share many of these same signaling molecules. So when signaling gets out of control with a chronically hyperactive immune system within the gut, these molecules find their way into the bone marrow. Here they alter the balance of bone remodeling activity. The more signaling molecules, the faster the bone resorbing osteoclasts destroy bone.

Gut microbes are responsible for maintaining a calm immune response; they also have major a influence on the level of inflammatory signaling molecules that circulate throughout the body. The more good bacteria you have in your gut, the less circulating inflammatory signaling molecules. Researchers have now linked the over production of these molecules to the aggressive bone loss that leads to osteoporosis.

Sjogren et al. showed that when laboratory mice were bred for digestive tracts free of any bacteria, the mice exhibited an abnormal increase bone density. Their bone mass actually became excessively dense. What these scientists found was that mice with no bacteria in their gut had fewer osteoclasts (bone cells that break down bone) in their bone and fewer T cells being made by their immune system. With fewer immune T cells, the mice weren't producing the signaling molecules that would also activate osteoclasts in bone marrow. The result, higher bone mass. When the researchers then put normal gut microbes back into the digestive system of these mice...what happened? The mice LOST bone density, but not so much that they got osteoporosis. The mice lost just enough that their bone density became normal! The mice went from having too much bone density when they didn't have any bacteria in their guts, to normal bone density when the gut was more healthy with good bacteria. By using a model of mice with no bacteria, the researchers were able to demonstrate how bacteria directly affect the release (or no release in the case of mice free of bacteria) of inflammatory signaling molecules.

In summary, gut bacteria are extremely important for maintaining a healthy immune system and in the regulation of bone mass. Eating a healthy diet high in fiber and low in refined sugars will help maintain good bacteria in the gut. If you have a history of antibiotic use talk with your health care provider about supplementing with probiotics.

Sjogren et al. 2012 The gut microbiota regulates bone mass in mice. Journal of Bone and Mineral Research 27(6):1357-1367.

Sunday, September 9, 2012

Flavonoids Increase Bone Mineral Density

When people ask me what is the most important thing they can do for improving bone health, I think they're expecting me to suggest a certain form of calcium supplement. There is no doubt, supplementing with quality calcium, such as that found in OsteoSustain and OsteoMineralBoost, is important, but remembering to take a few tablets each day is easy. What's more difficult is to remember to eat five to eight servings of fruits and vegetables, every day. So my answer to their question tends to be "EAT YOUR FRUITS AND VEGETABLES!" When you have bone loss, you need to do EVERYTHING you can to improve your overall health, and a diet rich in fruits and vegetables is the perfect place to start.

Fruits and vegetables are rich in vitamins, minerals, and phytochemicals called antioxidants. Without antioxidants we would not be able to neutralize the ravaging effects of free radicals and limit the oxidative stress that leads to cellular breakdown and aging. There are a number of classes (as well as subclasses) of naturally occurring phytochemicals: vitamins, carotenoids, curcuminoids, lignans and flavonoids. By consuming a diet poor in phytochemicals, we become susceptible to disease. In this month's issue of the Journal of Bone and Mineral Research, Welch et al. (2012) investigated the effect of different flavonoids on human bone density. Flavonoids are found in the pigments that give fruits and vegetables their rich yellow, orange, red and blue colors. Due to their extreme complexity, and variability in biological efficacy and availability, flavonoids have been further categorized into subclasses. These subclasses are: "flavonols, flavones, flavanones, flavan-3-ols and their oligomeric and polymeric forms (i.e. procyanides), isoflavones, and anthocyanins and other polymeric flavonoids."

One of the most intensely studied subclasses of flavonoids to be assessed for their effects on bone are the isolated components of soy called isoflavones. Supplementing with high doses (90 mg/day) of isoflavones have been shown to reduce bone loss (Ma et al. 2008) but this improvement may only be seen with high supplemental intake. When dietary isoflavones are studied for their effect on bone (for example, Mulligan et al. 2007) there is often no detectable improvement. With concerns that the estrogen-like effects of supplemental isoflavones can vary between estrogen-boosting and estrogen-blocking, depending upon the age and health of an individual, I have tended not to recommend supplemental soy isoflavones (including ipriflavone) to my patients. Soy in the diet is OK (unless you have a sensitivity to it) but I'm just not sold on them for inclusion in supplements.

What has become apparent to me with phytochemicals is that their value increases when consumed in their natural state (compared to extracting them and consuming them as supplements). There are over 4,000 flavonoids, and their beneficial effects are most powerful, and additive, when taken together. This is why a diet high in fruits and vegetables is superior to supplementing with individual phytochemicals. The reason is the "additive effect" from consuming the "whole."

In addition to confirming that a higher intake of plant-based flavonoids is associated with higher bone mineral density (BMD), Welch et al. found anthocyanins (a flavonoid and polyphenol) to be particularly important to bone health. They concluded that "a higher intake of anthocyanins was associated with a 3.4% and 3.1% higher BMD at the spine and hip, respectively."

My take home messages to you are: 1) the additive effect of flavonoids makes the consumption of fruits and vegetables superior to supplementing with extracts, and 2) the higher the anthocyanin content, the better that fruit or vegetable is going to be for bone health. Dried plumes, by the way, are rich in the purple flavonoids, anthocyanins.

Welch et al. 2012. Habitual flavonoid intakes are positively associated with bone mineral density in women. Journal of Bone and Mineral Research 27(9):1872-1878.

Friday, September 7, 2012

Vitamin E Decreases Bone Mass

In a study reported in Nature Medicine, Fujita et al. show that vitamin E in the alpha-tocopherol form is detrimental to bone health. Vitamin E is a potent antioxidant that protects against oxidative stress and the development of atherosclerosis. With oxidative stress being a major contributor to the development of osteoporosis, at first glance one would consider the antioxidant activity of vitamin E to be beneficial to bone health. Unfortunately, vitamin E's ability to reduce oxidative stress does not seem to counterbalance its negative effect on bone.

In this study out of Japan, mice supplemented with alpha-tocopherol showed reduced bone mass. The researchers found that vitamin E actually reduced bone density by increased a key protein that promoted osteoclastic bone resorption and accelerated bone loss. They concluded that "excess vitamin E is bad for the bones in humans..."

Please take note: If you supplement with vitamin E or take a multivitamin, make sure to read the label. Only use quality nutritional supplements that contain natural mixed tocopherols that are high in gamma-tocopherol.

Fujita et al. 2012. Vitamin E decreases bone mass by stimulating osteoclast fusion. Nature Medicine 18(4):589-594.

Two-Fold Increase in Fractures with Antidepressants

I thought I would briefly mention one more research article about antidepressants that just appeared in the Bone journal. I am not trying to belabor the point about antidepressants and bone loss but just making sure that if you take one of these medications (and I realize how important they can be sometimes for quality of life) that you will need to take extra vigilance in the care of your bones. Also, especially for mild to moderate depression or anxiety, make sure you explore psychotherapy and self-help books such as David D. Burn's Feeling Good. These can be extremely helpful alternatives to antidepressants.

This investigation (Rabenda et al. 2012) looked at the relationship between antidepressants and fracture risk by analyzing data from two international, phase III, randomized, placebo-controlled, double-blind studies (SOTI and TROPOS). It was determined that users of SSRI antidepressants had a "2-fold risk increase of nonvertebral [hip and forearm] fracture" and a "2.1-fold risk increase for subjects who were current users of TCAs [tricyclic antidepresants].

Rabenda et al. 2012. Risk of nonvertebral fractures among elderly postmenopausal women using antidepressants. Bone 51(4):674-679.

Wednesday, September 5, 2012

Antidepressants (SSRIs) Contribute to Osteoporosis

There are a host of medications that cause bone loss. Glucocorticoids (corticosteroids such as cortisone and prednisone) prescribed for reducing inflammation, have long been known to be the biggest offender. But another commonly prescribed group of medications, the selective serotonin reuptake inhibitors or SSRIs, have also come under scrutiny.

Serotonin is a neurotransmitter made from the amino acid tryptophan. It has been studied most extensively for its role in mood regulation. Approximately 1 to 2 percent of the body's production of serotonin is in the brain. SSRIs work by blocking serotonin re-uptake thereby increasing its availability within nerve synapses. The more serotonin available at the synapses, the better a person's mood. But the effects of serotonin are not limited to mood enhancement. This neurotransmitter is also involved in a person's response to hunger, sex, and sleep. In addition, it has neuro-regulatory effects in other parts of the body outside of the brain.

The rest of the body's serotonin is produced outside of the brain. Here it is involved with regulating activity of the heart, the gastrointestinal tract, and yes, the remodeling activity of bones. In recent years, doctors began to recognize a link between the use of SSRI medications and the diagnosis of osteoporosis. We are now beginning to understand why.

The majority (95%) of the body's serotonin is synthesized in the gut (duodenum). Here, serotonin stimulates peristalsis (gut motility) and increases vascular permeability. In 2008, scientists (Yadav et al.) at Columbia University discovered that serotonin was involved in yet another function--the regulation of bone remodeling. What the researchers found was that elevated levels of gut-derived serotonin can enter the circulation* and find its way to bone. Here, it inhibits bone formation by shutting down the cellular activity of osteoblasts (bone forming cells). This startling finding literally rocked the world of bone biology. Now we were seeing a possible connection between gut-derived serotonin, the enhancement of its activity by SSRIs, and bone loss.

In the September issue of Bone (2012) a review of the literature by Rizzoli et al. (European Society for Clinical and Economic Aspects of Osteoporosis) concluded that there is a link between the use of anti-depressant medications and increased risk of fracture. "The body of evidence suggests that SSRIs should be added to the list of medications that contribute to osteoporosis." The evidence is fairly clear now that SSRIs contribute to bone loss. But many questions still remain. Do SSRIs increase both brain serotonin levels and raise levels of gut-derived serotonin? Do SSRIs enhance the spillage of serotonin into the bloodstream and increase levels in bone marrow where it is now known to shut down bone formation? The answers to these questions appear to be yes but further research is necessary.


* In an earlier blog article, I wrote about MPV** (mean platelet volume) and its correlation to bone loss. Serotonin is carried predominantly by platelets in the blood. As MPV increases (a sign of inflammation and the release of large immature platelets), bone mineral density decreases. This correlation may well go beyond just the connection of inflammation to bone loss. When platelets are activated, one of the signaling molecules*** that they release is...serotonin! Only time will tell if this suspicious connection is involved in the development of osteoporosis (my bet is that it does).  As new research solves the mysteries of the serotonin/bone connection we, no doubt, will benefit in our ability to help reduce fracture risk. In the meantime, if you have osteopenia or osteoporosis and your MPV is elevated, increase your fruit and vegetable intake, supplement with curcumin, and take OsteoStim for its powerful antioxidant and bone building potential. Elevated MPV is also an indication of increased cardiovascular risk so talk with your doctor if it is high.

** MPV is a value commonly reported on a CBC lab test.

*** Activated platelets also release nucleotides such as ATP, ADP, UTP and UDP. Stay tuned for a future blog article on the effect of the extracellular nucleotide system on bone.


Rizzoli R., et al. 2012. Antidepressant medications and osteoporosis. Bone 51(3):606-613




Monday, September 3, 2012

Secondhand Smoke: Bone Loss

A major risk factor for osteoporosis is smoking. Active smokers average 4% less bone mineral density (BMD) compared to nonsmokers and they have a higher risk of fracture. But what about secondhand smoke? Do smokers increase the risk of osteoporosis to those non-smokers living in the same household? A recent study published in Osteoporosis International (Kim et al. 2012) says, yes.

Tobacco smoke, in addition to causing emphysema and cancer, can negatively affect bone health in several ways. "Nicotine, the most characteristic component of tobacco, is known to inhibit the formation of bone, and polycyclic aromatic hydrocarbons, benzopyrene, and 7,12-dimethylbenzanthracene are known to decrease bone mass and strength." Tobacco smoke also has "antiestrogenic effects and is also associated with low serum 25-OH vitamin D3 levels and low calcium absorption. Furthermore, menopause in female smokers has been reported to occur up to 2 years earlier than that in nonsmokers." 

In this study of over 2,000 postmenopausal Korean women, researchers concluded that secondhand smoke exposure "alters bone metabolism" and that there is a "significant association with increased risk of postmenopausal osteoporosis independent of other factors."

Kim, K.H., C.M. Lee, S. M. Park, et al. 2012. Secondhand smoke exposure and osteoporosis in never-smoking postmenopausal women: the Forth Korea National Health and Nutrition Examination Survey. Osteoporosis Int 10.1007/s00198-012-1987-9.

Sunday, September 2, 2012

Diuretics: Fracture Risk

There has been debate regarding the benefits or risks of using diuretic medications to reduce urine calcium loss in patients with osteoporosis. When I evaluate the literature, it is clear that diuretics for the treatment of osteoporosis is NOT the way to go. Diuretics not only appear to increase the risk of hip fractures due to their adverse effects on bone mineral density but they also increase urinary losses of vitamin B6, magnesium, potassium and zinc. This leads to low energy, metabolic acidosis and the increased risk for falls due to their adverse effects on a person's hemodynamics and equilibrium.

A study reported in Osteoporosis International (Berry et al., 2012) found "the risk of hip fracture was transiently elevated around twofold shortly after initiation of a loop or thiazide diuretic drug."

Although this study found no long term increase in hip fractures with the use of diuretics, a better alternative for reducing abnormally high urine calcium* loss is to increase fruit and vegetable intake to help neutralize the body's pH, and to supplement with vitamin K, potassium and boron. If you have excess calcium in your urine, try this plan: 1) increase fruits and vegetables to eight to ten servings a day, 2) eliminate high-phosphorus cola drinks, 3) moderate (or eliminate) your intake of red meats and avoid caffeine, 4) minimize your dairy intake (replace this calcium source with supplemental microcristalline hydroxyapatite or calcium citrate/malate--OsteoMineralBoost and OsteoSustain are perfect for this), and 5) supplement with Osteo-pHBalance our alkalinizing formula with potassium, spirulina and chlorella.

*Note: I frequently have patients tell me that their doctor prescribed them a diuretic in response to an abnormal result on their 24-hour urine calcium test. When asked if they refrained from taking calcium supplements before the test, they almost invariably report that they had not. If calcium supplements are taken during the collection of urine for this test, it will almost always return as abnormal (above 275 mg for women and 300 mg for men). To avoid erroneous test results, eat your regular diet and refrain from taking supplemental calcium for the 24 hours before and during the test.

Berry, S.D., Zhu, Y., Choi, H., Kiel, D.P., and Zhang, Y. 2012. Diuretic initiation and the acute risk of hip fracture. Osteoporosis Int DOI:10.1007/s00198-012-2053-3

Saturday, September 1, 2012

Osteopenia: Silent But Serious

Typically, we don't consider osteopenia (T-score of -1.0 to -2.4) as a serious threat to our health, but maybe we should. In a recent study out of the UK (Lynn et al., 2012) the authors found fractures in osteopenic individuals not to be uncommon. Distal long bones (such as the forearm, tibia, fibula and metatarsals) were the most common fracture sites. Interestingly, 45% of the individuals in this study were on bone protection treatment of some type at the time of their fracture.

The authors concluded that "careful clinical evaluation and a FRAX score assessment are important in patients with fragility fractures even when they have a category of osteopenia by DXA scan."

I have been telling patients for years how important it is to detect bone loss early. Having your first DXA scan at an earlier age (40 instead of 50 as is often recommended by physicians), and definitely if you sustain any minimal-trauma fracture, is good insurance for early detection of bone health issues. I can't tell you how many of my patients have had a metatarsal (foot) fracture from low-mileage running but their family physician did not follow up with a DXA scan to assess bone mineral density. Since it is so much easier to stop bone loss rather than to gain it back, why not find out if there is a problem BEFORE it becomes full blown osteoporosis? Osteopenia is always easier to work with than osteoporosis; there is valuable time to find solutions.

Lynn, M., Brannigan, S., Moniz, C. 2012. Osteopaenia: silent but serious threat for bone health - retrospective analysis of fragility fractures in osteopaenic patients. Osteo Int (Abstracts of the Osteoporosis and Bone Conference 2012) 23(Suppl 5):P92.
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