Dairy in adulthood: from foods to nutrient interactions on bone and skeletal muscle health

Abstract

The risk of fragility fractures exponentially increases with aging. Reduced mass and strength of both bone in osteoporosis and skeletal muscle in sarcopenia play a key role in the age-related incidence of fragility fractures. Undernutrition is often observed in the elderly, particularly in those subjects experiencing osteoporotic fractures, more likely as a cause than a consequence. Calcium (Ca), inorganic phosphate (Pi), vitamin D, and protein are nutrients that impact bone and skeletal muscle integrity. Deficiency in the supply of these nutrients increases with aging. Dairy foods are rich in Ca, Pi, and proteins and in many countries are fortified with vitamin D. Dairy foods are important souces of these nutrients and go a long way to meeting the recommendations, which increase with aging. This review emphaszes the interactions between these 4 nutrients, which, along with physical activity, act through cellular and physiological pathways favoring the maintenance of both bone and skeletal muscle structure and function.

Fig. 1.

Undernutrition and pathogenesis of hip fracture risk. Insufficiency in the 4 nutrients—Ca, Pi, vitamin D, and protein—can contribute to a reduction in both mass and strength of bone and skeletal muscle. The risk of falling is worsened by impairment in neuromuscular function and abnormalities in gait and balance. This dysfunction reduced the protective response that may prevent falling when stumbling. Undernutrition also decreases the soft tissue pad around the hip, thus increasing the impact of a fall on the proximal femur.

Fig. 2.

Need for additional Ca to reduce the risk of hip fracture with vitamin D supplementation. Evidence from a comparative meta-analysis of randomized controlled trials that oral vitamin D appears to reduce the risk of hip fracture only when Ca supplementation is added. The figure shows two forest plots of the risk of hip fracture between vitamin D and either placebo/no-treatment groups (left panel) or between vitamin D and Ca and placebo/no-treatment groups (right panel). The pooled estimate of the relative risk was statistically significant only with the combination of vitamin D and Ca. Adapted from Boonen et al. [28].

Fig. 3.

Schematic interaction of vitamin D and dietary protein on renal 1,25(OH)D production and thereby on intestinal Ca absorption. The transfer of dietary Ca from the intestinal lumen to the blood is stimulated by 1,25(OH)D, the renal production of which depends on its substrate, 25OHD, and IGF-I. The mechanism of intestinal Ca translocation depends of the presence of the vitamin D receptor (VDR), which in turn influences the transcription of several factors that are implicated in the transport of Ca across either the luminal or basolateral membranes or through the intracellular compartment of the enterocyte. CYP27B1: 25 hydroxyvitamin D-1α hydroxylase, TRPV6 = transient receptor potential cation channel, subfamily V, member 6, Calbindins = Ca binding proteins, PMCA1b = plasma membrane Ca ATPase 1b (Color figure available online.)

Fig. 4.

Bone mineralization process involving the interaction of Pi and Ca. (A) Bone forming cells, either osteoblasts or epiphyseal chondrocytes form vesicles, which bud from the plasma membrane and migrate in the nonmineralized organic matrix. (B) Matrix vesicles have the capacity to accumulate Pi through an Na-dependent Pi transporter, the driving force, and Ca through annexin channels. This accumulation leads to the formation of an impure form of hydroxyapatite crystal and its subsequent association with the collagen fibrils of the organic matrix. The bone forming cells are endowed with IGF-I receptor. The binding of IGF-I to this receptor stimulates the protein expression (mRNA) of the Na-dependent Pi transporter, which migrates to the plasma membrane of the bone forming cells. Adapted from Bonjour [12] (Color figure available online.)

Fig. 5.

Influence of phosphate on the urinary (A) and balance (B) of Ca in healthy adults. Results from a meta-analysis of intervention studies indicate that higher phosphate intakes were associated with decreased urine Ca (A) and increased Ca retention (B). The change in slope was not different whether the Ca intake was low (dotted regression line) or high (continuous regression line), indicating the absence of interaction in relation with the amount of dietary Ca. Adapted from Fenton et al. [66].

Fig. 6.

Interaction between dietary protein and mechanical loading on skeletal muscle cell. Dietary protein increases serum amino acids and IGF-I, which, through transporter and receptor localized in the skeletal muscle sarcolemma exert, through a complex intracellular pathway, an anabolic effect. Contractile forces resulting from mechanical loading also stimulate a complex molecular cascade. These pathways impact on the mammalian target of rapamycin complex (mTOR), which enhances several translation factors (70-kDa ribosomal protein S6, eukaryotic elongation factor 2, ribosomal protein S6). This simplified illustration schematizes the combined effects of dietary proteins, through amino acids and IGF-I, and mechanotransduction-mediated anabolic cell signaling on skeletal muscle mass and strength. Adapted from Pasiakos [93] (Color figure available online.)