Relationship between sodium intake and bone fragility in postmenopausal women

Presentation Number: SAT-261
Date of Presentation: June 15th, 2013

Kiyoko Nawata*1, Mika Yamauchi2, Shin Takaoka2, Ken-ichiro Tanaka2 and Toshitsugu Sugimoto2
1The University of Shimane, Matsue, Japan, 2Shimane University Faculty of Medicine, Izumo, Japan


Objectives: High sodium intake through salts can lead to increased calcium excretion. In addition, due to competition between sodium and calcium ions, reabsorption of calcium in the kidney is decreased. Increased sodium intake is positively correlated with urinary Ca excretion, and related to negative Ca balance. Excessive sodium intake has been reported to be associated with increases in bone resorption markers and decrease of bone mineral density (BMD). However, it remains unknown whether excessive sodium intake is related to the risk of fracture. We therefore examined the relationship between sodium intake and bone fragility and investigated whether this relationship was influenced by BMD, bone metabolic markers, intake of other nutrients and motor function. Methods: Subjects were 213 healthy postmenopausal women who had undergone osteoporosis screening. Levels of Ca, P, intact PTH, 25(OH)D, N-terminal propeptide of type I collagen (PINP) and C-terminal cross-linked telopeptide of type I collagen (CTX) were measured. The BMD of the lumbar spine (L2-4) and femoral neck (FN) was measured using DXA, the presence or absence of morphological vertebral fracture was determined, and the presence or absence of existing non-vertebral fracture was determined through physician interviews. Nutrient intakes (proteins, Ca, Mg, P, Na, vitamin D, vitamin K) were calculated using the Food Frequency Questionnaire (FFQ). Motor function tests included standing on one foot with closed eyes test and grip strength. Results: Mean values of age and BMI were 63±8 years and 22.9±3.1kg/m2, respectively. Sodium intake was 5211±1697mg. Levels of intact PTH, 25(OH)D, PINP, and CTX were 46±15pg/ml, 16.3±4.4ng/ml, 54.3±16.5ng/ml, and 0.40±0.15ng/ml, respectively, and levels of L2-4 and FN BMD were 0.84±0.15g/cm2 (T score -1.5±1.3, Z score 0.3±1.1) and 0.62±0.09g/cm2 (-1.5±0.8, 0.1±1.0), respectively. Sodium intake was not correlated with BMD, bone metabolic markers, muscle strength and balance ability. Logistic regression analysis of the effects of nutrient intake (divided into quartiles) on the risk of fracture revealed that highest sodium intake group (mean value 7561±1035mg) was a significant risk factor for non-vertebral fracture (odds ratio, 4.1(95%CI: 1.4-11.6), p<0.01) even after adjustments for age, BMI, intact PTH, 25(OH)D, CTX, BMD, and intake of other nutrients, standing on one foot with closed eyes test and grip strength.

Conclusion: These findings suggest that excessive sodium intake is a risk factor for bone fragility independent of BMD, bone metabolic markers, muscle strength and balance ability. It is important to consider excessive sodium intake in diet therapy for osteoporosis.


Nothing to Disclose: KN, MY, ST, KIT, TS