Osteoporosis and depression are major health problems of crisis proportions in postmenopausal women. Researchers have established a relationship between bone loss and depression, although few studies have focused on postmenopausal women. The purposes of this integrative review were to synthesize and summarize the available literature on: 1) the associations between bone loss and depression in postmenopausal women; and 2) potential variables that impact the associations between bone loss and depression in postmenopausal women. After searching the databases PubMed, CINAHL, Embase, and the Cochrane library between 2007 and 2017, 12 articles met the inclusion criteria. The majority of the included studies supported the relationship between depression and bone loss in postmenopausal women, although little information is offered as to why this relationship exists. This review summarizes the research that has been completed on depression and bone loss in postmenopausal women and identifies gaps in the literature. These findings will aid in the planning of future research and the development of health care recommendations.

In the United States, over 34 million American post-menopausal women have low bone mass (osteopenia) which increases their risk of osteoporosis and fractures. Calcium, vitamin D and exercise are recommended for prevention of osteoporosis, and bisphosphonates (BPs) are prescribed in women with osteoporosis. BPs may also be prescribed for women with low bone mass, but are more controversial due to the potential for adverse effects with long-term use. A bone loading exercise program (high-impact weight bearing and resistance training) promotes bone strength by preserving bone mineral density (BMD), improving bone structure, and by promoting bone formation at sites of mechanical stress. The sample for this study will be 309 women with low bone mass who are within 5 years post-menopause. Subjects are stratified by exercise history (≥2 high intensity exercise sessions per week; < 2 sessions per week) and randomized to a control or one of two treatment groups: 1) calcium + vitamin D (CaD) alone (Control); 2) a BP plus CaD (Risedronate); or 3) a bone loading exercise program plus CaD (Exercise). After 12 months of treatment, changes in bone structure, BMD, and bone turnover will be compared in the 3 groups. Primary outcomes for the study are bone structure measures (Bone Strength Index [BSI] at the tibia and Hip Structural Analysis [HSA] scores). Secondary outcomes are BMD at the hip and spine and serum biomarkers of bone formation (alkaline phosphase, AlkphaseB) and resorption (Serum N-terminal telopeptide, NTx). Our central hypothesis is that improvements in bone strength will be greater in subjects randomized to the Exercise group compared to subjects in either Control or Risedronate groups. Our research aims to decrease the risk of osteoporotic fractures by improving bone strength in women with low bone mass (pre-osteoporotic) during their first 5 years’ post-menopause, a time of rapid and significant bone loss. Results of this study could be used in developing a clinical management pathway for women with low bone mass at their peak period of bone loss that would involve lifestyle modifications such as exercises prior to medications such as BPs. Clinicaltrials.gov NCT02186600 . Initial registration: 7/7/2014.

Suppression of insulin-like growth factor 1 (IGF-1) and leptin secondary to low energy availability (LEA) may contribute to adverse effects on bone health. Whether a high-protein diet attenuates these effects has not been tested. Seven men completed three five-day conditions operationally defined as LEA (15 kcal kg fat-free mass (FFM)⁻¹·day⁻¹) with low protein (LEA-LP; 0.8 g protein·kg body weight (BW)⁻¹), LEA with high protein (LEA-HP; 1.7 g protein·kg BW⁻¹) and control (CON; 40 kcal·kg FFM⁻¹·day⁻¹, 1.7 g protein·kg BW⁻¹). In all conditions, participants expended 15 kcal·kg FFM⁻¹·day⁻¹ during supervised cycling sessions. Serum samples were analyzed for markers of bone turnover, IGF-1 and leptin. The decrease in leptin during LEA-LP (−65.6 ± 4.3%) and LEA-HP (−54.3 ± 16.7%) was greater than during CON (−25.4 ± 11.4%; p = 0.02). Decreases in P1NP (p = 0.04) and increases in CTX-I (p = 0.04) were greater in LEA than in CON, suggesting that LEA shifted bone turnover in favour of bone resorption. No differences were found between LEA-LP and LEA-HP. Thus, five days of LEA disrupted bone turnover, but these changes were not attenuated by a high-protein diet.