During the University of Colorado Department of Medicine’s annual Research Day, Associate Professor Christine Swanson, MD, MCR, delivered insights from her clinical research exploring the relationship between sleep and osteoporosis prevention.
Swanson, part of the Division of Endocrinology, Metabolism, and Diabetes, highlighted the complexity of osteoporosis—a condition typically associated with hormonal changes, aging, and lifestyle—but often lacking clear explanations in some patients.
Swanson emphasized the importance of investigating novel risk factors for osteoporosis, particularly those that coincide with life’s changes, such as sleep patterns.
She pointed out that individuals achieve their peak bone mineral density in their early to mid-20s, with men generally having higher density than women. This peak is crucial as it significantly influences the risk of fractures later in life.
As people age, their bone density tends to stabilize for a few decades until women reach menopause and men grow older, both of which are periods characterized by an accelerated decline in bone density.
Similarly, sleep patterns also deteriorate with age. People tend to experience shorter sleep durations, longer times to fall asleep, and a reduction in deep, restorative sleep known as slow-wave sleep.
Swanson further explained the intrinsic connection between sleep and bone health by discussing how genes regulating our internal clocks are also present in bone cells. These cells are active in bone formation and resorption—the process of bone renewal.
This activity is rhythmic and impacts the release of specific substances into the blood, which indicate the level of bone turnover.
Interestingly, the rhythm is more pronounced in bone resorption than in bone formation, suggesting that disturbances in sleep and circadian rhythms might directly affect bone health.
To delve deeper into how sleep impacts bone health, Swanson conducted a study where participants lived in a controlled environment without any cues of time, simulating the effects of jet lag or shift work by following a 28-hour daily schedule.
This setup mimicked severe circadian disruption and reduced sleep typical of night shift workers or frequent travelers.
The study revealed significant changes in bone turnover markers after this sleep and circadian rhythm disruption.
Both men and women showed declines in bone formation markers, with younger individuals experiencing more pronounced declines. Young women, in particular, displayed significant increases in bone resorption markers.
These findings suggest that insufficient bone formation coupled with increased bone resorption could, over time, lead to significant bone loss, increasing the risk of osteoporosis and fractures.
Swanson pointed out that younger women might be particularly vulnerable to these adverse effects of poor sleep on bone health.
Through her research, Swanson aims to shed light on the critical yet often overlooked link between sleep quality and bone health.
Her findings advocate for the importance of maintaining regular sleep patterns as a potential strategy for osteoporosis prevention, especially in populations at higher risk due to age and gender.
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The research findings can be found in the Journal of Clinical Endocrinology & Metabolism.
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