The assessment of bone mineral content and density of the lumbar spine and proximal femur in US submariners.

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The submarine environment is unique in that there is limited space and no sunlight, which may negatively affect skeletal health and lead to accelerated bone loss, osteoporosis, and fractures.


The primary purpose of this study was to determine whether there was an association with submarine service, specifically time spent at sea, and bone mineral content (BMC) and bone mineral density (BMD) of the lumbar spine and dual proximal femur (total hip and femoral neck) measured by DXA.


This is a cross-sectional study of 462 submariners 20-91 years old. Variables included in the analysis were age, height, race, alcohol intake, tobacco use, fracture history, conditions, and medications known to cause bone loss and osteoporosis and submarine service.


Of the submarine service predictors, only serving onboard a diesel submarine was determined to be independently associated with a reduction in BMD of the total hip and femur neck, while no submarine service predictor increased the odds of having low BMD. In submariners 50+ years old, the age-adjusted prevalence of osteopenia was 15.7 % (lumbar spine) and 40.4 % (femur neck), while the prevalence of osteoporosis was 4.8 % (lumbar spine) and 4.2 % (femur neck), rates that did not differ from NHANES 2005-2008. In submariners <50 years old, 3.1 % was below the expected range for age. The proportion of submariners 50+ years old that met the FRAX criteria for pharmacological treatment was 12 %.


Intermittent periods of submergence that can range from a few days to 3+ months do not appear to compromise skeletal health differently than the general population.





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Gasier, HG, LM Hughes, CR Young and AM Richardson (2014). The assessment of bone mineral content and density of the lumbar spine and proximal femur in US submariners. Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 25(9). pp. 2225–2234. 10.1007/s00198-014-2753-y Retrieved from

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Heath Gasier

Associate Professor in Anesthesiology

I am a physiologist who joined Duke University in 2019 after retiring from military service. My research has focused on understanding how oxidant stress impacts cellular and systems physiology. Initially, I studied in humans how hyperbaric oxygen (HBO2) within the therapeutic range and high altitude influence nitric oxide production, antioxidant defenses, tissue oxygenation and muscle performance. This work sparked my interest in redox biology and led me to train under Dr. Claude A. Piantadosi at Duke University. Here, I began to study in mice and rats the impact of extreme HBO2 on the central nervous system (CNS). The objectives were to identify in rodents the origin and mechanisms of CNS oxygen toxicity, and test targeted pharmacological intervention strategies. It was during this time that I became interested in heme oxygenase 1 (HO-1). During my final military assignment, I continued to work on HBO2 and CNS oxygen toxicity related research (pharmacological intervention) and initiated new studies examining how HO-1 induction influences musculoskeletal health in diet-induced obesity. These studies led to follow-on work aimed at determining the mechanisms of HO-1 induction and mitochondrial dynamic regulation in an in vitro model of diet-induced obesity. In addition, I was involved in research aimed at understanding how antioxidants influence skeletal muscle mitochondrial dynamics in rodents and cells exposed heat stress and extreme high altitude.

Since returning to Duke University, I continue to conduct research focused on understanding how oxidant stress induced by HBO2 and obesity influences mitochondrial dynamic regulation in the brain, lung and skeletal muscle. I am now studying how sarcopenia and gender influence these responses. I am also involved (Co-I) in research testing the efficacy of a home-based high intensity interval training program in COVID-19 critical illness and early parenteral nutrition in abdominal trauma victims. In both of these studies, my efforts will be directed towards measuring inflammation and mitochondrial quality control responses to the interventions, which are linked to HO-1 activation.

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