Anxiety or depression disorders can develop as a result of acute or chronic stress, and depression is often coupled with anxiety. Both conditions can alter the HPA response.1 Aging further activates the HPA, producing more glucocorticoids and stronger feelings of stress, anxiousness, and depression.2

The key molecular mediators between psychological stress and bone health are believed to be growth hormones, glucocorticoids, and inflammatory cytokines. Stress alters the levels of growth hormones by modifying the HPA axis, growth hormone-releasing hormones, and growth hormone-inhibiting hormones. When this balance is upset by chronic stress, a decrease in growth hormones can develop, leading to bone loss.2

Chronic stress, long known to affect the body’s physical health, has been associated with obesity, atherosclerosis, lung conditions, and diabetes. How psychological stress affects disease is not well understood, but several studies have shown that stress hormone signaling via the brain-immune connection is a significant contributor. Chronic stress can alter blood cell and platelet production and increase systemic inflammation, which can, in turn, negatively affect osteoclasts and osteoblasts; however, researchers caution that the roles of inflammatory factors in osteoporosis and in psychological stress are highly complex, context-dependent, and dose-dependent.1


Continue Reading

Shared Risk Factors

Lifestyle-related risk factors for developing osteoporosis, such as smoking, alcohol use, and substance abuse, may be influenced by stress. Smoking, in particular is a strong risk factor for developing osteoporosis, although the link is not well understood. Alcohol consumption is a significant risk factor for developing osteoporosis as well. Substance abuse, such as opioid addiction, occurs more often in persons with psychological stress-associated mental health disorders. Research has found that women addicted to opioids have increased rates of osteopenia and osteoporosis. Obesity also may be a risk factor for osteoporosis because of increased inactivity, as exercise can increase bone mass and decrease risk of fracture. In addition, obesity can increase systemic inflammation and the risk for type 2 diabetes, another known risk factor associated with developing osteoporosis-related fractures.1

Related Articles

Treatment Considerations

In the United States alone, osteoporosis accounts for >1.5 million fractures/y, and by 2025, treatment costs are estimated to eclipse $25 billion. An in-depth understanding of the mechanisms that affect stress and bone health is essential for determining a patient’s risk and providing treatment recommendations. It is important to note that pharmacological therapies used for mental health disorders and osteoporosis may have interacting effects, so interventions should be carefully weighed when making treatment recommendations.2

Treatments for osteoporosis include the following, but their possible effect on psychological stress should be considered before prescribing:

• Bisphosphonates

• Statins

• Denosumab

• Teriparatide

• Estrogen/selective estrogen receptor modulator

• Strontium ranelate

• Beta-blockers

• Exercise

Complementary, alternative, and integrative remedies, such as fish oil, calcium, magnesium, and vitamin D supplements, may offer benefits with fewer risks than traditional pharmacological interventions.1

Researchers concluded that further study is warranted to understand the “whole-health effects” of chronic psychological stress on osteoporosis and to develop a more personalized plan of care for patients.1

Follow @EndoAdvisor

References

1. Wippert PM, Rector M, Kuhn G, Wuertz-Kozak K. Stress and alterations in bones: an interdisciplinary perspective. Front Endocrinol (Lausanne). 2017;8:96.

2. Kelly RR, McDonald LT, Jensen NR, Sidles SJ, Larue AC. Impacts of psychological stress on osteoporosis: clinical implications and treatment interactions. Front Psychiatry. 2019;10.

3. Azuma K, Adachi Y, Hayashi H, Kubo KY. Chronic psychological stress as a risk factor of osteoporosis. J UOEH. 2015;37(4):245-253.

This article originally appeared on Rheumatology Advisor