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Common Prescription Drugs That Cause Bone Loss

Did you know that many commonly prescribed drugs cause bone loss?

Since writing the 2nd edition of Your Bones, I’ve learned a great deal more about the surprising number of prescription – and over-the-counter drugs – that promote bone loss.

Watch the video below to discover what motivated me to dive deeply into the research to determine 12 known drug classes that promote bone loss and what you can do to combat their bone-destructive effects.

12 Known Drug Classes That Cause Bone Loss

For each of the classes of drugs that cause bone loss, I’ve summarized the key information you need into the following three sections:

  • Used to: The conditions the drugs are prescribed to manage.
  • How and why the drug(s) cause bone loss: Description of how the drug negatively impacts bone building.
  • Drug Information: Additional information pertaining to the respective drug class including but not limited to studies conducted.

Where possible, I’ve suggested alternate drugs with less harmful effects on bone, which you can discuss with your doctor. If you must continue to take one of the many drugs that cause bone loss, the final section of this article focuses on what you can do to combat their adverse effects on your bones and lessen your risk of developing osteoporosis.

I have included the relevant research and studies in case you want to read them for yourself (links provided within the text and at the bottom of the article). And remember that this article should not be taken as medical advice. Always consult your doctor (you can share these studies with them too).

Please note, as I know some of you may ask, we are not able to mention specific drug brands – so trade names are not included. You can enter the class of drugs on Wikipedia for a listing of commonly prescribed examples.

For easy navigation, click on any of the subcategories to jump to that specific section.

  1. Anticonvulsants
  2. Benzodiazepines
  3. Antidepressants
  4. Insulin-Sensitizing Medications
  5. Opioid Pain Medications
  6. Glucocorticoid Medications
  7. Calcineurin Inhibitors
  8. Antacids, H-2 Blockers, Proton Pump Inhibitors
  9. Loop Diuretics
  10. Anti-Coagulants
  11. Thyroid Hormone Medications
  12. Contraceptives

Doctor in a consultation for drugs that cause osteoporosis

Anticonvulsants

Used to: Manage epilepsy, bipolar disorder, and neuropathic pain (e.g., pain resulting from diabetic neuropathy, spinal cord injury, multiple sclerosis, strokes, cancer chemotherapy)

How and why the drug(s) cause bone loss: These drugs interfere with our ability to absorb vitamin D and to metabolize it into the form that helps us absorb calcium.

Drug Information: Anticonvulsants can cause a deficiency of folate and/or vitamin B6, both of which are required to minimize homocysteine levels; a highly destructive inflammatory compound. High homocysteine levels boost inflammation throughout the body, and excess inflammation triggers the production and activity of osteoclasts, the specialized cells that break down bone.

Lastly, anticonvulsants reduce blood levels of vitamin K, which in its K1 form lowers inflammation, and in its K2 form, activates proteins that pull calcium into bone (osteocalcin), and keep calcium out of soft tissues (matrix Gla protein), like our blood vessels.

Ask your doctor about checking your vitamin D levels – both 25(OH)D, the form in which vitamin D is present in the bloodstream, and 1,25-D, the active hormonal form of vitamin D, which helps us absorb calcium.

If you are taking AlgaeCal Plus, you will get 1,600 IU of vitamin D3 daily, but you may require more. Also discuss supplementing with folate, B6, and vitamins K1 and K2. If you are taking AlgaeCal Plus, you will get 100 micrograms of vitamin K2 in its most effective (MK-7) form, but you may require more. The lab test used to determine whether your K2 needs are being met is a blood draw that checks levels of uncarboxylated osteocalcin (the protein directing calcium where it needs to go in your bones).

Benzodiazepines

Used to: Manage epilepsy, anxiety, insomnia, depression, schizophrenia, restless leg syndrome.

How and why the drug(s) cause bone loss: These drugs bind to and block off dopamine receptors in a part of the brain called the hypothalamus. By this action, the benzodiazepines prevent dopamine, an important neurotransmitter, from being secreted. Shutting down dopamine secretion causes levels of another hormone called prolactin to rise because dopamine is what turns off the pituitary gland’s secretion of prolactin.

Drug Information: High prolactin levels (a condition referred to in the medical literature as “hyperprolactinemia”) suppress the activity of the hypothalamic-pituitary-gonadal axis. This is a triad of endocrine glands that interacts and secretes a number of hormones involved in reproduction. The hypothalamus produces gonadotropin-releasing hormone (GnRH). The anterior portion of the pituitary gland produces luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the gonads (ovaries in women, testes in men) produce estrogen and testosterone, respectively. (More precisely, the pituitary’s secretion of FSH and LH are what signal the gonads to produce estrogen, progesterone, and testosterone.)

Since estrogen and progesterone play very important roles in maintaining healthy bones in women, inhibiting their production by inhibiting FSH and LH causes bone loss.  Estrogen prevents excessive activation of osteoclasts (the specialized cells that break down old bone), while progesterone activates osteoblasts (the specialized cells involved in building new bone), plus both hormones exert a number of other bone-protective effects. This is why the drop off in the production of estrogen and progesterone that occurs with menopause contributes to bone loss.

Even in men, estrogen is essential for bone health. Men convert a small, but very necessary, amount of testosterone into an estrogen that plays a critical role in maintaining men’s bones. That’s why drugs that disrupt testosterone production, such as the aromatase inhibitors used in the treatment of prostate cancer, cause bone loss in men.3-5

When I first wrote about this, I noted a 2008 study conducted in Spain that assessed risk factors for osteoporosis and fractures in 4,960 postmenopausal women aged 50 to 65 years. The results? The two top risk factors identified for low bone density were low intake of calcium and benzodiazepine use.6

Since then a number of other papers have reported on benzodiazepines not only causing bone loss but also increasing risk of falling – a double whammy of adverse effects that greatly increases risk for fracture.7-11

Particularly if you are a postmenopausal woman or a man over age 50, and you must continue to take a benzodiazepine, discuss bio-identical hormone replacement (BHRT) with your doctor. Even if you are a premenopausal woman or a younger man, it would still be a good idea to request tests to evaluate your prolactin levels and bone mineral density (BMD). Even better, ask to have all your hormone levels checked, and if they are severely compromised, consider BHRT.

Smiling woman looking up against trees at park during autumn

Antidepressants: SSRIs, MAIOs, Atypical Antipsychotics

Used to: SSRIs (selective serotonin reuptake inhibitors) and MAIOs (monoamine oxidase inhibitors) are used to manage depression, anxiety disorders, some personality disorders (e.g., obsessive-compulsive disorder, eating disorders) and premature ejaculation. MAOIs are also used to treat Parkinson’s disease. Atypical antipsychotics are used to treat schizophrenia, bipolar disorder, and autism. TCAs (Tricyclic antidepressants), used to manage depression, are still in use, although they have largely been replaced by SSRIs.

TCAs are less frequently prescribed now, but are still in use and have the same adverse effects as SSRIs, and possibly even worse effects on bone (see the discussion of the Kuopio Osteoporosis Risk Factor and Prevention Study (OSTPRE) below).

How and why the drug(s) cause bone loss: All these drugs inhibit dopamine production and neurotransmission, causing chronic elevation of the hormone prolactin, which disrupts HPA axis activity and the production of sex hormones, as explained above under Benzodiazepines.12-14

Drug Information: When first writing about the adverse effects on bone of antidepressant drugs I noted a study published 2011. This study involved over 27,000 postmenopausal women in Canada, which found selective serotonin reuptake inhibitors (SSRIs) increased risk for osteoporosis by 46%, atypical antipsychotics (tranquilizers, also called 2nd generation antipsychotics, increased risk by 55%, and benzodiazepines increased risk by 17%.15

Another very large study conducted in Spain—this one included more than 63,000 subjects—found SSRIs increased risk of osteoporotic fractures by 45%. MAOI antidepressants increased risk for osteoporosis by 15%, and benzodiazepines increased risk by 10%. A dose-effect relationship was seen with SSRIs and benzodiazepines – the longer any of these drugs were used, the greater the increase in risk for osteoporosis. In contrast, lithium, which is prescribed to manage bipolar disorder, was associated with a 37% lower risk for fracture.16

A study conducted looking into the effects of antidepressants on bone was published in the August 2016 issue of the journal Bone.  A total of 1,988 women (aged 57-67) participating in the Kuopio Osteoporosis Risk Factor and Prevention Study (OSTPRE) cohort were followed for 5 years. During this time, bone loss was found to be significantly accelerated in the 319 women who took antidepressants. Those using TCAs (tricyclic antidepressants) lost more than three times as much bone as women not taking antidepressants (-3.6mg/cm(2) vs. -1.1mg/cm). SSRIs also increased the rate of bone loss, and the higher the dose, the greater the amount of bone lost.17

This study followed up on an earlier 5-year study, published in 2007, that reported a 0.82% average yearly loss in hip bone BMD in postmenopausal SSRI users compared to a 0.47% loss in non-users.18 In the present study, the 5-year difference between SSRI users and non-users was smaller: postmenopausal SSRI users’ yearly hip bone loss was -0.22% compared to a loss of -0.08% in postmenopausal women not using these drugs.

But this new study raises concerns about TCAs. When I wrote about these drugs two years ago, the research had suggested TCA use did not increase bone loss. In one study, tricyclic antidepressants were associated with 43% lower risk for osteoporosis.19

Unfortunately, this newer study found that TCAs are not a better option and may be an even more damaging to our bones than SSRIs. The postmenopausal women taking tricyclic antidepressants in this study lost even more bone than women taking SSRIs. TCA users’ annual rate of bone loss was −0.35% compared to just −0.08% in women not taking antidepressants.

SSRIs are very commonly prescribed antidepressants. These drugs are supposed to increase brain levels of the neurotransmitter serotonin, by preventing its reuptake by the neurons that secrete it. However, SSRIs also inhibit dopamine production and neurotransmission which, as explained above under Benzodiazepines, causes high prolactin levels, endocrine dysfunction and bone loss.20

The research continues to report very high rates of osteopenia and osteoporosis in people taking any of the long-term psychoactive drugs (e.g., anticonvulsants, benzodiazepines, antidepressants), and the higher the dose and longer the drugs were taken, the greater the bone loss.

Young Caucasian women have been found to be especially vulnerable to developing high prolactin levels (hyperprolactinemia), with the resulting inhibition of estrogen and progesterone production, and bone loss. Younger women taking any of these drugs and experiencing menstrual problems (an indication that the drug is disrupting normal function of the hypothalamic-pituitary-gonadal axis) should immediately alert their doctors and request tests to evaluate their prolactin levels and BMD.

If you must take a psychoactive medication, please discuss which drug might be least harmful with your doctor. Some of these drugs have a lesser antagonizing effect on dopamine receptors in the brain. Others are potent dopamine receptor antagonists, and it is by antagonizing dopamine receptors that antipsychotic drugs cause hyperprolactinemia—and thus osteoporosis.

Conventional psychoactive drugs all cause hyperprolactinemia, but a few of the so-called “atypical” psychoactive drugs, supposedly, do not. The two following references are for the most recently published studies discussing this in the peer-reviewed medical literature: https://www.ncbi.nlm.nih.gov/pubmed/18477623https://www.ncbi.nlm.nih.gov/pubmed/15643097. Share these with your doctor and ask for help finding the psychoactive drug with the lowest prolactin-raising profile: 21-22

Working with an integrative, functional medicine or naturopathic physician who can help you understand and naturally correct the underlying causes of your health issues is your best option. Resources that can help you find these doctors are listed at the end of this article.Group of active senior runners outdoors, resting and hugging in windy cold weather.

Insulin-Sensitizing Medications

Used to:  Manage type 2 diabetes. The class of drugs is called thiazolidinediones (also known as the glitazones)

How and why the drug(s) cause bone loss: These drugs trigger mesenchymal stem cells (the precursor cells that live in your bone marrow and can become either osteoblasts, which build new bone, or adipocytes, which store fat) to become adipocytes (fat cells). By doing so, the thiazolidinedione drugs thin your bones and increase your production of visceral adipose tissue (VAT, belly fat), which is highly pro-inflammatory. VAT is linked to not only abdominal (apple-shaped) obesity, but also to insulin resistance, type 2 diabetes, and other inflammatory diseases, including osteoporosis.

Drug Information: In relation to your bones, chronic low-grade inflammation causes excessive activation of osteoclasts (the specialized cells that remove old or damaged bone), and too much osteoclast activity promotes bone loss. 23

Numerous studies have demonstrated that activation of PPAR-γ in mesenchymal stem cells causes them to become fat cells instead of osteoblasts. In everyday language: your body produces more fat and less bone-building osteoblasts. For those interested in biochemistry: more specifically, the glitazones (rosiglitazone and pioglitazone) cause bone loss because they are selective agonists of peroxisome proliferator-activated receptor-γ (PPAR-γ). (An agonist is a chemical that binds to a receptor and activates it, triggering the production of the biological response it produces.)

Another factor that causes mesenchymal stem cells to be fat cells rather than osteoblasts is a diet rich in arachidonic acid, an omega-6 fatty acid found in large amounts in conventionally raised animal products and farm-raised fish. Ensuring your intake of omega-3 fats is sufficient to counterbalance your consumption of omega-6s can help. Omega-3s help mesenchymal stem cells develop into osteoblasts.  The easiest, safest way to do this is to take Triple Power Omega 3 Fish Oil, a highly powerful supplement that AlgaeCal has developed.

One tablespoon daily will provide you with a hefty dose of omega-3s along with two potent anti-inflammatory agents, curcumin and astaxanthin.  You can also lower your intake of arachidonic acid by choosing organic meats, dairy products and eggs from pastured animals; these foods will have a much healthier ratio of omega-6: omega-3 fats.   

In addition to causing your body to produce fat instead of bone, the thiazolidinediones decrease the expression of insulin-like growth factor-I (IGF-1), a protein our bodies produce that promotes bone formation.

These two actions already secure the thiazolidinediones a top spot on the list of bone-busting drugs, but here’s the kicker: The thiazolidinediones also stimulate osteoclast development and activity. So, these drugs attack your bones from both ends of the spectrum: they suppress bone building and increase bone breakdown.

Long-term treatment with thiazolidinediones increases the risk of fractures by up to 4-fold in postmenopausal women and in men. Risk correlates with the duration of thiazolidinedione treatment and gets really significant within 12 to 18 months.24

The most recent paper, a review discussing all the effects of these drugs, tells us they increase our risk not only for bone fractures, but also for fluid retention, heart failure, and bladder cancer. And they also raise levels of LDL cholesterol. LDL is the form of cholesterol that becomes harmful when damaged by inflammation, which the thiazolidinediones promote by increasing the production of pro-inflammatory belly fat.25

If you have insulin resistance or type 2 diabetes and must take an insulin-sensitizing agent, ask your doctor about using metformin rather than one of the glitazones. Metformin has a positive effect on osteoblast differentiation, and therefore a neutral or even potentially protective effect on bone.26

Many studies have now shown that a whole foods Mediterranean-type diet – a delicious, satisfying 40%-fat diet with flavorful extra virgin olive oil and walnuts, almonds and hazelnuts– and regular exercise can help combat type 2 diabetes, eliminate excess body fat, boost your energy (and your sex life), slow the aging process, and protectthe health of your bones.27-34

For help with super quick (15 minutes or less) & easy recipes that will immediately become your favorites, see the non-profit, World’s Healthiest Foods website www.whfoods.org. And look for my recipes posted on the AlgaeCal blog.

Opioid Pain Medications

Used to: Manage chronic pain. Morphine (sold under more than 100 trade names), Codeine, Hydrocodone, Oxycodone, Methadone, Tramadol are all types of opioid pain medications.

How and why the drug(s) cause bone loss:  Opioid drugs disrupt normal regulation of hormone production in the hypothalamic-pituitary axis (HPA). They increase the production of prolactin, which inhibits the production of estrogen and testosterone (see the full explanation above under Benzodiazepines); inhibit production of DHEA, which is the precursor in your body’s hormone production assembly line for testosterone and estrogen; and increase production of thyroid stimulating hormone, which directly suppresses bone remodeling.35

Drug Information: The use of opioids as a long-term treatment for chronic pain has increased so dramatically that opioid-induced deficiency of androgens (the hormones, DHEA and testosterone) has been given its own acronym in the medical literature: OPIAD.36

In addition to destroying your bones, opioid-induced hormone dysregulation may lead to menstrual irregularities and reduced fertility in premenopausal women. In pre- and postmenopausal women and in men, it may also cause sexual dysfunction, fatigue, depression, a loss of muscle strength and mass.37

If you must take an opioid medication for chronic pain, particularly if you are a postmenopausal woman or a man over age 50, discuss bio-identical hormone replacement (BHRT) with your doctor. Even if you are a premenopausal woman or a younger man, it would still be a good idea to request tests to evaluate your prolactin levels and BMD. Even better, ask to have all your hormone levels checked, and if they are severely compromised, consider BHRT.

And you can greatly lessen opioid medication’s damaging effects on your bones by ensuring you get optimal amounts of all the nutrients bones require. AlgaeCal Plus will be a huge help, providing plant-based calcium, vitamins D3 and K2, C boron and other important trace minerals. Also, lowering your overall inflammation by eating a healthy, whole foods Mediterranean-type diet, and taking Triple Power Omega 3 Fish Oil to ensure adequate omega-3s plus the anti-inflammatory protection of curcumin and astaxanthin. Plus, getting as much regular weight-bearing exercise as you can tolerate.

Girl smells sunflower in the sun - vitamin D

Glucocorticoid Medications

Used to: Manage allergies, asthma, autoimmune diseases.

How and why the drug(s) cause bone loss: Glucocorticoids suppress osteoblasts’ bone-building activity and hence bone formation, while, at the same time, osteoclast (bone-resorbing cells) numbers are either unchanged or slightly increased resulting in bone loss.

Drug Information: Glucocorticoids induce production of a protein called caspase 3 and other proteins that play key roles in cellular apoptosis (cell-suicide) in osteoblasts and osteocytes (what osteoblasts become after they begin secreting the bone matrix). So, glucocorticoids cause both osteoblasts and osteocytes to self-destruct. Osteocytes play a central role in skeletal sensing of the need for bone repair and in bone repair itself, so glucocorticoids’ induction of caspase 3 results in weakening of bone (within 6 months) — even when glucocorticoids are used at very low doses.

Glucocorticoids change the balance between receptor activator for NF-κB ligand (RANKL) and osteoprotegerin (OPG). RANKL is produced by osteoblasts and osteocytes (what osteoblasts become as they lay down new bone). It’s a key regulator of bone-resorbing osteoclast activation and survival. Osteoblasts and osteocytes also produce OPG, which is a decoy receptor for RANKL and thus inhibits RANKL from activating osteoclasts. The balance between RANKL and OPG is a key deciding factor of how much bone resorption is and will be happening (more RANKL = more bone breakdown; more OPG = less bone breakdown). Glucocorticoids tip this balance strongly in favor of RANKL.

Glucocorticoids also cause an increase in the production of macrophage colony-stimulating factor, a pro-inflammatory cytokine (signaling molecule) that triggers the production of more pro-inflammatory cytokines; inflammation further increases RANKL production and activation, thus further increasing the production and activity of osteoclasts. Glucocorticoids also directly prolong the lifespan of mature osteoclasts.

Glucocorticoids inhibit Wnt protein expression in mature (bone-building) osteoblasts, and this results in the precursor cells of osteoblasts (mesenchymal stem cells) becoming adipocytes (fat cells) instead of osteoblasts.

Glucocorticoids deplete vitamin D3.

Not surprisingly, BMD drops 6-12% within the first year of glucocorticoid use, and approximately 3% per year following. Fracture risk escalates up to 75% within the first 3 months.38-39

If you must take a glucocorticoid, you can still greatly lessen its bone-blasting effects by ensuring you get optimal amounts of all the nutrients bones require (AlgaeCal Plus will be a huge help), lowering your overall inflammation (eating a healthy, whole foods Mediterranean-type diet, and taking Triple Power), and getting regular weight-bearing exercise.

Calcineurin Inhibitors

Used to: Suppress immune system rejection of organ transplants. Typically given in combination with glucocorticoids in patients undergoing organ transplantation to help prevent organ rejection. Also now used to treat dry eye syndrome (keratoconjunctivitis sicca).

How and why the drug(s) cause bone loss:  These drugs markedly increase bone resorption via two mechanisms: they disrupt vitamin D metabolism and therefore calcium absorption, and cause secondary hyperparathyroidism.

Drug Information: Secondary hyperparathyroidism occurs as a protective response when calcium levels drop too low in the bloodstream, which they do when vitamin D is deficient or its metabolism is disrupted. In response, parathyroid hormone is secreted to trigger calcium release from bone, so calcium can be restored to its required levels in the bloodstream. When parathyroid levels are continuously elevated, calcium gets continuously withdrawn from bone.40-41

If you must take a calcineurin inhibitor, your needs for vitamin D3 will be increased. Ask your doctor about testing not only your 25(OH)D levels, but your 1,25-D level as well, and helping you to determine how much supplemental vitamin D3 you require. And ensure you are providing your bones with all the other key nutrients they must have, in addition to vitamin D3, to maintain themselves by taking AlgaeCal Plus.

Antacids, H-2 Blockers, Proton Pump Inhibitors

Used to: Manage indigestion, heartburn, GERD (gastroesophageal reflux disease)

How and why the drug(s) cause bone loss:  Antacids neutralize stomach acid after it has been produced. Without stomach acid, calcium cannot be made soluble, which is necessary for its absorption. Stomach acid is also required for the digestion of food. Many vitamins (particularly B12) and minerals required for healthy bones are not freed from the food matrix and rendered available for absorption without the action of stomach acid.

Drug Information: H-2 blockers block the action of the histamine-producing cells in the stomach lining, which signal the acid producing cells to secrete HCl (stomach acid), thus preventing the production of stomach acid.

Proton pump inhibitors block the proton pump inside the cells in the stomach lining that produce and secrete stomach acid. Proton pump inhibitors (PPIs) are the most potent of the acid-blockers; just one PPI pill can reduce stomach acid secretion by 90-95% for a full 24 hours.

In addition, both H2-blockers and PPIs increase risk for chronic kidney disease. Vitamin D is converted into its active, hormonal form, 1,25-D, in our kidneys. This is the form in which vitamin D helps us absorb calcium. When our kidneys are not working well, our ability to absorb calcium is severely compromised. Once daily use of PPIs increases risk of chronic kidney disease by 15%; twice daily PPI use increases risk by 46%. Twice daily use of H2 blockers increases risk for chronic kidney disease by 39%.

Chronic use of PPIs is associated with significantly increased risk for chronic kidney disease and fracture.42-49

If you are taking one of these drugs, please work with a doctor who can help you figure out the cause(s) of your indigestion, heartburn or GERD. Your body may be reacting to some food(s) you regularly eat. You could have some unhealthy strains of bacteria in your digestive tract. You could be unable to effectively deal with the stress in your life because your genetic inheritance gave you slow versions of the enzymes that clear out cortisol. These are a few among the many potential reasons for digestive unhappiness, none of which are cured by taking stomach acid-suppressing drugs, and all of which can be safely, naturally treated – and cured –not just “managed” with a drug that destroys your bones.

Because your digestion is compromised, you will be unable to effectively release the vitamins and minerals your bones require from the foods you eat. The nutrients in supplements do not have to be disassociated from foods; they become readily available with much less digestive effort. If you are not already taking AlgaeCal Plus and Triple Power, this is yet one more reason to do so: these supplements can greatly improve the availability to you of the nutrients your bones require.

Doctor Measuring blood pressure - blood pressure meds are drugs that cause osteoporosis

Loop Diuretics

Used to: Manage high blood pressure, heart failure, liver cirrhosis, and certain kidney diseases.

How and why the drug(s) cause bone loss: Loop diuretics directly increase urinary elimination of calcium, which causes a lowering of calcium’s concentration in the bloodstream. The lowering of calcium in the blood triggers the secretion of parathyroid hormone, which mobilizes calcium’s release from bone by increasing bone turnover.

Drug Information: Loop diuretics also increase sodium loss, often to the point of causing “hyponatremia,” an electrolyte disturbance in which the sodium ion concentration in the blood is lower than normal.  Approximately one-third of total body sodium resides in the bone, with 40% of bone sodium content being exchangeable with sodium in the bloodstream. A moderate but persistent loss of both bone sodium and calcium either indirectly, via an increased urination caused by loop diuretics, or directly, by hyponatremia [low sodium]-induced bone resorption, adversely impacts bone strength and increases fracture risk.

Hyponatremia also increases bone resorption by increasing osteoclasts’ formation and their bone resorbing activity.

Add to this the depletion in blood volume caused by all forms of diuretics, which increases the likelihood of dizziness when sitting up or rising into standing position (the medical term for this is “postural hypotension”), and you have the perfect set up for a fall, which further increases your risk for a fracture.

Loop diuretics may also deplete magnesium, which, after calcium, is the most important mineral required for bone health.50-56

The most recently published study discussing risk factors for osteoporosis, published in the May 2016 issue of the journal Endocrine, found loop diuretics increased odds for developing osteoporosis by a whopping 70%.

Only one other factor was found to increase risk for osteoporosis more than loop diuretics: former treatment with osteoporosis drugs, which increased odds of continuing to have osteoporosis by 350%! Think about what this tells us about the actual effects of these drugs on our bones!

In contrast to loop diuretics, the use of thiazide diuretics lowered odds of developing osteoporosis by 30% – and so did regular, heavy exercise.57

The takeaway here: if you must take a diuretic, use one of the thiazide diuretics (ask your doctor), and not a loop diuretic. And get some weight-bearing exercise – every day.

Anti-Coagulants

Used to: Some anti-coagulants prevent excessive blood clot formation, and others prevent deep vein thrombosis and pulmonary embolisms.

Commonly prescribed examples: There are several types, but low molecular weight types appear to be the least harmful to bone.

How and why the drug(s) cause bone loss: Anti-coagulants used to prevent excessive blood clot formation also prevent vitamin K recycling and therefore the activation of osteocalin, a vitamin K-dependent protein that brings calcium into bone, and matrix Gla protein, a vitamin K-dependent protein that prevents calcium from depositing in soft tissues, e.g., blood vessels, heart, kidneys, breast, brain.

Drug Information: The most common type of anti-coagulant does not impact cortical bone, but rapidly decreases trabecular bone volume by disrupting vitamin D metabolism and inducing secondary hyperparathyroidism, discussed above under Calcineurin Inhibitors. (If bones were like M&Ms, cortical bone would be the hard, outer candy shell and trabecular bone, the soft chocolate interior.) The result is a significant drop in osteoblast production and activity, and in osteoid surface in the bone. (Osteoids are what osteoblasts become after they begin depositing the bone matrix.)  In addition, these harmful effects are accompanied by a large increase in osteoclasts and bone resorption activity.58-59

The low molecular weight version may be less destructive to bone than other forms.  In contrast to the common unfractionated anti-coagulant, which is known to cause bone loss, a study just published (July 2016) found the use of the low-molecular-weight version during pregnancy did not increase loss of BMD.60-61

If you must continue to take an anti-coagulant, share this paper with your doctor and discuss switching to a low-molecular weight version. Also, consider taking Triple Power. Numerous studies show omega-3s – specifically compounds called “resolvins” that our bodies make when metabolizing EPA and DHA – prevent excessive blood clot formation (the medical term is thrombosis).62

Discuss with your doctor taking 2 tablespoons of Triple Power daily rather than the basic dose of 1 tablespoon. You might share the following two recent studies, which have shown (1) supplemental omega-3s greatly lessen likelihood of thrombus (clot) formation, (2) individuals with cardiovascular disease require a higher dose of omega-3s than those without cardiovascular issues.63-64

Thyroid Hormone Medications

Used to: Manage hypothyroidism (underactive thyroid). People are commonly given a synthetic thyroid hormone (a man-made version of thyroxine T4) sold under various trade names.

How and why the drug(s) cause bone loss: In 25% of patients, the dose of synthetic thyroid hormone prescribed is slightly higher than what is actually needed.65 Furthermore, an individual’s dosage requirement may change, so a dose that was initially right on may later turn out to be greater than what is needed. And too much thyroid hormone promotes bone loss.

Drug Information: A dose of synthetic thyroid hormone, even slightly in excess of need, causes suppression of TSH (thyroid-stimulating hormone). TSH directly protects bone by inhibiting the production of osteoclasts.66

In addition, low TSH is an indication of hyperthyroidism, a condition in which the thyroid is producing too much thyroid hormone (or in this case, in which the dose of supplemental thyroid hormone is too high). Hyperthyroidism significantly increases bone turnover and reduces bone mineral density (BMD). Although bone formation and bone resorption both increase, bone resorption far outpaces bone formation, so the end result is bone loss.

TSH should be monitored regularly and thyroid hormone dosage adjusted according to results in anyone on long-term thyroid hormone replacement therapy. This is rarely done. If you’re taking thyroid hormone, make sure you are checked at least twice yearly, and your dose adjusted if indicated.67-68

contraceptives cause osteoporosis

Contraceptives: Birth Control Pills, IUDs, Birth Control Shots

Used to: Prevent pregnancy. Oral contraceptives (birth control pills) contain either a combination of patented versions of estrogen (i.e., not bio-identical to normal human estrogen) along with patented versions of progesterone (called “progestins”) or just a progestin.

Birth control shots contain long-acting progestin-only contraceptive. They’re taken via injection every 3 months. IUDs that dispense the progestin are also often prescribed.

How and why the drug(s) cause bone loss:  Oral contraceptives lower blood levels of vitamin B6 and vitamin B12, causing levels of homocysteine to rise because its clearance requires these B vitamins. High levels of homocysteine promote inflammation and are associated with both cardiovascular disease and osteoporosis, in particular, with hip fractures.

Drug Information: One of the ways homocysteine harms bone, specifically, is by inhibiting an enzyme (called lysyl-oxydase) that plays an important role in collagen crosslink formation; this results in a weakened bone matrix. Homocysteine also causes the balance between RANKL and OPG to shift in favor of RANKL, promoting osteoclast production and activity. (RANKL and OPG are explained in the section on Glucocorticoids above.

Lastly, high homocysteine greatly increases oxidative stress (inflammation) throughout the body, another key instigator of osteoclast production and activity.69-70

Birth control pills, whether they contain only a patented version of estrogen or combine the “estrogen” with a “progestin,” patented analog of progesterone, work by inhibiting follicular development and preventing ovulation. For this reason, both types of birth control pills prevent ovulation and therefore formation of the corpus luteum, which is what produces progesterone. Birth control pills thus prevent the production of progesterone, and progesterone plays a key role in the development of osteoblasts.71-78

In the Canadian Multicentre Osteoporosis Study, oral contraceptive users had bone mineral density scores 2.3% to 3.7% lower than women who had never used oral contraceptives.79

One of the progestin-only contraceptives, medroxyprogesterone acetate, is the most widely used contraceptive worldwide. It’s given by injection every 3 months.

Because of its wide use in younger women and documentation that administration it may be associated with a loss of BMD, FDA has attached a black box warning to labels.80

Another progestin-only contraceptive, now being used in women as young as 14 years of age, is the IUD containing a progestin called levonorgestrel. IUDs containing levonorgestrel not only prevent ovulation, but typically cause amenorrhea (cessation of menstruation). Obviously, this is not helpful to young women, who are supposed to be building up their peak bone mass.

A recent meta-analysis estimated a BMD increase of 0.5% per year in women with normal ovulation, but a decrease in BMD of 0.7% per year in young women with ovulatory disturbances (anovulation—no ovulation, or short luteal phase). Studies show that they cause serious disturbances to your body.81


Drug-Induced Bone Loss Can Be Effectively Combatted

If you are having difficulty getting your doctor to monitor the effects on your bones of the medications you are being prescribed to manage — epilepsy, depression, anxiety or insomnia, restless leg syndrome, type 2 diabetes, chronic pain, allergies, asthma, autoimmune diseases, dry eyes, indigestion, heartburn, GERD, high blood pressure, liver disease, kidney disease, hypothyroidism, or use of birth control pills or IUDs – please share this information with your doctor.

The references cited are the most recent papers in the peer-reviewed medical journals. (And they include the PubMed IDs [PMID #], making it extremely quick and simple to locate these papers on PubMed). Educate your doctor, so you can get the health care you deserve. If your doctor refuses to become educated, find another, more competent physician.

Ideally, work with a physician knowledgeable about integrative, functional and/or naturopathic medicine, who can help you identify the underlying causes of your health issues and help you restore your health using effective and safe, natural means.

In the Resources section of Your Bones, I’ve provided a full list of medical organizations you can contact to help you find physicians in your area who can help you restore your health naturally. I cannot list them all here, but three such national groups are:

Your bones need all the nutrients they require to remodel, rebuild and maintain healthy structure and function.


Takeaways

Today we discussed 12 known drugs classes that cause bone loss. Unfortunately, these drugs are commonly prescribed. In fact, you may be taking one or more yourself right now…

If you are, know that you don’t wait for your bones to become weaker. Even if you must continue to take one or more of these drugs that cause bone loss, findings show that “active management” of bone loss in those with psychoactive drug-associated osteopenia/osteoporosis “can halt or even reverse this process.” And the same principle applies regardless of the drug category82

Intelligent “active management” means supplying your bones with optimal amounts of all the nutrients they require to remodel, rebuild and maintain healthful structure and function. You can do this by eating a healthful, whole foods, preferably organic, Mediterranean-type diet and taking AlgaeCal Plus and Triple Power.  And don’t forget regular weight-bearing exercise; it sends “build!” signals to your bones, improves your mood, keeps you trim, and boosts your energy.

Please share this information with friends and family

An ounce of prevention – in the form of a natural bone-building program targeted to combat the metabolic disturbances caused by these bone-busting drugs – can help prevent much needless misery.


Author: Lara Pizzorno, MDIV, MA, LMT

Best-selling author of “Your Bones: How You Can Prevent Osteoporosis and Have Strong Bones for Life – Naturally” and a member of the American Medical Writers Association with 30+ years of experience specializing in bone health. Lara is the Editor of Longevity Medicine Review (www.lmreview.com) as well as a Senior Medical Editor for SaluGenecists Inc., and Integrative Medicine Advisors, LLC.