Anabolic Osteoporosis

Anabolic Osteoporosis

Written by Ben Bunting: BA, PGCert. (Sport & Exercise Nutrition) // British Army Physical Training Instructor // S&C Coach.


Anabolic osteoporosis is a condition that can occur as a result of long-term use of anabolic steroids.

These steroids, often used by athletes and bodybuilders to enhance muscle growth and performance, can have detrimental effects on bone health.

This article delves into the connection between anabolic steroids and osteoporosis, highlighting the risks and providing crucial information for those considering or currently using these substances.

Understanding Anabolic Steroids and Osteoporosis

Anabolic steroids are synthetic substances that mimic the effects of testosterone in the body.

While they can have benefits for muscle growth and athletic performance, they also come with serious risks, including the development of osteoporosis.

Osteoporosis is a condition characterized by weak and brittle bones, making individuals more susceptible to fractures and other bone-related issues.

This article aims to provide a comprehensive understanding of the link between anabolic steroids and osteoporosis, shedding light on the potential dangers and encouraging informed decision-making when it comes to steroid use.

How Anabolic Steroids Affect Bone Health

Anabolic steroids have a direct impact on bone health, and not in a positive way.

These synthetic substances interfere with the normal process of bone remodeling, which is essential for maintaining strong and healthy bones.

Research shows that steroids disrupt the balance between bone formation and bone resorption, leading to a net loss of bone density over time.

This loss of bone density increases the risk of fractures and osteoporosis.

Additionally, a study published in 2000 demonstrates that steroids can also decrease the production of collagen, a protein that provides structural support to bones.

This further weakens the bones and makes them more susceptible to injury. It is crucial for individuals considering steroid use to understand the potential consequences on their bone health and make informed decisions to protect their long-term well-being.

The Risks and Side Effects of Steroid Use

The use of anabolic steroids comes with a range of risks and side effects, including those that directly impact bone health.

Other side effects of steroid use include hormonal imbalances, liver damage, cardiovascular problems, and psychological effects.

It is important for individuals considering steroid use to weigh these risks and make informed decisions about their health and well-being.

Preventing and Treating Osteoporosis in Steroid Users

If you are using anabolic steroids or considering their use, it is crucial to take steps to prevent and treat osteoporosis.

First and foremost, it is important to consult with a healthcare professional who can provide guidance and monitor your bone health.

They may recommend regular bone density scans to assess your bone density and identify any changes over time.

Additionally, they may prescribe medications such as bisphosphonates or hormone replacement therapy to help prevent bone loss and maintain bone strength.

It is also important to engage in weight-bearing exercises, such as walking or weightlifting, as these activities can help improve bone density.

Finally, ensuring a balanced diet that includes adequate calcium and vitamin D is essential for maintaining strong bones.

By taking these proactive measures, individuals using anabolic steroids can minimize their risk of developing osteoporosis and protect their long-term bone health. 

Anabolic Osteoporosis Treatments

Teriparatide is an anabolic agent prescribed to postmenopausal osteoporosis patients to increase bone mineral density (BMD) and decrease vertebral and non-vertebral fracture rates, and also used in men and glucocorticoid-induced osteoporosis patients; its benefits may wane over time though.

Current pharmaceutical treatments for osteoporosis aim to decrease bone resorption but do not restore disordered skeletal architecture. Only osteoanabolic agents such as teriparatide, abaloparatide and romosozumab stimulate bone formation.

Anti-resorptive agents

Though advances have been made in osteoporosis therapy, current options remain limited and only enable modest increases in bone mineral density (BMD) and reduction of nonvertebral fractures by 20% to 40%.3, it remains important for those at high risk of fracture to consider using anabolic agents with antiresorptive therapies as treatment options.

Current anabolic agents available include bisphosphonates, SERMs and calcitonin. While these drugs have been shown to help decrease skeletal fractures, their effectiveness depends on both timing of administration and magnitude of change in bone strength.

Anabolic agents aid bone formation through direct actions on cells within the bone marrow, while also being capable of inhibiting loss. Anabolics accomplish this feat by increasing mesenchymal stem cell differentiation into mature osteoblasts and suppressing bone-resorbing factors like Sclerostin/Wnts expression.

These agents also impact the osteoblast-marrow axis by increasing secretion of parathyroid hormone (PTH) and PTH-related peptide (PTHrP), both acting through PTH receptors to have mitogenic properties for cells within the osteoblast lineage, while inhibiting osteoblast apoptosis.

They also induce expression of IGF-1, an anabolic agent known for stimulating mesenchymal stem cells to differentiate into osteoblasts while suppressing Notch signaling involved with suppressed differentiation and osteoporosis.

PTH, Teriparatide and Abaloparatide exert their anabolic effects by acting directly as agonists on the osteoblast-marrow axis.

By increasing calcium ion concentrations within bone marrow while simultaneously raising levels of phosphorus in bloodstream they are able to accelerate bone formation while simultaneously blocking activation of RANKL which serves as receptor for bone-resorbing factor transforming growth factor beta (TGF).

This prevents osteoclasts from breaking down bone by blocking activation of TGF receptor activation via blocking activation of TGF receptor RANKL receptor which activated via blocking activation of TGF TGF TGF.

Abaloparatide's recent research shows that PTH and teriparatide, when administered together for 12 months, significantly improve femoral strength compared to either medication used alone. However, due to being conducted on only a limited sample size of patients this result should be interpreted with care.

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Anti-remodeling agents

Antiresorptive agents like bisphosphonates and denosumab can be effective medications in improving bone mineral density (BMD) and decreasing fracture risk.

However, they cannot restore bone mass or architecture and therefore the risk of fragility fracture remains high.

Anabolic treatment may be more suitable in these high risk patients with recent or recurrent fractures, very low BMD, glucocorticoid use and falls to promote mass gain while simultaneously decreasing fracture risk.

Bone is an intricate tissue that undergoes continuous remodelling to maintain homeostasis in both health and disease.

This is through an equilibrium between bone resorption and formation, controlled by osteoclasts responsible for clearing away dead bone fragments in fracture healing, while anabolic therapies, like teriparatide and abaloparatide, promote bone formation by inhibiting osteoclast activity.

There are other cellular and molecular mechanisms involved with bone formation regulation including cytokines, chemokines and growth factors; all potential targets but their development and delivery into skeletal organs is complex.

Studies of sequential and combination treatments for osteoporosis have explored various sequential and combination medications designed to increase bone mineral density (BMD) and decrease fracture risk.

Evidence shows that one course of teriparatide significantly increasing BMD while decreasing vertebral and non-vertebral fractures in postmenopausal women.

Teriparatide/denosumab treatment appears to produce greater BMD gains and reductions of vertebral and non-vertebral fractures than either drug alone.

These results demonstrate that taking a multimodal approach may be the best strategy for producing significant skeletal benefits for patients with established osteoporosis.

Physicians must however carefully consider which sequence of antiresorptive and anabolic treatments to implement for maximum efficacy.


Teriparatide is an anti-osteoporosis treatment administered through subcutaneous injection.

It increases bone mineral density among postmenopausal women and men, prevents vertebral fractures and improves skeletal microarchitecture/volume/microarchitecture as well as decreasing risk of non-vertebral fractures.

This makes it the only licensed anabolic agent proven to improve fracture outcomes.

It is also effective against male osteoporosis as well as glucocorticoid-induced osteoporosis. Taken subcutaneously daily, subcutaneous injection is recommended.

Most antiresorptive agents for osteoporosis inhibit bone resorption and remodeling, so are generally classified as antiresorptive agents.

Recombinant parathyroid hormone (iPTH) and teriparatide stand out by stimulating bone formation via binding to R0 conformations PTH1 receptors which have higher affinity than N1 ones.

Additionally they only last 24 months before bone resorption outweighs bone formation limiting their use further.

Studies have revealed that when treatment ceases, its anabolic effect diminishes significantly, although why this happens is unknown.

Potential theories include downregulation of PTH1R or depletion of bone cell precursors.

Therefore, to maintain these anabolic benefits it may be beneficial to combine teriparatide with another antiresorptive agent like bisphosphonates in order to extend its anabolic benefits for longer.

Studies have demonstrated that when combined, teriparatide and bisphosphonates can work to decrease both vertebral and non-vertebral fractures.

This is likely due to how bisphosphonates interfere with calcitonin's action on bone resorption by blocking its enzyme.

One method for increasing bone density with Teriparatide is cyclical treatment, where patients take three months on and three off every year of taking it.

Although cyclical treatment was found to provide less overall benefit than continuous use, it did significantly reduce vertebral fracture rates.

Teriparatide is one of the more costly therapies approved, yet it still helps reduce vertebral and non-vertebral osteoporosis fractures and increase BMD.

Furthermore, its side effects include low risk of osteosarcoma complications. As with all therapies, however, this one must be discussed thoroughly with patients and their healthcare team.

Risk must be communicated effectively so as to strike an appropriate balance between potential osteosarcoma risks and clinical benefits of taking this drug.


Abaloparatide is an anabolic medication designed to increase bone density by targeting PTH receptors, and has been shown to decrease fracture risk among postmenopausal women with osteoporosis.

Taken as a monthly injection, Abaloparatide represents the first anabolic medication ever shown to reduce fractures risk.

However, while it does not represent a cure, this therapy can improve quality of life for people living with osteoporosis while possibly eliminating surgical interventions required to treat hip fractures after having had hip replacement or other orthopedic surgeries.

Abaloparatide differs from teriparatide by having a shorter activation time and less of an effect on calcium absorption.

Studies have demonstrated it to stimulate osteoclast-mediated calcium release from bone, increase distal renal tubular calcium reabsorption.

However, it has significantly less of an impact on intestinal calcium absorption, reduce vertebral and nonvertebral fractures among women with osteoporosis, improve their skeletal outcomes after 18 months of treatment, as well as decrease osteoporosis-related fractures among them.

The drug, a pyridinic acid amide, is taken orally and excreted through urine. With an active half-life of 1.7 hours and rapid excretion by nonspecific proteolytic degradation, it does not lead to hypercalcemia in healthy volunteers and tolerated by those with renal impairment.

While studies in rats have implicated it with increased risks of bone cancer (osteosarcoma), its effect in humans remains unknown and therefore it should not be taken by those with breast or prostate cancer history or family histories of bone cancer risk.

Individuals living with osteoporosis should visit their physicians and participate in an osteoporosis support group to increase awareness and discuss management methods. Regular appointments with rheumatologists, endocrinologists and orthopedists for monitoring of calcium and phosphorus levels as well as fracture evaluation are also advised.

Additionally, a physician can recommend exercise programs designed to strengthen bones while also offering nutritional recommendations that can lower the risk of osteoporosis.


Long-term use of steroids (glucocorticoids) may result in osteoporosis - a condition where bones become fragile and fractures more likely.

This occurs because glucocorticoids reduce levels of calcium and phosphorous that are essential to bone formation.

Postmenopausal women taking oral steroids could experience rapid bone loss as a result.

It's vital that individuals taking anabolic steroid medications discuss potential bone loss risks with their healthcare provider in order to mitigate against possible loss as soon as possible or treat it.

Corticosteroid-induced osteoporosis is a prevalent issue, commonly occurring among those suffering from asthma, rheumatoid arthritis, lupus and inflammatory bowel disease.

Other conditions causing this bone loss include adrenal disease, pituitary disorders multiple sclerosis cancer.

The rate of bone loss depends on length and dose of use as well as genetics and environmental factors; typically most rapid bone loss occurs six months post initiation of oral steroid medication while inhaled steroids may less likely impact bone density than oral versions.

To combat anabolic osteoporosis numerous anabolic agents have been developed, including teriparatide, abaloparatide and romosozumab. Each of these compounds helps increase bone formation and BMD through unique mechanisms.

Teriparatide and abaloparatide are synthetic analogues of PTH with differing affinity for the calcineurin receptor (Rg1).

Abaloparatide has greater affinity for R0 conformation of Rg1, and thus less tendency to cause transient bone loss at cortical sites.

Romosozumab is a monoclonal antibody against Sclerostin produced naturally by osteoclasts to suppress bone formation; loss-of-function mutations of Sclerostin lead to bone mass disorder Sclerosteosis. Thus increasing BMD while simultaneously decreasing resorption by inhibiting Sclerostin-RANK ligand interaction.

Anabolic therapies have demonstrated greater efficacy than antiresorptive medications at preventing fractures, but are limited by cost and parenteral administration requirements.

Recently published health technology assessments (HTAs) indicate that both teriparatide and romosozumab may be cost-effective solutions in patients at very high risk for fracture.

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